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ESP: PubMed Auto Bibliography 25 Jun 2026 at 01:55 Created:
Microbiome
It has long been known that every multicellular organism coexists with large prokaryotic ecosystems — microbiomes — that completely cover its surfaces, external and internal. Recent studies have shown that these associated microbiomes are not mere contamination, but instead have profound effects upon the function and fitness of the multicellular organism. We now know that all MCEs are actually functional composites, holobionts, composed of more prokaryotic cells than eukaryotic cells and expressing more prokaryotic genes than eukaryotic genes. A full understanding of the biology of "individual" eukaryotes will now depend on an understanding of their associated microbiomes.
Created with PubMed® Query: microbiome[tiab] NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2026-06-22
CmpDate: 2026-06-22
Application of 16S rRNA gene amplicon sequencing in the investigation of novel ovine skin lesions in Norway.
Frontiers in veterinary science, 13:1802983.
BACKGROUND: Contagious ovine digital dermatitis (CODD) is a globally emerging polymicrobial foot disease in sheep that causes severe welfare and economic problems. Currently, there is no validated commercial laboratory diagnostic test for CODD, and the current 'gold standard' is the pathological scoring of foot lesions. In this study, we used a combination of gross pathological lesion scoring and 16S rRNA gene amplicon sequencing of the bacterial microbiome to investigate novel suspected CODD foot lesions identified in three Norwegian abattoirs.
METHODS: We conducted 16S rRNA gene amplicon sequencing of biopsy samples from novel Norwegian foot lesions (n = 30), footrot lesions (n = 7), and healthy skin (n = 30), and the results were compared with sequenced biopsy samples from a previous study of sheep from the United Kingdom (UK) with CODD lesions (n = 31) and healthy foot skin (n = 7). A UK veterinarian with clinical experience in CODD performed the pathological scoring of the novel Norwegian foot lesions using photographic images collected at the Norwegian abattoirs.
RESULTS: Gross pathology and bacterial microbiome compositional analysis revealed that the novel CODD-like lesions were pathologically and bacteriologically distinct from healthy skin, CODD lesions, and footrot lesions. The novel CODD-like lesions presented as ulceration in the skin region immediately dorsal to the coronary band, extending distally below the carpus/tarsus, and were associated with hair loss, haemorrhage, and crusting. A comparison of the bacterial microbiota in the novel CODD-like lesions with those found in healthy skin, CODD lesions, and footrot lesions revealed that the bacterial communities were significantly different in terms of diversity, phylogeny, and microbial composition.
CONCLUSION: Gross pathological lesion description, used in combination with 16S rRNA gene sequencing of the bacterial microbiome, demonstrated that the novel Norwegian skin lesions involved a dysbiosis that differed substantially from what has been previously described for CODD lesions and that the lesions were highly unlikely to be CODD. Further studies on the aetiopathogenesis of this novel sheep hoof condition should enable improved diagnosis.
Additional Links: PMID-42328067
PubMed:
Citation:
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@article {pmid42328067,
year = {2026},
author = {Duncan, JS and Angell, JW and Lenzi, L and Liu, X and Staton, GJ and Evans, NJ and Gilhuus, M},
title = {Application of 16S rRNA gene amplicon sequencing in the investigation of novel ovine skin lesions in Norway.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1802983},
pmid = {42328067},
issn = {2297-1769},
abstract = {BACKGROUND: Contagious ovine digital dermatitis (CODD) is a globally emerging polymicrobial foot disease in sheep that causes severe welfare and economic problems. Currently, there is no validated commercial laboratory diagnostic test for CODD, and the current 'gold standard' is the pathological scoring of foot lesions. In this study, we used a combination of gross pathological lesion scoring and 16S rRNA gene amplicon sequencing of the bacterial microbiome to investigate novel suspected CODD foot lesions identified in three Norwegian abattoirs.
METHODS: We conducted 16S rRNA gene amplicon sequencing of biopsy samples from novel Norwegian foot lesions (n = 30), footrot lesions (n = 7), and healthy skin (n = 30), and the results were compared with sequenced biopsy samples from a previous study of sheep from the United Kingdom (UK) with CODD lesions (n = 31) and healthy foot skin (n = 7). A UK veterinarian with clinical experience in CODD performed the pathological scoring of the novel Norwegian foot lesions using photographic images collected at the Norwegian abattoirs.
RESULTS: Gross pathology and bacterial microbiome compositional analysis revealed that the novel CODD-like lesions were pathologically and bacteriologically distinct from healthy skin, CODD lesions, and footrot lesions. The novel CODD-like lesions presented as ulceration in the skin region immediately dorsal to the coronary band, extending distally below the carpus/tarsus, and were associated with hair loss, haemorrhage, and crusting. A comparison of the bacterial microbiota in the novel CODD-like lesions with those found in healthy skin, CODD lesions, and footrot lesions revealed that the bacterial communities were significantly different in terms of diversity, phylogeny, and microbial composition.
CONCLUSION: Gross pathological lesion description, used in combination with 16S rRNA gene sequencing of the bacterial microbiome, demonstrated that the novel Norwegian skin lesions involved a dysbiosis that differed substantially from what has been previously described for CODD lesions and that the lesions were highly unlikely to be CODD. Further studies on the aetiopathogenesis of this novel sheep hoof condition should enable improved diagnosis.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Canine Tooth Microbiome Gingival Index: a new microbiome-derived measure of gingival health validated by nutritional intervention.
Frontiers in veterinary science, 13:1839039.
INTRODUCTION: Periodontitis affects over 80% of dogs over 3 years of age, progressing irreversibly from gingivitis due to an imbalance in the subgingival microbial community that triggers an immune response. Early diagnosis of gingivitis is challenging, often relying on visible redness or bleeding noticed by pet owners or professionals. Therefore, an easy-to-interpret, clinically relevant, and responsive measurement tool based on the subgingival microbiome is needed to facilitate early diagnosis of oral health issues. We developed the Canine Tooth Microbiome Gingival Index (CTMGI), a single-score metric derived from subgingival plaque microbiome data and machine learning models, and validated its responsiveness via nutritional intervention.
METHODS: We collected subgingival plaque microbiome profiles from 692 tooth samples of 347 dogs, generated through 16S amplicon sequencing. For the machine learning models, the tooth gingivitis scores were dichotomized into healthy (gingivitis score <3) and unhealthy (gingivitis score ≥3), along with other clinical scores such as tooth recession, pocket depth, and attachment loss. The raw data were split into training and test sets, and five distinct machine learning models were employed to identify features that distinguish healthy from gingivitis sites.
RESULTS: The two top-performing models-random forest and logistic regression-yielded 22 unique features. These 22 features included the sum of early and late colonizers, the phyla actinobacteria and proteobacteria, and other bacterial species. The CTMGI was derived from the 22 features, categorized as "positive" or "negative" based on their influence on gingivitis. The CTMGI classification cutoff score was set at -0.12 with a Receiver Operating Characteristics-Area Under the Curve (ROC-AUC) of 0.761, a sensitivity of 0.701, and a specificity of 0.752. A score greater than -0.12 was found to indicate a "healthy" gingival condition; otherwise, it indicated "unhealthy." Furthermore, we conducted a nutritional intervention study to validate the responsiveness of the CTMGI, in which the test food, which has documented oral health benefits, resulted in a significantly higher CTMGI score (1.32) compared to the control food, which offers no oral health benefits (0.66).
DISCUSSION: Overall, this study developed and validated a quantitative, single-score, microbiome-based metric that is clinically translatable for the assessment of early-stage canine gingival health. Furthermore, its demonstrated responsiveness to nutritional intervention suggests that this index can serve as a prognostic measure.
Additional Links: PMID-42328069
PubMed:
Citation:
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@article {pmid42328069,
year = {2026},
author = {Hollar, R and Cochrane, CY and Green, N and Coffman, L and Scherl, D and Badri, DV},
title = {Canine Tooth Microbiome Gingival Index: a new microbiome-derived measure of gingival health validated by nutritional intervention.},
journal = {Frontiers in veterinary science},
volume = {13},
number = {},
pages = {1839039},
pmid = {42328069},
issn = {2297-1769},
abstract = {INTRODUCTION: Periodontitis affects over 80% of dogs over 3 years of age, progressing irreversibly from gingivitis due to an imbalance in the subgingival microbial community that triggers an immune response. Early diagnosis of gingivitis is challenging, often relying on visible redness or bleeding noticed by pet owners or professionals. Therefore, an easy-to-interpret, clinically relevant, and responsive measurement tool based on the subgingival microbiome is needed to facilitate early diagnosis of oral health issues. We developed the Canine Tooth Microbiome Gingival Index (CTMGI), a single-score metric derived from subgingival plaque microbiome data and machine learning models, and validated its responsiveness via nutritional intervention.
METHODS: We collected subgingival plaque microbiome profiles from 692 tooth samples of 347 dogs, generated through 16S amplicon sequencing. For the machine learning models, the tooth gingivitis scores were dichotomized into healthy (gingivitis score <3) and unhealthy (gingivitis score ≥3), along with other clinical scores such as tooth recession, pocket depth, and attachment loss. The raw data were split into training and test sets, and five distinct machine learning models were employed to identify features that distinguish healthy from gingivitis sites.
RESULTS: The two top-performing models-random forest and logistic regression-yielded 22 unique features. These 22 features included the sum of early and late colonizers, the phyla actinobacteria and proteobacteria, and other bacterial species. The CTMGI was derived from the 22 features, categorized as "positive" or "negative" based on their influence on gingivitis. The CTMGI classification cutoff score was set at -0.12 with a Receiver Operating Characteristics-Area Under the Curve (ROC-AUC) of 0.761, a sensitivity of 0.701, and a specificity of 0.752. A score greater than -0.12 was found to indicate a "healthy" gingival condition; otherwise, it indicated "unhealthy." Furthermore, we conducted a nutritional intervention study to validate the responsiveness of the CTMGI, in which the test food, which has documented oral health benefits, resulted in a significantly higher CTMGI score (1.32) compared to the control food, which offers no oral health benefits (0.66).
DISCUSSION: Overall, this study developed and validated a quantitative, single-score, microbiome-based metric that is clinically translatable for the assessment of early-stage canine gingival health. Furthermore, its demonstrated responsiveness to nutritional intervention suggests that this index can serve as a prognostic measure.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Exploring the effects of sugarcane bagasse extracts on human gut microbiota via fecal batch fermentation.
Journal of food science and technology, 63(7):1311-1322.
UNLABELLED: This study investigated the effects of four sugarcane bagasse (SB) extracts, namely crude carbohydrates (CC), crude polyphenols (CP), partially purified carbohydrates (PPC), and partially purified polyphenols (PPP), on the gut microbiome using an in vitro human gut model. Both CP and PPC had strong modulatory effects on the gut microbiota. Treatment with CP increased species richness and resulted in the highest reduction in the growth of Enterobacteriaceae, which are pathogenic bacteria, while stimulating the growth of the beneficial bacteria Peptostreptococcaceae, Lachnospiraceae, Ruminococcaceae, and Bacteroidaceae. Treatment with PPC decreased the proportion of Peptostreptococcaceae and increased the proportion of Porphyromonadaceae. Moreover, supplementation with PPC tended to promote propionic acid production compared to the control and was significantly higher than the PPP treatment (p < 0.05). These findings suggested that CP and PPC derived from SB positively influenced the modulation of the gut microbiota profile, making them potential candidates for prebiotic applications.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13197-025-06284-1.
Additional Links: PMID-42328136
PubMed:
Citation:
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@article {pmid42328136,
year = {2026},
author = {Pongsuwanporn, T and Arunmas, E and Tunsagool, P and Chitprasert, P and Nakphaichit, M},
title = {Exploring the effects of sugarcane bagasse extracts on human gut microbiota via fecal batch fermentation.},
journal = {Journal of food science and technology},
volume = {63},
number = {7},
pages = {1311-1322},
pmid = {42328136},
issn = {0022-1155},
abstract = {UNLABELLED: This study investigated the effects of four sugarcane bagasse (SB) extracts, namely crude carbohydrates (CC), crude polyphenols (CP), partially purified carbohydrates (PPC), and partially purified polyphenols (PPP), on the gut microbiome using an in vitro human gut model. Both CP and PPC had strong modulatory effects on the gut microbiota. Treatment with CP increased species richness and resulted in the highest reduction in the growth of Enterobacteriaceae, which are pathogenic bacteria, while stimulating the growth of the beneficial bacteria Peptostreptococcaceae, Lachnospiraceae, Ruminococcaceae, and Bacteroidaceae. Treatment with PPC decreased the proportion of Peptostreptococcaceae and increased the proportion of Porphyromonadaceae. Moreover, supplementation with PPC tended to promote propionic acid production compared to the control and was significantly higher than the PPP treatment (p < 0.05). These findings suggested that CP and PPC derived from SB positively influenced the modulation of the gut microbiota profile, making them potential candidates for prebiotic applications.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13197-025-06284-1.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Longitudinal remodeling of gastric microbiota following Helicobacter pylori eradication reveals an eradication-associated microbial signature in gastric cancer.
Frontiers in cellular and infection microbiology, 16:1848437.
INTRODUCTION: Helicobacter pylori (H. pylori) is a major cause of gastric cancer (GC); however, GC also develops in H. pylori-negative patients, and the characteristics of non-H. pylori microbial communities remain unclear.
METHODS: We characterized gastric microbiota in patients with GC according to H. pylori status, sex, GC subtype, and longitudinal changes following H. pylori eradication therapy. Gastric corpus mucosal samples were collected from 35 patients with GC who underwent endoscopic therapy and longitudinal follow-up. Some patients were followed for more than 10 years, and gastric microbiota were analyzed using 16S rRNA gene sequencing.
RESULTS: H. pylori-negative samples exhibited significantly higher microbial diversity and distinct community structures compared with H. pylori-positive samples, which was consistent across sex and GC subtypes. Multiple non-H. pylori taxa were enriched in H. pylori-negative samples, including organisms with reported urease and nitrate-reducing activities. Longitudinal analyses demonstrated that successful eradication induced significant but non-uniform microbial shifts, whereas persistent infection maintained stable H. pylori-dominated profiles. Notably, species-level analyses revealed selective and H. pylori eradication-specific microbial changes, with Actinomyces naeslundii consistently enriched only in the H. pylori eradicated group across longitudinal modeling and differential abundance analyses. Functional prediction analyses revealed a reduced representation of host-pathogen interaction-related pathways in H. pylori-negative samples.
DISCUSSION: These findings suggest that H. pylori-negative gastric microbiota harbor functionally distinct microbial communities that may contribute to gastric carcinogenesis through alternative microbial and ecological pathways. In addition, H. pylori eradication revealed a longitudinal remodeling of gastric microbiota.
Additional Links: PMID-42328161
PubMed:
Citation:
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@article {pmid42328161,
year = {2026},
author = {Song, CH and Choi, Y and Kim, N and Ha, S and Park, JH and Lee, HK and Shin, CM and Ahn, S},
title = {Longitudinal remodeling of gastric microbiota following Helicobacter pylori eradication reveals an eradication-associated microbial signature in gastric cancer.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1848437},
pmid = {42328161},
issn = {2235-2988},
mesh = {Humans ; *Stomach Neoplasms/microbiology ; *Helicobacter Infections/drug therapy/microbiology/complications ; *Helicobacter pylori/drug effects ; Male ; Female ; RNA, Ribosomal, 16S/genetics ; Middle Aged ; Longitudinal Studies ; *Gastrointestinal Microbiome ; Gastric Mucosa/microbiology ; Aged ; Anti-Bacterial Agents/therapeutic use ; Bacteria/classification/genetics/isolation & purification ; DNA, Bacterial/genetics/chemistry ; },
abstract = {INTRODUCTION: Helicobacter pylori (H. pylori) is a major cause of gastric cancer (GC); however, GC also develops in H. pylori-negative patients, and the characteristics of non-H. pylori microbial communities remain unclear.
METHODS: We characterized gastric microbiota in patients with GC according to H. pylori status, sex, GC subtype, and longitudinal changes following H. pylori eradication therapy. Gastric corpus mucosal samples were collected from 35 patients with GC who underwent endoscopic therapy and longitudinal follow-up. Some patients were followed for more than 10 years, and gastric microbiota were analyzed using 16S rRNA gene sequencing.
RESULTS: H. pylori-negative samples exhibited significantly higher microbial diversity and distinct community structures compared with H. pylori-positive samples, which was consistent across sex and GC subtypes. Multiple non-H. pylori taxa were enriched in H. pylori-negative samples, including organisms with reported urease and nitrate-reducing activities. Longitudinal analyses demonstrated that successful eradication induced significant but non-uniform microbial shifts, whereas persistent infection maintained stable H. pylori-dominated profiles. Notably, species-level analyses revealed selective and H. pylori eradication-specific microbial changes, with Actinomyces naeslundii consistently enriched only in the H. pylori eradicated group across longitudinal modeling and differential abundance analyses. Functional prediction analyses revealed a reduced representation of host-pathogen interaction-related pathways in H. pylori-negative samples.
DISCUSSION: These findings suggest that H. pylori-negative gastric microbiota harbor functionally distinct microbial communities that may contribute to gastric carcinogenesis through alternative microbial and ecological pathways. In addition, H. pylori eradication revealed a longitudinal remodeling of gastric microbiota.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Stomach Neoplasms/microbiology
*Helicobacter Infections/drug therapy/microbiology/complications
*Helicobacter pylori/drug effects
Male
Female
RNA, Ribosomal, 16S/genetics
Middle Aged
Longitudinal Studies
*Gastrointestinal Microbiome
Gastric Mucosa/microbiology
Aged
Anti-Bacterial Agents/therapeutic use
Bacteria/classification/genetics/isolation & purification
DNA, Bacterial/genetics/chemistry
RevDate: 2026-06-22
CmpDate: 2026-06-22
Impact of probiotic supplementation on salivary function, oral microbiota, and gut health: a systematic review.
Frontiers in cellular and infection microbiology, 16:1816010.
INTRODUCTION: Probiotics, which are classified as helpful living microorganisms, have demonstrated the ability to improve salivary function, inhibit pathogens like Streptococcus mutans, and modify the oral and gut microbiota. The aims of this systematic review was to assess their effects on salivary function, oral microbiota, and gut health.
METHODS: Literature search was done in PubMed, Scopus, Web of Science, Science Direct and Cochrane were performed. Randomized controlled trials were included which involved human subjects receiving probiotic supplementation Outcomes assessed were salivary parameters (flow rate, buffering capacity, pH, biomarkers), oral microbiota changes, and gut health indicators. Study selection, data extraction, and risk of bias assessment (RoB 2.0) were performed independently by two reviewers. Due to heterogeneity, meta-analysis was not conducted.
RESULTS: A total of six systematic reviews were included in this review. Probiotic supplementation was associated with improvements in salivary parameters, including buffering capacity and plaque pH, and reductions in cariogenic bacteria such as Streptococcus mutans. Probiotics demonstrated beneficial effects on gut microbiota and gastrointestinal symptoms, supporting an oral-gut microbiota interaction. Risk of bias ranged from low to high across studies. Overall, evidence suggested beneficial effects, though heterogeneity and methodological limitations reduced certainty.
CONCLUSIONS: Probiotics have been shown to provide modest, strain-specific benefits for modulating the oral microbiota and certain salivary parameters, with more precise molecular and clinical evidence for gut effects.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420251243347, identifier CRD420251243347.
Additional Links: PMID-42328170
PubMed:
Citation:
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@article {pmid42328170,
year = {2026},
author = {Kumar, G and Jena, S and Nelson, VK and Baig, HA and Alanazi, ZA and Alanazi, BK and Alanazi, FSZ and Awad R, AA},
title = {Impact of probiotic supplementation on salivary function, oral microbiota, and gut health: a systematic review.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1816010},
pmid = {42328170},
issn = {2235-2988},
mesh = {Humans ; *Probiotics/administration & dosage ; *Saliva/microbiology/physiology ; *Mouth/microbiology ; Randomized Controlled Trials as Topic ; *Dietary Supplements ; *Microbiota/drug effects ; *Gastrointestinal Tract/microbiology ; *Gastrointestinal Microbiome/drug effects ; Streptococcus mutans ; },
abstract = {INTRODUCTION: Probiotics, which are classified as helpful living microorganisms, have demonstrated the ability to improve salivary function, inhibit pathogens like Streptococcus mutans, and modify the oral and gut microbiota. The aims of this systematic review was to assess their effects on salivary function, oral microbiota, and gut health.
METHODS: Literature search was done in PubMed, Scopus, Web of Science, Science Direct and Cochrane were performed. Randomized controlled trials were included which involved human subjects receiving probiotic supplementation Outcomes assessed were salivary parameters (flow rate, buffering capacity, pH, biomarkers), oral microbiota changes, and gut health indicators. Study selection, data extraction, and risk of bias assessment (RoB 2.0) were performed independently by two reviewers. Due to heterogeneity, meta-analysis was not conducted.
RESULTS: A total of six systematic reviews were included in this review. Probiotic supplementation was associated with improvements in salivary parameters, including buffering capacity and plaque pH, and reductions in cariogenic bacteria such as Streptococcus mutans. Probiotics demonstrated beneficial effects on gut microbiota and gastrointestinal symptoms, supporting an oral-gut microbiota interaction. Risk of bias ranged from low to high across studies. Overall, evidence suggested beneficial effects, though heterogeneity and methodological limitations reduced certainty.
CONCLUSIONS: Probiotics have been shown to provide modest, strain-specific benefits for modulating the oral microbiota and certain salivary parameters, with more precise molecular and clinical evidence for gut effects.
https://www.crd.york.ac.uk/PROSPERO/view/CRD420251243347, identifier CRD420251243347.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Probiotics/administration & dosage
*Saliva/microbiology/physiology
*Mouth/microbiology
Randomized Controlled Trials as Topic
*Dietary Supplements
*Microbiota/drug effects
*Gastrointestinal Tract/microbiology
*Gastrointestinal Microbiome/drug effects
Streptococcus mutans
RevDate: 2026-06-22
CmpDate: 2026-06-22
Oral human papillomavirus infection aligns with a coordinated bacterial microbiome inferred virulence ecology.
Frontiers in cellular and infection microbiology, 16:1821266.
BACKGROUND: The biological relationship between oral human papillomavirus (HPV) infection and the community-level virulence ecology of the oral bacterial microbiome remains unresolved due to taxon-centric analyses. We profiled non-cancer oral HPV infection status and the ecological virulence architecture of the oral bacterial microbiome by integrating with bacterial genomics.
METHODS: We used publicly available 16S rRNA gene sequencing data of the oral bacterial microbiome from 127 participants. Raw sequencing reads were quality filtered, denoised and taxonomically assigned at the genus level using standard amplicon-processing pipelines. Oral HPV status was derived from the original study metadata. Microbiome structure was characterised using diversity metrics, unsupervised ecotype and multivariate analyses. To interrogate functional organisation, bacterial genera were mapped to curated virulence-associated domains from published bacterial genomics databases. Variance partitioning was performed using PERMANOVA analysis to assess the independent contributions of HPV status and virulence ecology.
RESULTS: We observed a gross overlap across oral HPV groups (64 HPV-negative and 63 HPV-positive) with no dominant bacterial microbiome taxa after multiple-testing correction (all FDR > 0.10). Alpha diversity was modestly higher in HPV-positive samples, but differences were not statistically significant (Median difference = 0.18; 95% CI 0.05-0.41, p = 0.12). Unsupervised ecotype analysis identified three independent bacterial microbiome states, none defined by HPV status (All p > 0.20). In the multivariate PERMANOVA analysis, microbial diversity (R² = 8.9%, p < 0.001) and virulence ecology (R² = 3.9%, p < 0.001) explained significantly more community bacterial microbiome variance than HPV status (R² = 0.9%, p = 0.24). The structured network-level reprogramming of taxa and genera virulence ecology by HPV status showed almost similar genus-virulence coordination, particularly within adhesion, invasion and immune-interface modules and no significant differences in the mean virulence module abundance (all Cliff's δ < 0.15). HPV-positivity aligned more with high virulence-pressure, low terrain of the oral bacterial microbiome ecological landscapes. Relative to the protected terrain (Q1), HPV positivity was more frequent in the higher-pressure ecological states, with odds ratios of 3.62 for Q2 (95% CI 1.19-11.06; p=0.024), 3.13 for Q3 (95% CI 1.02-9.58; p=0.045), and 3.68 for Q4 (95% CI 1.06-12.77; p=0.040). The strongest point estimate was observed in the low-diversity, high-pressure danger zone (Q4).
CONCLUSIONS: In this hypothesis generation study, oral HPV infection aligns with coordinated inferred virulence ecology of the oral bacterial microbiome rather than discrete taxonomic or abundance-based changes.
Additional Links: PMID-42328172
PubMed:
Citation:
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@article {pmid42328172,
year = {2026},
author = {Chambuso, R and Alajrami, S and Wali Jan, N and Allam, M and Desai, V and Mohamed, YS and Al-Marzooq, F},
title = {Oral human papillomavirus infection aligns with a coordinated bacterial microbiome inferred virulence ecology.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1821266},
pmid = {42328172},
issn = {2235-2988},
mesh = {Humans ; *Papillomavirus Infections/virology/microbiology ; *Microbiota ; RNA, Ribosomal, 16S/genetics ; *Human Papillomavirus Viruses/pathogenicity ; *Bacteria/classification/genetics/pathogenicity/isolation & purification ; *Mouth/microbiology/virology ; Virulence ; Female ; Phylogeny ; Sequence Analysis, DNA ; DNA, Bacterial/genetics/chemistry ; },
abstract = {BACKGROUND: The biological relationship between oral human papillomavirus (HPV) infection and the community-level virulence ecology of the oral bacterial microbiome remains unresolved due to taxon-centric analyses. We profiled non-cancer oral HPV infection status and the ecological virulence architecture of the oral bacterial microbiome by integrating with bacterial genomics.
METHODS: We used publicly available 16S rRNA gene sequencing data of the oral bacterial microbiome from 127 participants. Raw sequencing reads were quality filtered, denoised and taxonomically assigned at the genus level using standard amplicon-processing pipelines. Oral HPV status was derived from the original study metadata. Microbiome structure was characterised using diversity metrics, unsupervised ecotype and multivariate analyses. To interrogate functional organisation, bacterial genera were mapped to curated virulence-associated domains from published bacterial genomics databases. Variance partitioning was performed using PERMANOVA analysis to assess the independent contributions of HPV status and virulence ecology.
RESULTS: We observed a gross overlap across oral HPV groups (64 HPV-negative and 63 HPV-positive) with no dominant bacterial microbiome taxa after multiple-testing correction (all FDR > 0.10). Alpha diversity was modestly higher in HPV-positive samples, but differences were not statistically significant (Median difference = 0.18; 95% CI 0.05-0.41, p = 0.12). Unsupervised ecotype analysis identified three independent bacterial microbiome states, none defined by HPV status (All p > 0.20). In the multivariate PERMANOVA analysis, microbial diversity (R² = 8.9%, p < 0.001) and virulence ecology (R² = 3.9%, p < 0.001) explained significantly more community bacterial microbiome variance than HPV status (R² = 0.9%, p = 0.24). The structured network-level reprogramming of taxa and genera virulence ecology by HPV status showed almost similar genus-virulence coordination, particularly within adhesion, invasion and immune-interface modules and no significant differences in the mean virulence module abundance (all Cliff's δ < 0.15). HPV-positivity aligned more with high virulence-pressure, low terrain of the oral bacterial microbiome ecological landscapes. Relative to the protected terrain (Q1), HPV positivity was more frequent in the higher-pressure ecological states, with odds ratios of 3.62 for Q2 (95% CI 1.19-11.06; p=0.024), 3.13 for Q3 (95% CI 1.02-9.58; p=0.045), and 3.68 for Q4 (95% CI 1.06-12.77; p=0.040). The strongest point estimate was observed in the low-diversity, high-pressure danger zone (Q4).
CONCLUSIONS: In this hypothesis generation study, oral HPV infection aligns with coordinated inferred virulence ecology of the oral bacterial microbiome rather than discrete taxonomic or abundance-based changes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Papillomavirus Infections/virology/microbiology
*Microbiota
RNA, Ribosomal, 16S/genetics
*Human Papillomavirus Viruses/pathogenicity
*Bacteria/classification/genetics/pathogenicity/isolation & purification
*Mouth/microbiology/virology
Virulence
Female
Phylogeny
Sequence Analysis, DNA
DNA, Bacterial/genetics/chemistry
RevDate: 2026-06-22
CmpDate: 2026-06-22
Investigating the diversity of intratumoral microbiota in high-grade serous ovarian cancer with varying platinum sensitivity.
Frontiers in cellular and infection microbiology, 16:1652322.
BACKGROUND: Ovarian cancer remains the most lethal gynecological malignancy. However, no studies have investigated the differences in intratumoral microbiota among patients with varying platinum sensitivity. This study aims to explore the intratumoral microbiota of ovarian cancer in relation to different sensitivities to platinum-based chemotherapy.
METHODS: Tumor samples were collected from ovarian cancer patients exhibiting different platinum-sensitive statuses and subjected to microbiome (16S rRNA gene sequencing) analyses. Following DNA extraction and PCR amplification, library construction and sequencing were performed. The differences in intratumoral microbiota across various groups were analyzed both individually and collectively using a range of bioinformatics approaches.
RESULTS: A total of 22 patients with high-grade serous ovarian cancer participated in this study, including 6 from the platinum-sensitive recurrent group, 8 from the platinum-resistant recurrent group, and 8 from the platinum-refractory group. Bacterial diversity within the intratumoral microbiota, phylogenetic profiles of microbial communities, as well as functional predictions and bacterial phenotypes all exhibited significant differences among these three groups. At the phylum level, Firmicutes, Actinobacteria, and Acidobacteria were significantly more abundant in the platinum-refractory group compared to both the platinum-sensitive recurrent group and the platinum-resistant recurrent group. Additionally, genera Lactococcus and Corynebacterium showed significant enrichment in the platinum-refractory group relative to both other groups.
CONCLUSIONS: This study is pioneering in identifying variations in intratumoral microbiota associated with differing sensitivities to platinum therapy in ovarian cancer patients; these findings may provide valuable insights for future mechanistic research.
Additional Links: PMID-42328173
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@article {pmid42328173,
year = {2026},
author = {Cheng, X and Xiao, L and Ye, L and Wang, X and Zhao, Q and Chen, Y and Zhou, R and Xu, X and Ni, J and Guo, W and Chen, X},
title = {Investigating the diversity of intratumoral microbiota in high-grade serous ovarian cancer with varying platinum sensitivity.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1652322},
pmid = {42328173},
issn = {2235-2988},
mesh = {Humans ; Female ; *Ovarian Neoplasms/microbiology/drug therapy/pathology ; *Microbiota/genetics/drug effects ; RNA, Ribosomal, 16S/genetics ; *Platinum/therapeutic use/pharmacology ; *Bacteria/classification/genetics/isolation & purification/drug effects ; Phylogeny ; Drug Resistance, Neoplasm ; *Antineoplastic Agents/therapeutic use/pharmacology ; Middle Aged ; DNA, Bacterial/genetics/chemistry ; Sequence Analysis, DNA ; Aged ; Adult ; },
abstract = {BACKGROUND: Ovarian cancer remains the most lethal gynecological malignancy. However, no studies have investigated the differences in intratumoral microbiota among patients with varying platinum sensitivity. This study aims to explore the intratumoral microbiota of ovarian cancer in relation to different sensitivities to platinum-based chemotherapy.
METHODS: Tumor samples were collected from ovarian cancer patients exhibiting different platinum-sensitive statuses and subjected to microbiome (16S rRNA gene sequencing) analyses. Following DNA extraction and PCR amplification, library construction and sequencing were performed. The differences in intratumoral microbiota across various groups were analyzed both individually and collectively using a range of bioinformatics approaches.
RESULTS: A total of 22 patients with high-grade serous ovarian cancer participated in this study, including 6 from the platinum-sensitive recurrent group, 8 from the platinum-resistant recurrent group, and 8 from the platinum-refractory group. Bacterial diversity within the intratumoral microbiota, phylogenetic profiles of microbial communities, as well as functional predictions and bacterial phenotypes all exhibited significant differences among these three groups. At the phylum level, Firmicutes, Actinobacteria, and Acidobacteria were significantly more abundant in the platinum-refractory group compared to both the platinum-sensitive recurrent group and the platinum-resistant recurrent group. Additionally, genera Lactococcus and Corynebacterium showed significant enrichment in the platinum-refractory group relative to both other groups.
CONCLUSIONS: This study is pioneering in identifying variations in intratumoral microbiota associated with differing sensitivities to platinum therapy in ovarian cancer patients; these findings may provide valuable insights for future mechanistic research.},
}
MeSH Terms:
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Humans
Female
*Ovarian Neoplasms/microbiology/drug therapy/pathology
*Microbiota/genetics/drug effects
RNA, Ribosomal, 16S/genetics
*Platinum/therapeutic use/pharmacology
*Bacteria/classification/genetics/isolation & purification/drug effects
Phylogeny
Drug Resistance, Neoplasm
*Antineoplastic Agents/therapeutic use/pharmacology
Middle Aged
DNA, Bacterial/genetics/chemistry
Sequence Analysis, DNA
Aged
Adult
RevDate: 2026-06-22
CmpDate: 2026-06-22
Progressive microbial alterations in the human gut and lung across early life: implications for translational medicine.
Frontiers in cellular and infection microbiology, 16:1739520.
Early life represents a critical window for the establishment and maturation of the human microbiome. The sterile womb paradigm remains dominant in the field, but in utero microbial colonization is highly controversial due to challenges related to low-biomass contamination. After birth, the intestinal and pulmonary microbial communities undergo a programmed succession shaped by factors such as delivery mode, feeding practices, and environmental exposures, and they bidirectionally regulate host immune and metabolic homeostasis via the gut-lung axis. Dysbiosis during early life is closely associated with allergic diseases, metabolic disorders, and respiratory illnesses. This review summarizes the dynamic succession patterns of the intestinal and pulmonary microbiota during early life, analyzes the methodological origins of the ongoing controversy over in utero colonization, delineates the developmental characteristics of the pulmonary microbiome at distinct stages, and systematically discusses the translational potential, clinical risks, and ethical challenges of microbiome-targeted interventions. Collectively, this review aims to provide a theoretical reference for early-life health protection and disease prevention.
Additional Links: PMID-42328178
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Citation:
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@article {pmid42328178,
year = {2026},
author = {Zhao, Y and Gao, Y and Li, X and Georgian, EM and Pinkerton, KE and Zhang, C},
title = {Progressive microbial alterations in the human gut and lung across early life: implications for translational medicine.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1739520},
pmid = {42328178},
issn = {2235-2988},
mesh = {Humans ; *Lung/microbiology ; *Translational Research, Biomedical ; *Gastrointestinal Microbiome ; Dysbiosis/microbiology ; *Microbiota ; *Gastrointestinal Tract/microbiology ; Translational Science, Biomedical ; Infant, Newborn ; },
abstract = {Early life represents a critical window for the establishment and maturation of the human microbiome. The sterile womb paradigm remains dominant in the field, but in utero microbial colonization is highly controversial due to challenges related to low-biomass contamination. After birth, the intestinal and pulmonary microbial communities undergo a programmed succession shaped by factors such as delivery mode, feeding practices, and environmental exposures, and they bidirectionally regulate host immune and metabolic homeostasis via the gut-lung axis. Dysbiosis during early life is closely associated with allergic diseases, metabolic disorders, and respiratory illnesses. This review summarizes the dynamic succession patterns of the intestinal and pulmonary microbiota during early life, analyzes the methodological origins of the ongoing controversy over in utero colonization, delineates the developmental characteristics of the pulmonary microbiome at distinct stages, and systematically discusses the translational potential, clinical risks, and ethical challenges of microbiome-targeted interventions. Collectively, this review aims to provide a theoretical reference for early-life health protection and disease prevention.},
}
MeSH Terms:
show MeSH Terms
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Humans
*Lung/microbiology
*Translational Research, Biomedical
*Gastrointestinal Microbiome
Dysbiosis/microbiology
*Microbiota
*Gastrointestinal Tract/microbiology
Translational Science, Biomedical
Infant, Newborn
RevDate: 2026-06-22
CmpDate: 2026-06-22
Tree-Structured Orthonormal Decomposition of the Aitchison Simplex.
ArXiv pii:2606.11646.
Compositional data -- vectors encoding relative proportions -- arise across scientific domains, including ecology, geochemistry, and genomics. The features in these data often come with known hierarchical structure (e.g., taxonomies, phylogenies, ontologies), yet existing methods either ignore this structure, discard the intrinsic Aitchison geometry, are designed for binary trees, or yield incomplete coordinate systems. We describe PolyILR, a canonical orthonormal decomposition of the Aitchison tangent space aligned with any tree topology. Our construction defines a weighted local geometry at each internal node capturing full branching structure, then lifts these to a global orthonormal basis where every coordinate corresponds to a specific tree location. On microbiome and single-cell benchmarks, PolyILR yields stable, interpretable features and enables inference at multiscale tree resolution. We also establish a novel theoretical connection to softmax classifiers, suggesting possible applications to probabilistic modeling.
Additional Links: PMID-42328291
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Citation:
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@article {pmid42328291,
year = {2026},
author = {Yamada, D and Zhang, Q and Pence, T and Bendlin, BB and Rey, F and Singh, V},
title = {Tree-Structured Orthonormal Decomposition of the Aitchison Simplex.},
journal = {ArXiv},
volume = {},
number = {},
pages = {},
pmid = {42328291},
issn = {2331-8422},
abstract = {Compositional data -- vectors encoding relative proportions -- arise across scientific domains, including ecology, geochemistry, and genomics. The features in these data often come with known hierarchical structure (e.g., taxonomies, phylogenies, ontologies), yet existing methods either ignore this structure, discard the intrinsic Aitchison geometry, are designed for binary trees, or yield incomplete coordinate systems. We describe PolyILR, a canonical orthonormal decomposition of the Aitchison tangent space aligned with any tree topology. Our construction defines a weighted local geometry at each internal node capturing full branching structure, then lifts these to a global orthonormal basis where every coordinate corresponds to a specific tree location. On microbiome and single-cell benchmarks, PolyILR yields stable, interpretable features and enables inference at multiscale tree resolution. We also establish a novel theoretical connection to softmax classifiers, suggesting possible applications to probabilistic modeling.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Global trends in Alzheimer's disease randomized controlled trials: a bibliometric analysis.
Dementia & neuropsychologia, 20:e20250423.
UNLABELLED: Alzheimer's disease (AD) is the most common form of dementia worldwide, creating substantial clinical and socioeconomic burdens. Randomized controlled trials (RCTs) provide the highest level of evidence to evaluate interventions, yet global publication trends and thematic evolution have not been systematically analyzed.
OBJECTIVE: As far as we are aware, there has been no bibliometric analysis that has thoroughly assessed RCTs in AD, despite their pivotal influence on the development of treatment and prevention strategies. Therefore, in this study, we conducted a bibliometric mapping analysis of global RCTs on AD.
METHODS: A bibliometric analysis of human RCTs on AD from September 2010 to September 2025 was conducted using PubMed and Web of Science. VOSviewer was employed for keyword co-occurrence, co-authorship mapping, and co-citation analyses to identify research themes, collaborations, and temporal trends.
RESULTS: A total of 4,482 RCTs were identified, revealing five main themes: pharmacological interventions, lifestyle and prevention strategies, pathophysiological mechanisms, cognitive and behavioral interventions, and clinical trial methodology. After 2015, focus shifted from traditional pharmacology to multidomain, prevention-oriented, and precision-driven approaches. Emerging topics included digital health, gut microbiome, and machine learning. Collaboration networks highlighted the dominance of the US and Europe, with rapid growth in Asia and emerging regions.
CONCLUSION: Findings indicate a paradigm shift in AD RCTs toward integrative, technology-enabled designs, emphasizing both pharmacological and non-pharmacological strategies. These trends can guide future global research priorities and intervention development.
Additional Links: PMID-42328310
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Citation:
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@article {pmid42328310,
year = {2026},
author = {Hosseinpoor-Dashatani, S and Ebrahimi, N},
title = {Global trends in Alzheimer's disease randomized controlled trials: a bibliometric analysis.},
journal = {Dementia & neuropsychologia},
volume = {20},
number = {},
pages = {e20250423},
pmid = {42328310},
issn = {1980-5764},
abstract = {UNLABELLED: Alzheimer's disease (AD) is the most common form of dementia worldwide, creating substantial clinical and socioeconomic burdens. Randomized controlled trials (RCTs) provide the highest level of evidence to evaluate interventions, yet global publication trends and thematic evolution have not been systematically analyzed.
OBJECTIVE: As far as we are aware, there has been no bibliometric analysis that has thoroughly assessed RCTs in AD, despite their pivotal influence on the development of treatment and prevention strategies. Therefore, in this study, we conducted a bibliometric mapping analysis of global RCTs on AD.
METHODS: A bibliometric analysis of human RCTs on AD from September 2010 to September 2025 was conducted using PubMed and Web of Science. VOSviewer was employed for keyword co-occurrence, co-authorship mapping, and co-citation analyses to identify research themes, collaborations, and temporal trends.
RESULTS: A total of 4,482 RCTs were identified, revealing five main themes: pharmacological interventions, lifestyle and prevention strategies, pathophysiological mechanisms, cognitive and behavioral interventions, and clinical trial methodology. After 2015, focus shifted from traditional pharmacology to multidomain, prevention-oriented, and precision-driven approaches. Emerging topics included digital health, gut microbiome, and machine learning. Collaboration networks highlighted the dominance of the US and Europe, with rapid growth in Asia and emerging regions.
CONCLUSION: Findings indicate a paradigm shift in AD RCTs toward integrative, technology-enabled designs, emphasizing both pharmacological and non-pharmacological strategies. These trends can guide future global research priorities and intervention development.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.
International journal of biological sciences, 22(11):5754-5779.
Inflammatory bowel disease (IBD) arises from dysregulated interactions among the gut microbiota, immune system, and intestinal epithelium. Intestinal macrophages are central to these processes, yet are often viewed primarily as downstream inflammatory effectors. Here, we present a conceptual review that reframes intestinal macrophages as metabolic sensors and regulatory hubs that orchestrate inflammatory persistence or resolution. We propose a Macrophage-Orchestrated Metabolic Sensor (MOMS) framework organized into three coordinated layers: Sense, in which macrophages detect microbial- and host-derived metabolites; Switch, in which metabolic and epigenetic reprogramming stabilizes intracellular inflammatory or reparative states; and Command, in which these stabilized states drive epithelial repair, immune-cell recruitment, or fibrotic remodeling. Integrating evidence from immunometabolism, microbiome research, and single-cell biology, we identify key molecular nodes-including METTL3 and NLRP3-as programmable regulators of macrophage fate. The MOMS framework generates testable predictions linking macrophage metabolic states to disease severity and treatment responsiveness, and provides a conceptual foundation for precision macrophage-directed therapies in IBD and related immune-metabolic disorders.
Additional Links: PMID-42328447
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Citation:
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@article {pmid42328447,
year = {2026},
author = {Guan, G and Sun, X and Chen, Y and Guo, Q and Dong, Y},
title = {Macrophage-Orchestrated Metabolic Sensing Drives IBD Pathogenesis: A Framework for Targeted Therapy.},
journal = {International journal of biological sciences},
volume = {22},
number = {11},
pages = {5754-5779},
pmid = {42328447},
issn = {1449-2288},
mesh = {*Macrophages/metabolism ; Humans ; *Inflammatory Bowel Diseases/metabolism/immunology/therapy ; Animals ; Gastrointestinal Microbiome/physiology ; },
abstract = {Inflammatory bowel disease (IBD) arises from dysregulated interactions among the gut microbiota, immune system, and intestinal epithelium. Intestinal macrophages are central to these processes, yet are often viewed primarily as downstream inflammatory effectors. Here, we present a conceptual review that reframes intestinal macrophages as metabolic sensors and regulatory hubs that orchestrate inflammatory persistence or resolution. We propose a Macrophage-Orchestrated Metabolic Sensor (MOMS) framework organized into three coordinated layers: Sense, in which macrophages detect microbial- and host-derived metabolites; Switch, in which metabolic and epigenetic reprogramming stabilizes intracellular inflammatory or reparative states; and Command, in which these stabilized states drive epithelial repair, immune-cell recruitment, or fibrotic remodeling. Integrating evidence from immunometabolism, microbiome research, and single-cell biology, we identify key molecular nodes-including METTL3 and NLRP3-as programmable regulators of macrophage fate. The MOMS framework generates testable predictions linking macrophage metabolic states to disease severity and treatment responsiveness, and provides a conceptual foundation for precision macrophage-directed therapies in IBD and related immune-metabolic disorders.},
}
MeSH Terms:
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*Macrophages/metabolism
Humans
*Inflammatory Bowel Diseases/metabolism/immunology/therapy
Animals
Gastrointestinal Microbiome/physiology
RevDate: 2026-06-22
CmpDate: 2026-06-22
Exploring the Role of Skin Microbiota in Autoimmune Skin Diseases from a Bidirectional Mendelian Randomization Perspective.
Clinical, cosmetic and investigational dermatology, 19:607307.
BACKGROUND: The etiologies of psoriasis, localized scleroderma (LoS), and systemic lupus erythematosus (SLE) remain incompletely understood. Although skin microbiota are implicated in cutaneous immune homeostasis, their causal relationships with autoimmune skin diseases are unclear.
OBJECTIVE: To investigate bidirectional causal associations between skin microbiota and psoriasis, LoS, and SLE.
METHODS: Summary-level genome-wide association study (GWAS) data for 1656 skin microbiome traits were obtained from public resources, and GWAS data for psoriasis, LoS, and SLE were obtained from FinnGen version 9. Two-sample Mendelian randomization (MR) was performed using inverse-variance weighting as the primary method, supplemented by MR-Egger regression, weighted median, simple mode, weighted mode, heterogeneity tests, pleiotropy assessment, MR-PRESSO, and leave-one-out analysis.
RESULTS: Forward MR identified skin microbiota traits associated with the risk of psoriasis, LoS, and SLE. Specifically, 4, 5, and 5 microbiota traits were positively associated with these diseases, respectively, whereas 4, 3, and 8 traits were inversely associated. Reverse MR suggested that psoriasis, LoS, and SLE may also influence skin microbiota composition: psoriasis and LoS were associated with increased abundance of 4 and 1 microbiota traits, respectively, and psoriasis, LoS, and SLE were associated with reduced abundance of 8, 6, and 2 traits, respectively. Most significant associations showed no strong evidence of heterogeneity or horizontal pleiotropy.
CONCLUSION: This bidirectional MR study provides genetic evidence supporting reciprocal relationships between skin microbiota and autoimmune skin diseases. The findings are exploratory and require replication in larger multi-ancestry cohorts and functional validation before clinical translation.
Additional Links: PMID-42328488
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Citation:
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@article {pmid42328488,
year = {2026},
author = {Wang, J and Wang, X and Tao, X and Yang, Q and Zhang, M and Wang, Y and Liu, S},
title = {Exploring the Role of Skin Microbiota in Autoimmune Skin Diseases from a Bidirectional Mendelian Randomization Perspective.},
journal = {Clinical, cosmetic and investigational dermatology},
volume = {19},
number = {},
pages = {607307},
pmid = {42328488},
issn = {1178-7015},
abstract = {BACKGROUND: The etiologies of psoriasis, localized scleroderma (LoS), and systemic lupus erythematosus (SLE) remain incompletely understood. Although skin microbiota are implicated in cutaneous immune homeostasis, their causal relationships with autoimmune skin diseases are unclear.
OBJECTIVE: To investigate bidirectional causal associations between skin microbiota and psoriasis, LoS, and SLE.
METHODS: Summary-level genome-wide association study (GWAS) data for 1656 skin microbiome traits were obtained from public resources, and GWAS data for psoriasis, LoS, and SLE were obtained from FinnGen version 9. Two-sample Mendelian randomization (MR) was performed using inverse-variance weighting as the primary method, supplemented by MR-Egger regression, weighted median, simple mode, weighted mode, heterogeneity tests, pleiotropy assessment, MR-PRESSO, and leave-one-out analysis.
RESULTS: Forward MR identified skin microbiota traits associated with the risk of psoriasis, LoS, and SLE. Specifically, 4, 5, and 5 microbiota traits were positively associated with these diseases, respectively, whereas 4, 3, and 8 traits were inversely associated. Reverse MR suggested that psoriasis, LoS, and SLE may also influence skin microbiota composition: psoriasis and LoS were associated with increased abundance of 4 and 1 microbiota traits, respectively, and psoriasis, LoS, and SLE were associated with reduced abundance of 8, 6, and 2 traits, respectively. Most significant associations showed no strong evidence of heterogeneity or horizontal pleiotropy.
CONCLUSION: This bidirectional MR study provides genetic evidence supporting reciprocal relationships between skin microbiota and autoimmune skin diseases. The findings are exploratory and require replication in larger multi-ancestry cohorts and functional validation before clinical translation.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Multi-omics study on traditional Xiaoqu of Fangxian Huangjiu: Unveiling interactions among physicochemical factors, microbiome and volatile flavor compounds.
Food chemistry: X, 35:103849.
Xiaoqu is the key fermentation starter of Huangjiu, with its microbial profile closely linking to the flavor quality. This study investigated Fangxian Xiaoqu (FXXQ) and corresponding Fangxian Huangjiu (FXHJ) by physicochemical analysis, microbiomics, and flavoromics. Results showed significant variations in physicochemical properties, with Weissella and Saccharomycopsis identified as dominant bacteria and fungi, respectively. A total of 255 bacterial and 151 fungal differential taxa in FXXQ were identified, as well as 76 volatile flavor compounds in FXHJ, including ten newly reported for FXHJ. Correlation analysis revealed acid protease activity as the most critical physicochemical factor shaping bacterial communities, while alcohol-producing capacity dominated fungal communities. Esters content was positively correlated with the abundances of Leuconostoc and Staphylococcus, and alcohols content with that of Saccharomycopsis. This study provides theoretical support for standardizing the preparation of FXXQ and regulating the flavor of the final FXHJ product.
Additional Links: PMID-42328624
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@article {pmid42328624,
year = {2026},
author = {Ren, X and Wen, Q and Cui, L and Cao, T and Hu, D and Liu, H and Wu, J and Ren, Q and Huang, M and Zhao, D and Li, H},
title = {Multi-omics study on traditional Xiaoqu of Fangxian Huangjiu: Unveiling interactions among physicochemical factors, microbiome and volatile flavor compounds.},
journal = {Food chemistry: X},
volume = {35},
number = {},
pages = {103849},
pmid = {42328624},
issn = {2590-1575},
abstract = {Xiaoqu is the key fermentation starter of Huangjiu, with its microbial profile closely linking to the flavor quality. This study investigated Fangxian Xiaoqu (FXXQ) and corresponding Fangxian Huangjiu (FXHJ) by physicochemical analysis, microbiomics, and flavoromics. Results showed significant variations in physicochemical properties, with Weissella and Saccharomycopsis identified as dominant bacteria and fungi, respectively. A total of 255 bacterial and 151 fungal differential taxa in FXXQ were identified, as well as 76 volatile flavor compounds in FXHJ, including ten newly reported for FXHJ. Correlation analysis revealed acid protease activity as the most critical physicochemical factor shaping bacterial communities, while alcohol-producing capacity dominated fungal communities. Esters content was positively correlated with the abundances of Leuconostoc and Staphylococcus, and alcohols content with that of Saccharomycopsis. This study provides theoretical support for standardizing the preparation of FXXQ and regulating the flavor of the final FXHJ product.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Modulatory effect of porous silicon water-formulated catechin on gut microbiome in chronic unpredictable mild stress-induced dementia in a rat model.
Frontiers in pharmacology, 17:1778580.
Stress-induced dysbiosis exacerbates mental health by modulating the nervous system and gut permeability. In this study, we investigate the therapeutic potential of porous silicon water-mixed catechin in alleviating chronic stress-induced dementia in rats. In a 28-day study, chronic unpredictable mild stress (CUMS)-induced rats were treated with Lactobacillus acidophilus (2.5 × 10^9 CFU, p.o), porous silicon water (7 mg/kg, p.o), catechin (30 mg/kg, p.o), and porous silicon water-mixed catechin (PSC) (7 mg and 30 mg/kg, p.o). The effect of porous silicon water-mixed catechin was evaluated through behavioral studies, plasma acetylcholinesterase activity, plasma glutamate, brain reactive oxygen species (ROS), brain endogenous anti-oxidant enzymes, metagenomics analysis, and histological examination of the prefrontal cortex and hippocampus. Administration of PSC significantly improved spatial learning and memory by reducing escape latency time and increased exploratory behavior in the open platform. PSC significantly inhibited acetylcholinesterase enzyme activity and restored endogenous antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GSH) while reducing lipid peroxidation (LPO) compared to the CUMS group. In addition, PSC decreased the brain ROS levels, as determined by a fluorescence assay, and reduced plasma glutamate levels. 16S rRNA V3-V4 metagenomic analysis revealed a significant increase in microbial diversity (Shannon index: 7.52), microbial richness (Chao1 index: 1059.41), β-diversity index, and overall taxonomic abundance in treated rats. CUMS-induced morphological alterations in the hippocampus and prefrontal cortex were significantly improved following PSC administration. In the present study, Pearson correlation coefficient (r) demonstrates an association between gut microbial abundance and AChE activity. Hence, it has been concluded that PSC treatment may significantly modulate the gut microbiome and improve cognition in chronic unpredictable mild stress-induced dementia.
Additional Links: PMID-42328632
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@article {pmid42328632,
year = {2026},
author = {Alnasser, SM and Ravikumar, S and Jayaraman, S and Selvaraj, D and Gunasekaran, V},
title = {Modulatory effect of porous silicon water-formulated catechin on gut microbiome in chronic unpredictable mild stress-induced dementia in a rat model.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1778580},
pmid = {42328632},
issn = {1663-9812},
abstract = {Stress-induced dysbiosis exacerbates mental health by modulating the nervous system and gut permeability. In this study, we investigate the therapeutic potential of porous silicon water-mixed catechin in alleviating chronic stress-induced dementia in rats. In a 28-day study, chronic unpredictable mild stress (CUMS)-induced rats were treated with Lactobacillus acidophilus (2.5 × 10^9 CFU, p.o), porous silicon water (7 mg/kg, p.o), catechin (30 mg/kg, p.o), and porous silicon water-mixed catechin (PSC) (7 mg and 30 mg/kg, p.o). The effect of porous silicon water-mixed catechin was evaluated through behavioral studies, plasma acetylcholinesterase activity, plasma glutamate, brain reactive oxygen species (ROS), brain endogenous anti-oxidant enzymes, metagenomics analysis, and histological examination of the prefrontal cortex and hippocampus. Administration of PSC significantly improved spatial learning and memory by reducing escape latency time and increased exploratory behavior in the open platform. PSC significantly inhibited acetylcholinesterase enzyme activity and restored endogenous antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GSH) while reducing lipid peroxidation (LPO) compared to the CUMS group. In addition, PSC decreased the brain ROS levels, as determined by a fluorescence assay, and reduced plasma glutamate levels. 16S rRNA V3-V4 metagenomic analysis revealed a significant increase in microbial diversity (Shannon index: 7.52), microbial richness (Chao1 index: 1059.41), β-diversity index, and overall taxonomic abundance in treated rats. CUMS-induced morphological alterations in the hippocampus and prefrontal cortex were significantly improved following PSC administration. In the present study, Pearson correlation coefficient (r) demonstrates an association between gut microbial abundance and AChE activity. Hence, it has been concluded that PSC treatment may significantly modulate the gut microbiome and improve cognition in chronic unpredictable mild stress-induced dementia.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Pathogenetic and clinical aspects of fibromyalgia: one year in review 2026.
Clinical and experimental rheumatology, 44(6):1057-1068.
Fibromyalgia (FM) is a complex chronic pain condition with a multifaceted pathogenesis and heterogeneous clinical presentation. This narrative review summarises the most relevant studies published in 2025 on the pathogenetic and clinical aspects of FM. Central sensitisation remains the main neurobiological mechanism, supported by evidence of increased ascending nociceptive signalling, impaired descending inhibition, network reorganisation and autonomic dysfunction. Emerging findings have also explored a possible role for non-classical autoimmune mechanisms, as patient-derived IgG has been shown to induce pain hypersensitivity and bind dorsal root ganglion neurons and satellite glial cells, suggesting potential interactions between immune and metabolic pathways. The gut microbiome is increasingly implicated, showing reduced diversity, distinct signatures, and transferable pain phenotypes. Genetic studies identify a predominantly neuronal architecture involving 26 loci linked to proteins essential for neuronal function. Oxidative stress remains a major hypothesis, supported by elevated biomarkers and preclinical evidence for mitochondrial-targeted strategies. Early-life stress may selectively affect the right amygdala, contributing to long-term vulnerability. Clinically, pain in FM appears heterogeneous and may not be entirely explained by a purely nociplastic paradigm, as some studies have suggested the presence of neuropathic-like features in at least a subset of patients. Likewise, residual pain in inflammatory arthritis remains a multifactorial and incompletely characterised entity, potentially sharing some mechanisms with FM while also encompassing distinct and broader pathophysiological processes. Cognitive dysfunction (fibrofog) represents a multidimensional clinical construct whose underlying mechanisms remain only partially understood. FM is also associated with high affective burden, systemic symptoms, and reduced muscle performance consistent with dynapenia. Stigma and symptom invisibility continue to negatively affect care, while sex and gender influence disease expression and burden. Digital health and AI offer new opportunities but also raise concerns regarding misinformation. Overall, current evidence supports a multidimensional view of FM and highlights the need for updated diagnostic criteria and more integrated, personalised models of care.
Additional Links: PMID-42328952
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PubMed:
Citation:
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@article {pmid42328952,
year = {2026},
author = {Iannuccelli, C and Favretti, M and Bianchi, B and Dolcini, G and Cauli, C and Ferraro, V and Gioia, C and Bazzichi, L and Atzeni, F and Batticciotto, A and Galli, F and Varrassi, G and Ablin, JN and Gualtierotti, R and Conti, F and Di Franco, M and Salaffi, F and Sarzi-Puttini, P and Di Carlo, M and , },
title = {Pathogenetic and clinical aspects of fibromyalgia: one year in review 2026.},
journal = {Clinical and experimental rheumatology},
volume = {44},
number = {6},
pages = {1057-1068},
doi = {10.55563/clinexprheumatol/asx3uo},
pmid = {42328952},
issn = {0392-856X},
mesh = {Humans ; *Fibromyalgia/physiopathology/etiology/psychology/genetics ; Nociplastic Pain ; Central Nervous System Sensitization ; Oxidative Stress ; Animals ; },
abstract = {Fibromyalgia (FM) is a complex chronic pain condition with a multifaceted pathogenesis and heterogeneous clinical presentation. This narrative review summarises the most relevant studies published in 2025 on the pathogenetic and clinical aspects of FM. Central sensitisation remains the main neurobiological mechanism, supported by evidence of increased ascending nociceptive signalling, impaired descending inhibition, network reorganisation and autonomic dysfunction. Emerging findings have also explored a possible role for non-classical autoimmune mechanisms, as patient-derived IgG has been shown to induce pain hypersensitivity and bind dorsal root ganglion neurons and satellite glial cells, suggesting potential interactions between immune and metabolic pathways. The gut microbiome is increasingly implicated, showing reduced diversity, distinct signatures, and transferable pain phenotypes. Genetic studies identify a predominantly neuronal architecture involving 26 loci linked to proteins essential for neuronal function. Oxidative stress remains a major hypothesis, supported by elevated biomarkers and preclinical evidence for mitochondrial-targeted strategies. Early-life stress may selectively affect the right amygdala, contributing to long-term vulnerability. Clinically, pain in FM appears heterogeneous and may not be entirely explained by a purely nociplastic paradigm, as some studies have suggested the presence of neuropathic-like features in at least a subset of patients. Likewise, residual pain in inflammatory arthritis remains a multifactorial and incompletely characterised entity, potentially sharing some mechanisms with FM while also encompassing distinct and broader pathophysiological processes. Cognitive dysfunction (fibrofog) represents a multidimensional clinical construct whose underlying mechanisms remain only partially understood. FM is also associated with high affective burden, systemic symptoms, and reduced muscle performance consistent with dynapenia. Stigma and symptom invisibility continue to negatively affect care, while sex and gender influence disease expression and burden. Digital health and AI offer new opportunities but also raise concerns regarding misinformation. Overall, current evidence supports a multidimensional view of FM and highlights the need for updated diagnostic criteria and more integrated, personalised models of care.},
}
MeSH Terms:
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Humans
*Fibromyalgia/physiopathology/etiology/psychology/genetics
Nociplastic Pain
Central Nervous System Sensitization
Oxidative Stress
Animals
RevDate: 2026-06-22
CmpDate: 2026-06-22
The microbiota-gut-brain axis in fibromyalgia: a scoping review.
Clinical and experimental rheumatology, 44(6):1088-1103.
OBJECTIVES: Fibromyalgia (FM) is a nociplastic pain condition characterised by widespread pain, fatigue, cognitive dysfunction and multisystem involvement. Increasing evidence implicates the microbiota-gut-brain axis (MGBA) as a potential contributor to its complex pathophysiology. This scoping review maps contemporary evidence (2020-2026) on MGBA alterations in FM across microbial, metabolic, neuroimmune and translational dimensions.
METHODS: This review was conducted following the Arksey and O'Malley framework, as refined by Levac et al. and the Joanna Briggs Institute, and reported in accordance with PRISMAScR guidelines. A systematic search of PubMed/MEDLINE, EMBASE, Web of Science and Scopus identified studies published between January 2020 and March 2026. Eligible studies included primary clinical, translational and preclinical investigations evaluating microbiota composition, microbial metabolites, intestinal permeability, neuroimmune signalling, or microbiometargeted interventions in FM. Narrative and systematic reviews were used only to contextualise findings and were not counted among the included studies.
RESULTS: Of 1,365 records identified, 39 studies were included in the final synthesis. Across studies, findings were heterogeneous but most frequently described alterations in gut microbiota composition, including reduced diversity and depletion of butyrate-producing taxa such as Faecalibacterium prausnitzii, along with shifts in Bifidobacterium and Prevotella. Key metabolic perturbations encompassed reduced short-chain fatty acid production and dysregulated tryptophan metabolism. Increased intestinal permeability and activation of neuroimmune pathways were additionally documented. Microbiota profiles were associated with clinically relevant outcomes including pain intensity, fatigue, and cognitive dysfunction. Interventional evidence remains limited but suggests emerging therapeutic potential.
CONCLUSIONS: The MGBA represents a biologically plausible and integrative framework for FM, linking peripheral and central mechanisms. Current evidence remains heterogeneous and largely associative. Future research should prioritise longitudinal, mechanistically driven studies to advance microbiome-informed diagnostic and therapeutic strategies.
Additional Links: PMID-42328953
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PubMed:
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@article {pmid42328953,
year = {2026},
author = {Varrassi, G and Chelidze, K and Tran, YV and Van Pham, PV and Al Alwany, AA and Encinas, MN and Sarzi-Puttini, P and Myrcik, D and Corriero, A and Farì, G and Leoni, MLG},
title = {The microbiota-gut-brain axis in fibromyalgia: a scoping review.},
journal = {Clinical and experimental rheumatology},
volume = {44},
number = {6},
pages = {1088-1103},
doi = {10.55563/clinexprheumatol/5yhjub},
pmid = {42328953},
issn = {0392-856X},
mesh = {Humans ; *Fibromyalgia/microbiology/physiopathology/metabolism/immunology ; *Gastrointestinal Microbiome/physiology ; *Brain-Gut Axis/physiology ; *Brain/physiopathology ; Animals ; Nociplastic Pain ; },
abstract = {OBJECTIVES: Fibromyalgia (FM) is a nociplastic pain condition characterised by widespread pain, fatigue, cognitive dysfunction and multisystem involvement. Increasing evidence implicates the microbiota-gut-brain axis (MGBA) as a potential contributor to its complex pathophysiology. This scoping review maps contemporary evidence (2020-2026) on MGBA alterations in FM across microbial, metabolic, neuroimmune and translational dimensions.
METHODS: This review was conducted following the Arksey and O'Malley framework, as refined by Levac et al. and the Joanna Briggs Institute, and reported in accordance with PRISMAScR guidelines. A systematic search of PubMed/MEDLINE, EMBASE, Web of Science and Scopus identified studies published between January 2020 and March 2026. Eligible studies included primary clinical, translational and preclinical investigations evaluating microbiota composition, microbial metabolites, intestinal permeability, neuroimmune signalling, or microbiometargeted interventions in FM. Narrative and systematic reviews were used only to contextualise findings and were not counted among the included studies.
RESULTS: Of 1,365 records identified, 39 studies were included in the final synthesis. Across studies, findings were heterogeneous but most frequently described alterations in gut microbiota composition, including reduced diversity and depletion of butyrate-producing taxa such as Faecalibacterium prausnitzii, along with shifts in Bifidobacterium and Prevotella. Key metabolic perturbations encompassed reduced short-chain fatty acid production and dysregulated tryptophan metabolism. Increased intestinal permeability and activation of neuroimmune pathways were additionally documented. Microbiota profiles were associated with clinically relevant outcomes including pain intensity, fatigue, and cognitive dysfunction. Interventional evidence remains limited but suggests emerging therapeutic potential.
CONCLUSIONS: The MGBA represents a biologically plausible and integrative framework for FM, linking peripheral and central mechanisms. Current evidence remains heterogeneous and largely associative. Future research should prioritise longitudinal, mechanistically driven studies to advance microbiome-informed diagnostic and therapeutic strategies.},
}
MeSH Terms:
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Humans
*Fibromyalgia/microbiology/physiopathology/metabolism/immunology
*Gastrointestinal Microbiome/physiology
*Brain-Gut Axis/physiology
*Brain/physiopathology
Animals
Nociplastic Pain
RevDate: 2026-06-22
Mechanisms by which proline reductase of Clostridioides difficile promotes efficient metabolism and disease progression in vivo.
mBio [Epub ahead of print].
UNLABELLED: Clostridioides difficile is a toxin-producing pathogen that opportunistically infects those with a depleted gut microbiome, often triggered by antibiotic use. C. difficile preferentially utilizes Stickland amino acids, including proline, to promote energy generation and growth for colonization. We evaluated host outcomes from infection with wild-type and ΔprdB mouse-infective C. difficile ATCC 43255 strains to investigate how proline metabolism modulates C. difficile's pathogenesis and interactions with commensals in an enriched gut nutrient environment. While gnotobiotic mice infected with the ΔprdB mutant succumbed to infection, they showed delayed colonization and toxin production, thereby extending their survival. In vivo C. difficile transcriptomic analyses demonstrated a shift from Stickland fermentation to carbohydrate metabolism in the ΔprdB mutant. To investigate functions of C. difficile's proline reductase in interactions with the commensal microbiota, we evaluated infection outcomes in mice co-colonized with the disease-promoting commensal Clostridium sardiniense (CSAR). One-third of CSAR and ΔprdB-infected mice survived, while co-colonized mice with the wild-type strain rapidly succumbed within 48 h. In vivo transcriptomic analyses from co-colonized mice identified additional metabolic defects in the ΔprdB mutant, including failure to express oxidative Stickland pathways and ornithine fermentations to harness CSAR-produced ornithine, suggesting conversion of the mutant into a glycolytic strain that was now in direct competition with CSAR for carbohydrate substrates. CSAR remained metabolically active during the ΔprdB infection through its mucin degradation and polysaccharide and disaccharide metabolism. Our findings illustrate critical functions of C. difficile's proline reductase in coordinating early metabolism to facilitate gut colonization, including interactions with a cross-feeding commensal species.
IMPORTANCE: Clostridioides difficile is a spore-forming bacterium that commonly causes pseudomembranous colitis in patients exposed to antibiotics, with infections leading to 30,000 deaths annually in the United States. We conducted further in vitro and in vivo analyses to determine how proline reductase modulates C. difficile colonization, growth, and metabolism, and showed that this pathway is critical to Clostridium sardiniense's ability to cross-feed with the pathogen to cause toxic megacolon. We demonstrated that sporulation and toxin production are delayed when C. difficile's proline reductase pathway is interrupted through the deletion of the prdB gene. Survival was enhanced in mice co-colonized with C. sardiniense and the C. difficile ΔprdB mutant, as C. difficile relies on glycolytic pathways over Stickland fermentations. The present findings support the central role of proline reductase metabolism in early pathogen growth, metabolism, and toxin, and as a potential therapeutic target against C. difficile infection.
Additional Links: PMID-42328975
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PubMed:
Citation:
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@article {pmid42328975,
year = {2026},
author = {Cersosimo, LM and Graham, M and Monestier, A and Pavao, A and Worley, JN and Peltier, J and Dupuy, B and Bry, L},
title = {Mechanisms by which proline reductase of Clostridioides difficile promotes efficient metabolism and disease progression in vivo.},
journal = {mBio},
volume = {},
number = {},
pages = {e0118026},
doi = {10.1128/mbio.01180-26},
pmid = {42328975},
issn = {2150-7511},
abstract = {UNLABELLED: Clostridioides difficile is a toxin-producing pathogen that opportunistically infects those with a depleted gut microbiome, often triggered by antibiotic use. C. difficile preferentially utilizes Stickland amino acids, including proline, to promote energy generation and growth for colonization. We evaluated host outcomes from infection with wild-type and ΔprdB mouse-infective C. difficile ATCC 43255 strains to investigate how proline metabolism modulates C. difficile's pathogenesis and interactions with commensals in an enriched gut nutrient environment. While gnotobiotic mice infected with the ΔprdB mutant succumbed to infection, they showed delayed colonization and toxin production, thereby extending their survival. In vivo C. difficile transcriptomic analyses demonstrated a shift from Stickland fermentation to carbohydrate metabolism in the ΔprdB mutant. To investigate functions of C. difficile's proline reductase in interactions with the commensal microbiota, we evaluated infection outcomes in mice co-colonized with the disease-promoting commensal Clostridium sardiniense (CSAR). One-third of CSAR and ΔprdB-infected mice survived, while co-colonized mice with the wild-type strain rapidly succumbed within 48 h. In vivo transcriptomic analyses from co-colonized mice identified additional metabolic defects in the ΔprdB mutant, including failure to express oxidative Stickland pathways and ornithine fermentations to harness CSAR-produced ornithine, suggesting conversion of the mutant into a glycolytic strain that was now in direct competition with CSAR for carbohydrate substrates. CSAR remained metabolically active during the ΔprdB infection through its mucin degradation and polysaccharide and disaccharide metabolism. Our findings illustrate critical functions of C. difficile's proline reductase in coordinating early metabolism to facilitate gut colonization, including interactions with a cross-feeding commensal species.
IMPORTANCE: Clostridioides difficile is a spore-forming bacterium that commonly causes pseudomembranous colitis in patients exposed to antibiotics, with infections leading to 30,000 deaths annually in the United States. We conducted further in vitro and in vivo analyses to determine how proline reductase modulates C. difficile colonization, growth, and metabolism, and showed that this pathway is critical to Clostridium sardiniense's ability to cross-feed with the pathogen to cause toxic megacolon. We demonstrated that sporulation and toxin production are delayed when C. difficile's proline reductase pathway is interrupted through the deletion of the prdB gene. Survival was enhanced in mice co-colonized with C. sardiniense and the C. difficile ΔprdB mutant, as C. difficile relies on glycolytic pathways over Stickland fermentations. The present findings support the central role of proline reductase metabolism in early pathogen growth, metabolism, and toxin, and as a potential therapeutic target against C. difficile infection.},
}
RevDate: 2026-06-22
Long-read metagenomics reveals stable resistome and microbiome in treated Italian slaughterhouse wastewater: a preliminary study.
Microbiology spectrum [Epub ahead of print].
Antimicrobial resistance (AMR) poses a major threat to global health, and food production environments are increasingly recognized as potential reservoirs and dissemination points for resistant bacteria and antimicrobial resistance genes (ARGs). Slaughterhouse wastewater contains complex microbial communities originating from multiple animal sources and processing activities, yet the effectiveness of current treatment processes in mitigating microbiological and resistome-associated risks remains poorly understood. In this study, we applied high-throughput long-read metagenomic sequencing to characterize microbial community composition and resistome profiles in wastewater samples collected before and after physicochemical treatment from four Italian slaughterhouses. Taxonomic profiling revealed a diverse microbiome dominated by Bacillota and Pseudomonadota, along with DNA assigned to potentially clinically relevant taxa, including members of the ESKAPE group. Resistome analysis identified 96 ARGs conferring resistance to 16 antimicrobial classes. Comparative analyses of pre- and post-treatment samples showed no significant changes in microbial community structure, alpha- and beta-diversity metrics, or ARG profiles. These findings indicate that the applied coagulation-flocculation-based treatment has limited effects on the relative composition of the wastewater microbiome and resistome, as detected by shotgun metagenomics. Our results suggest that slaughterhouse wastewater may act as a persistent environmental reservoir of antimicrobial resistance determinants and highlight the need for enhanced treatment strategies and resistome-oriented surveillance within a One Health framework. Given the limited sample size and the preliminary nature of this investigation, these findings should be interpreted as exploratory and hypothesis-generating, rather than broadly generalizable.IMPORTANCEAntimicrobial resistance is a growing global health concern that extends beyond clinical settings into agricultural and environmental systems. Slaughterhouses represent critical interfaces where microbial communities from livestock, processing environments, and wastewater converge, creating opportunities for the persistence and dissemination of antimicrobial resistance genes. Despite the widespread use of physicochemical treatments to reduce organic load and suspended solids in slaughterhouse wastewater, their impact on microbial communities and resistome remains poorly characterized. By applying long-read metagenomic sequencing, this study provides a comprehensive characterization of the microbiome and resistome in slaughterhouse wastewater before and after treatment. Our findings show that commonly applied coagulation-flocculation treatments do not substantially alter the relative structure of microbial communities or the diversity of resistance genes. These results highlight the potential role of slaughterhouse wastewater as an environmental reservoir for antimicrobial resistance and emphasize the need for improved treatment technologies and systematic surveillance strategies to mitigate the environmental dissemination of resistance determinants in line with the One Health approach.
Additional Links: PMID-42328985
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PubMed:
Citation:
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@article {pmid42328985,
year = {2026},
author = {Pallotti, S and Nigro, ME and Albini, E and Russo, E and Carpi, FM and Falconi, M and Torbidoni-Baldassari, B and Giuliodori, AM and Petrelli, D and Beccacece, L and Pezzotti, G and Magistrali, CF and Massacci, FR and Napolioni, V},
title = {Long-read metagenomics reveals stable resistome and microbiome in treated Italian slaughterhouse wastewater: a preliminary study.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0156226},
doi = {10.1128/spectrum.01562-26},
pmid = {42328985},
issn = {2165-0497},
abstract = {Antimicrobial resistance (AMR) poses a major threat to global health, and food production environments are increasingly recognized as potential reservoirs and dissemination points for resistant bacteria and antimicrobial resistance genes (ARGs). Slaughterhouse wastewater contains complex microbial communities originating from multiple animal sources and processing activities, yet the effectiveness of current treatment processes in mitigating microbiological and resistome-associated risks remains poorly understood. In this study, we applied high-throughput long-read metagenomic sequencing to characterize microbial community composition and resistome profiles in wastewater samples collected before and after physicochemical treatment from four Italian slaughterhouses. Taxonomic profiling revealed a diverse microbiome dominated by Bacillota and Pseudomonadota, along with DNA assigned to potentially clinically relevant taxa, including members of the ESKAPE group. Resistome analysis identified 96 ARGs conferring resistance to 16 antimicrobial classes. Comparative analyses of pre- and post-treatment samples showed no significant changes in microbial community structure, alpha- and beta-diversity metrics, or ARG profiles. These findings indicate that the applied coagulation-flocculation-based treatment has limited effects on the relative composition of the wastewater microbiome and resistome, as detected by shotgun metagenomics. Our results suggest that slaughterhouse wastewater may act as a persistent environmental reservoir of antimicrobial resistance determinants and highlight the need for enhanced treatment strategies and resistome-oriented surveillance within a One Health framework. Given the limited sample size and the preliminary nature of this investigation, these findings should be interpreted as exploratory and hypothesis-generating, rather than broadly generalizable.IMPORTANCEAntimicrobial resistance is a growing global health concern that extends beyond clinical settings into agricultural and environmental systems. Slaughterhouses represent critical interfaces where microbial communities from livestock, processing environments, and wastewater converge, creating opportunities for the persistence and dissemination of antimicrobial resistance genes. Despite the widespread use of physicochemical treatments to reduce organic load and suspended solids in slaughterhouse wastewater, their impact on microbial communities and resistome remains poorly characterized. By applying long-read metagenomic sequencing, this study provides a comprehensive characterization of the microbiome and resistome in slaughterhouse wastewater before and after treatment. Our findings show that commonly applied coagulation-flocculation treatments do not substantially alter the relative structure of microbial communities or the diversity of resistance genes. These results highlight the potential role of slaughterhouse wastewater as an environmental reservoir for antimicrobial resistance and emphasize the need for improved treatment technologies and systematic surveillance strategies to mitigate the environmental dissemination of resistance determinants in line with the One Health approach.},
}
RevDate: 2026-06-22
Cost-effectiveness of Microbiota Restoration Therapies for Recurrent Clostridioides difficile Infection.
The American journal of gastroenterology pii:00000434-990000000-02218 [Epub ahead of print].
BACKGROUND: Recurrent Clostridioides difficile infection (rCDI) is associated with substantial morbidity, healthcare utilization, and costs. FDA-approved microbiota-based therapies, fecal microbiota spores, live-brpk (VOS) and fecal microbiota, live-jslm (RBL), reduce recurrence risk, but cost-effective placement within the rCDI treatment pathway remains uncertain.
METHODS: We performed a U.S. payer-perspective cost-effectiveness analysis using decision-tree modeling according to CHEERS 2022 guidelines. Adult with rCDI entered the model after the first or second recurrence and were followed for <1 year. Effectiveness inputs were derived from ECOSPOR III/IV (VOS), PUNCH CD3/CD3-OLS (RBL) trials, and published literature for standard-of-care (SoC) comparators. Outcomes included costs (2025 USD), quality-adjusted life-years (QALYs), and incremental cost-effectiveness ratios (ICERs). Probabilistic and deterministic sensitivity analyses were performed using a willingness-to-pay threshold of $150,000/QALY. ICERs were interpreted across $50,000, $100,000, $120,000, and $150,000/QALY.
RESULTS: After the first recurrence, RBL was cost-effective versus SoC alone ($25,415/QALY). Early initiation remained favorable compared with delayed use for VOS ($27,239/QALY) and RBL ($26,704/QALY). After the second recurrence, VOS remained cost-effective versus SoC (ICER $53,983/QALY), whereas RBL exceeded the willingness-to-pay threshold (ICER $171,496/QALY). Exploratory cross-trial VOS-versus-RBL comparisons yielded ICERs of $124,636/QALY after first recurrence and $137,350/QALY after second recurrence, indicating threshold-sensitive product-to-product comparisons.
CONCLUSIONS: Earlier initiation of microbiota-based therapies after the first CDI recurrence provides greater health benefits at acceptable cost-effectiveness thresholds compared with delayed use, supporting earlier integration into rCDI treatment strategies. VOS-versus-RBL comparisons should be interpreted as exploratory indirect comparisons pending comparative real-world or head-to-head data.
Additional Links: PMID-42329003
Publisher:
PubMed:
Citation:
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@article {pmid42329003,
year = {2026},
author = {Berry, P and Bharadiya, V and Pardi, DS and Khanna, S},
title = {Cost-effectiveness of Microbiota Restoration Therapies for Recurrent Clostridioides difficile Infection.},
journal = {The American journal of gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ajg.0000000000004083},
pmid = {42329003},
issn = {1572-0241},
abstract = {BACKGROUND: Recurrent Clostridioides difficile infection (rCDI) is associated with substantial morbidity, healthcare utilization, and costs. FDA-approved microbiota-based therapies, fecal microbiota spores, live-brpk (VOS) and fecal microbiota, live-jslm (RBL), reduce recurrence risk, but cost-effective placement within the rCDI treatment pathway remains uncertain.
METHODS: We performed a U.S. payer-perspective cost-effectiveness analysis using decision-tree modeling according to CHEERS 2022 guidelines. Adult with rCDI entered the model after the first or second recurrence and were followed for <1 year. Effectiveness inputs were derived from ECOSPOR III/IV (VOS), PUNCH CD3/CD3-OLS (RBL) trials, and published literature for standard-of-care (SoC) comparators. Outcomes included costs (2025 USD), quality-adjusted life-years (QALYs), and incremental cost-effectiveness ratios (ICERs). Probabilistic and deterministic sensitivity analyses were performed using a willingness-to-pay threshold of $150,000/QALY. ICERs were interpreted across $50,000, $100,000, $120,000, and $150,000/QALY.
RESULTS: After the first recurrence, RBL was cost-effective versus SoC alone ($25,415/QALY). Early initiation remained favorable compared with delayed use for VOS ($27,239/QALY) and RBL ($26,704/QALY). After the second recurrence, VOS remained cost-effective versus SoC (ICER $53,983/QALY), whereas RBL exceeded the willingness-to-pay threshold (ICER $171,496/QALY). Exploratory cross-trial VOS-versus-RBL comparisons yielded ICERs of $124,636/QALY after first recurrence and $137,350/QALY after second recurrence, indicating threshold-sensitive product-to-product comparisons.
CONCLUSIONS: Earlier initiation of microbiota-based therapies after the first CDI recurrence provides greater health benefits at acceptable cost-effectiveness thresholds compared with delayed use, supporting earlier integration into rCDI treatment strategies. VOS-versus-RBL comparisons should be interpreted as exploratory indirect comparisons pending comparative real-world or head-to-head data.},
}
RevDate: 2026-06-22
Anatomical, physiological, and luminal adaptations occurring in an ileoanal pouch: opportunities for improving outcomes.
Inflammatory bowel diseases pii:8713123 [Epub ahead of print].
BACKGROUND: The ileal pouch represents a unique adaptation of the ileum to serve the dual roles of nutrient absorption, fecal storage, and evacuation in a new luminal microenvironment. However, the adaptation process produces early histological inflammation and therefore clues in the development of pouchitis may lie in how the ileal pouch adapts.
AIMS: This narrative review explored anatomical and luminal ileal pouch adaptations, with a goal of designing clinical strategies that can strengthen the resilience of the pouch mucosa.
METHODS: A comprehensive PubMed search was conducted, and findings were critically examined and summarized.
RESULTS: Physiologically, the ileum must acquire key adaptive features, such as water and electrolyte reabsorption and distention capabilities to support optimal pouch function. However, other adaptations, such as severe villous blunting and alterations in bile acid metabolism, may accelerate an inflammatory environment. The benefits of retaining ileal type characteristics such as aspects of mucosal architecture are unclear, whereas changes in permeability and epithelial nutrient utilization remain incompletely characterized. Significant knowledge gaps remain regarding the optimal pouch microenvironment, including how the microbiome and its metabolites contribute to pouchitis development, and current therapies to manage pouchitis have yielded limited success. Mechanistically informed studies that explore the dynamic interplay between pouch structure, microbiota, and dietary influences are needed to better design targeted therapies.
CONCLUSIONS: The ileal pouch undergoes a series of adaptations that are not fully understood. This review integrates current evidence to better understand these adaptations, highlights clinically relevant implications, and identifies key areas where further mechanistic investigation is needed.
Additional Links: PMID-42329028
Publisher:
PubMed:
Citation:
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@article {pmid42329028,
year = {2026},
author = {Rhys-Jones, D and Gibson, PR and Halmos, EP and Segal, JP and Ardalan, Z and Yao, CK},
title = {Anatomical, physiological, and luminal adaptations occurring in an ileoanal pouch: opportunities for improving outcomes.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag111},
pmid = {42329028},
issn = {1536-4844},
support = {//Monash University/ ; },
abstract = {BACKGROUND: The ileal pouch represents a unique adaptation of the ileum to serve the dual roles of nutrient absorption, fecal storage, and evacuation in a new luminal microenvironment. However, the adaptation process produces early histological inflammation and therefore clues in the development of pouchitis may lie in how the ileal pouch adapts.
AIMS: This narrative review explored anatomical and luminal ileal pouch adaptations, with a goal of designing clinical strategies that can strengthen the resilience of the pouch mucosa.
METHODS: A comprehensive PubMed search was conducted, and findings were critically examined and summarized.
RESULTS: Physiologically, the ileum must acquire key adaptive features, such as water and electrolyte reabsorption and distention capabilities to support optimal pouch function. However, other adaptations, such as severe villous blunting and alterations in bile acid metabolism, may accelerate an inflammatory environment. The benefits of retaining ileal type characteristics such as aspects of mucosal architecture are unclear, whereas changes in permeability and epithelial nutrient utilization remain incompletely characterized. Significant knowledge gaps remain regarding the optimal pouch microenvironment, including how the microbiome and its metabolites contribute to pouchitis development, and current therapies to manage pouchitis have yielded limited success. Mechanistically informed studies that explore the dynamic interplay between pouch structure, microbiota, and dietary influences are needed to better design targeted therapies.
CONCLUSIONS: The ileal pouch undergoes a series of adaptations that are not fully understood. This review integrates current evidence to better understand these adaptations, highlights clinically relevant implications, and identifies key areas where further mechanistic investigation is needed.},
}
RevDate: 2026-06-22
Canagliflozin attenuates Parkinson's disease and is associated with modulation of gut-inflammasome-brain axis in rats.
Inflammopharmacology [Epub ahead of print].
Recent evidence links gut dysbiosis and the gut-brain axis to the pathophysiology of Parkinson's disease (PD), which is considered one of the most common neurodegenerative illnesses and is characterized by motor symptoms and a gradual loss of nigral dopaminergic neurons. Canagliflozin (CANA), a sodium-glucose cotransporter-2 inhibitor with emerging anti-inflammatory and antioxidant properties, has recently gained attention for its neuroprotective effects beyond glycemic control. This research aimed to examine the neuroprotective potential of CANA in a rat model of PD, focusing on its potential effect on the gut-inflammasome-brain axis. Rats were treated with rotenone (ROT) (2 mg/kg, subcutaneous) and/or CANA (20 mg/kg, oral) for 30 consecutive days. Behavioral assessment (n = 13), biochemical assays (n = 6), and histological and immunohistochemical analysis (n = 3) were performed. Microbiome profiling (n = 3) using 16S rRNA amplicon sequencing was conducted using three pooled fecal samples/group, with each pool prepared from fecal material collected from three rats and fecal metabolomic profiling (n = 5) was performed to assess microbial metabolites. ROT intoxication caused significant motor impairments, including decreased locomotor activity, poor coordination, and increased catalepsy. Further histological examination demonstrated dopaminergic neuronal loss and α-synuclein aggregation in the substantia nigra and striatum. CANA treatment enhanced motor function, conserved neuronal integrity, and decreased α-synuclein accumulation. Moreover, ROT altered the gut microbiota with selective taxonomic shifts, including enriched abundance of Parabacteroides and Ruminococcaceae with depleted Prevotella-related taxa, in addition to fecal metabolite profile alteration. Consequently, it increased colonic oxidative stress and weakened tight junctions, all of which enhanced LPS translocation. This systemic endotoxemia generated oxidative stress, dyslipidemia, and NF-κB/NLRP3 inflammasome activation. Conversely, CANA restored gut microbial balance and their metabolites, and gut integrity, decreased LPS leakage, and reduced systemic and central oxidative stress and inflammation, preventing inflammasome activation and α-synuclein aggregation. Collectively, these findings suggest that CANA may exert neuroprotective effects in ROT-induced PD associated with modulating the gut-inflammasome-brain axis.
Additional Links: PMID-42329290
PubMed:
Citation:
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@article {pmid42329290,
year = {2026},
author = {Gamal, NK and Fakhry, R and Hatem, Y and Rashed, E and Marzouk, R and Bukr, AKM and Safwat, K and Mamdouh, M and AbdElFatah, A and Atallah, A and Attia, H and Ayoub, IM and George, MY},
title = {Canagliflozin attenuates Parkinson's disease and is associated with modulation of gut-inflammasome-brain axis in rats.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {42329290},
issn = {1568-5608},
abstract = {Recent evidence links gut dysbiosis and the gut-brain axis to the pathophysiology of Parkinson's disease (PD), which is considered one of the most common neurodegenerative illnesses and is characterized by motor symptoms and a gradual loss of nigral dopaminergic neurons. Canagliflozin (CANA), a sodium-glucose cotransporter-2 inhibitor with emerging anti-inflammatory and antioxidant properties, has recently gained attention for its neuroprotective effects beyond glycemic control. This research aimed to examine the neuroprotective potential of CANA in a rat model of PD, focusing on its potential effect on the gut-inflammasome-brain axis. Rats were treated with rotenone (ROT) (2 mg/kg, subcutaneous) and/or CANA (20 mg/kg, oral) for 30 consecutive days. Behavioral assessment (n = 13), biochemical assays (n = 6), and histological and immunohistochemical analysis (n = 3) were performed. Microbiome profiling (n = 3) using 16S rRNA amplicon sequencing was conducted using three pooled fecal samples/group, with each pool prepared from fecal material collected from three rats and fecal metabolomic profiling (n = 5) was performed to assess microbial metabolites. ROT intoxication caused significant motor impairments, including decreased locomotor activity, poor coordination, and increased catalepsy. Further histological examination demonstrated dopaminergic neuronal loss and α-synuclein aggregation in the substantia nigra and striatum. CANA treatment enhanced motor function, conserved neuronal integrity, and decreased α-synuclein accumulation. Moreover, ROT altered the gut microbiota with selective taxonomic shifts, including enriched abundance of Parabacteroides and Ruminococcaceae with depleted Prevotella-related taxa, in addition to fecal metabolite profile alteration. Consequently, it increased colonic oxidative stress and weakened tight junctions, all of which enhanced LPS translocation. This systemic endotoxemia generated oxidative stress, dyslipidemia, and NF-κB/NLRP3 inflammasome activation. Conversely, CANA restored gut microbial balance and their metabolites, and gut integrity, decreased LPS leakage, and reduced systemic and central oxidative stress and inflammation, preventing inflammasome activation and α-synuclein aggregation. Collectively, these findings suggest that CANA may exert neuroprotective effects in ROT-induced PD associated with modulating the gut-inflammasome-brain axis.},
}
RevDate: 2026-06-22
Immunomodulatory and Gut Microbiota-Regulating Effects of Lactobacillus helveticus LH76 in Healthy Adults: Preclinical Safety Assessment and a Randomized, Double-Blind, Placebo-Controlled Trial.
Probiotics and antimicrobial proteins [Epub ahead of print].
Lactobacillus helveticus LH76 is a candidate strain with potential probiotic properties, but its safety and functional effects have not been comprehensively characterized. In this study, we systematically evaluated the safety profile and potential immunomodulatory and gut microbiota-modulating effects of LH76 through integrated genomic, preclinical, and clinical approaches. Preclinical safety assessment included whole-genome sequencing and bioinformatics analyses (AMRFinder, CARD, ResFinder, VFDB, and PathogenFinder), in vitro assays of hemolysis, biogenic amine production, and cytotoxicity in Caco-2 cells, as well as a 14-day acute oral toxicity study in mice. An 8-week randomized, double-blind, placebo-controlled trial was subsequently conducted in healthy adults to assess safety, immune-related biomarkers (IgA, IgM, IgG, C3, C4, LL-37, and calprotectin), and gut microbiota composition by 16 S rRNA sequencing. LH76 showed no detectable antibiotic resistance or classical virulence genes, no hemolytic activity, negligible biogenic amine production, and no detectable cytotoxicity in vitro, while no adverse effects or pathological abnormalities were observed in vivo. In the clinical trial, LH76 was well tolerated and was not associated with adverse changes in hematological, biochemical, or metabolic parameters. Compared with placebo, LH76 supplementation was associated with increased serum IgM and C3 levels, decreased C4 and LL-37 levels, increased microbial richness, and relative enrichment of genera including Blautia and Bifidobacterium. PICRUSt2-based analysis further suggested shifts in predicted microbial metabolic pathways, although these findings remain inferential. Overall, LH76 demonstrated a favorable safety profile, was well tolerated in healthy adults at the administered daily dose of 3 × 10[10] CFU/day for 8 weeks and showed an acute oral LD50 exceeding 2 × 10[10] CFU/kg in mice. These findings support further investigation of LH76 in larger and more mechanistic studies.
Additional Links: PMID-42329317
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Citation:
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@article {pmid42329317,
year = {2026},
author = {Song, S and Ding, L and Yang, T and Liu, J and Wang, Z and Qin, Y and Tan, X and Xu, F and Liang, T},
title = {Immunomodulatory and Gut Microbiota-Regulating Effects of Lactobacillus helveticus LH76 in Healthy Adults: Preclinical Safety Assessment and a Randomized, Double-Blind, Placebo-Controlled Trial.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42329317},
issn = {1867-1314},
abstract = {Lactobacillus helveticus LH76 is a candidate strain with potential probiotic properties, but its safety and functional effects have not been comprehensively characterized. In this study, we systematically evaluated the safety profile and potential immunomodulatory and gut microbiota-modulating effects of LH76 through integrated genomic, preclinical, and clinical approaches. Preclinical safety assessment included whole-genome sequencing and bioinformatics analyses (AMRFinder, CARD, ResFinder, VFDB, and PathogenFinder), in vitro assays of hemolysis, biogenic amine production, and cytotoxicity in Caco-2 cells, as well as a 14-day acute oral toxicity study in mice. An 8-week randomized, double-blind, placebo-controlled trial was subsequently conducted in healthy adults to assess safety, immune-related biomarkers (IgA, IgM, IgG, C3, C4, LL-37, and calprotectin), and gut microbiota composition by 16 S rRNA sequencing. LH76 showed no detectable antibiotic resistance or classical virulence genes, no hemolytic activity, negligible biogenic amine production, and no detectable cytotoxicity in vitro, while no adverse effects or pathological abnormalities were observed in vivo. In the clinical trial, LH76 was well tolerated and was not associated with adverse changes in hematological, biochemical, or metabolic parameters. Compared with placebo, LH76 supplementation was associated with increased serum IgM and C3 levels, decreased C4 and LL-37 levels, increased microbial richness, and relative enrichment of genera including Blautia and Bifidobacterium. PICRUSt2-based analysis further suggested shifts in predicted microbial metabolic pathways, although these findings remain inferential. Overall, LH76 demonstrated a favorable safety profile, was well tolerated in healthy adults at the administered daily dose of 3 × 10[10] CFU/day for 8 weeks and showed an acute oral LD50 exceeding 2 × 10[10] CFU/kg in mice. These findings support further investigation of LH76 in larger and more mechanistic studies.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
The human breast milk microbiome: a landscape review of its composition, origins, and impact on infant health.
Archives of microbiology, 208(9):.
Breast milk has long been recognized as the optimal source of nutrition for newborns, yet emerging research has revealed an additional dimension of its complexity: a diverse and dynamic microbial community. The breast milk microbiome constitutes one of the earliest and most consequential sources of microbial colonization in the infant gut, with direct relevance to neonatal immune development and long-term health. The core milk microbiome, dominated by Staphylococcus, Streptococcus, Lactobacillus, and Bifidobacterium, arrives principally via the entero-mammary pathway, maternal skin, and retrograde infant oral transfer, and is substantially modulated by maternal factors including diet, mode of delivery, antibiotic use, BMI, and lactation stage. Beyond live microorganisms, human milk oligosaccharides serve as critical prebiotics that selectively promote beneficial microbial taxa in the infant gut, while also exhibiting direct antimicrobial and immunomodulatory properties. Extracellular vesicles in breast milk carry bioactive payload, including proteins, microRNAs, and microbial components, that influence infant gut epithelial development and immune signaling, representing an underexplored frontier in milk biology. This review synthesizes current knowledge on the composition, origins, and functional significance of the breast milk microbiome. Based on a wide-ranging literature survey, the functional roles of the breast milk microbiome in colonization resistance, immune education, and metabolic programming in the developing infant are evaluated. Disruptions to this microbial community have been associated with conditions such as infant colic, atopic disease, and obesity. By mapping the available literature, we identify emerging research trends in the breast milk microbiome research and their translational implications for infant health optimization.
Additional Links: PMID-42329433
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@article {pmid42329433,
year = {2026},
author = {Koynova-Tenchov, R},
title = {The human breast milk microbiome: a landscape review of its composition, origins, and impact on infant health.},
journal = {Archives of microbiology},
volume = {208},
number = {9},
pages = {},
pmid = {42329433},
issn = {1432-072X},
mesh = {Humans ; *Milk, Human/microbiology ; *Infant Health ; *Microbiota ; Female ; Infant ; Infant, Newborn ; Oligosaccharides ; Bacteria/classification/isolation & purification/genetics ; Gastrointestinal Microbiome ; },
abstract = {Breast milk has long been recognized as the optimal source of nutrition for newborns, yet emerging research has revealed an additional dimension of its complexity: a diverse and dynamic microbial community. The breast milk microbiome constitutes one of the earliest and most consequential sources of microbial colonization in the infant gut, with direct relevance to neonatal immune development and long-term health. The core milk microbiome, dominated by Staphylococcus, Streptococcus, Lactobacillus, and Bifidobacterium, arrives principally via the entero-mammary pathway, maternal skin, and retrograde infant oral transfer, and is substantially modulated by maternal factors including diet, mode of delivery, antibiotic use, BMI, and lactation stage. Beyond live microorganisms, human milk oligosaccharides serve as critical prebiotics that selectively promote beneficial microbial taxa in the infant gut, while also exhibiting direct antimicrobial and immunomodulatory properties. Extracellular vesicles in breast milk carry bioactive payload, including proteins, microRNAs, and microbial components, that influence infant gut epithelial development and immune signaling, representing an underexplored frontier in milk biology. This review synthesizes current knowledge on the composition, origins, and functional significance of the breast milk microbiome. Based on a wide-ranging literature survey, the functional roles of the breast milk microbiome in colonization resistance, immune education, and metabolic programming in the developing infant are evaluated. Disruptions to this microbial community have been associated with conditions such as infant colic, atopic disease, and obesity. By mapping the available literature, we identify emerging research trends in the breast milk microbiome research and their translational implications for infant health optimization.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Milk, Human/microbiology
*Infant Health
*Microbiota
Female
Infant
Infant, Newborn
Oligosaccharides
Bacteria/classification/isolation & purification/genetics
Gastrointestinal Microbiome
RevDate: 2026-06-22
Rethinking Head and Neck Atopic Dermatitis: Pathogenic Axes and Emerging Therapeutic Directions.
American journal of clinical dermatology [Epub ahead of print].
Head and neck atopic dermatitis represents a common and clinically challenging phenotype of atopic dermatitis, characterized by anatomical selectivity, chronicity, and variable therapeutic response. Increasing evidence indicates that head and neck atopic dermatitis is not merely a regional extension of generalized disease, but a distinct phenotype shaped by the convergence of regional barrier fragility, a lipid-rich sebaceous microenvironment, microbiome imbalance, particularly involving Malassezia species, and a mixed immune signature integrating type 2, type 17, and type 22 inflammatory pathways. These factors promote persistent inflammation, psoriasiform features, and relative treatment refractoriness in the head and neck region. The clinical relevance of this phenotype has increased in the era of targeted therapies, as persistent or de novo facial involvement has been reported during biologic treatment, most notably with interleukin-4Rα blockade. Dupilumab-associated head and neck dermatitis exemplifies a pathway shift characterized by suppression of type 2 inflammation alongside exaggerated interleukin-22 and aryl hydrocarbon receptor-driven epithelial stress responses, providing mechanistic insight into paradoxical inflammation and incomplete regional control. Advances in immunobiology are beginning to translate into more tailored therapeutic strategies. Interleukin-13-selective biologics, systemic and topical Janus kinase inhibitors, and emerging agents targeting tissue-resident memory T-cell pathways offer new opportunities to address the dominant inflammatory circuits active in this region. Although comparative data remain limited, these approaches raise the possibility of improved control in selected patients with difficult-to-treat head and neck involvement. This review synthesizes current evidence on the pathogenic hallmarks of head and neck atopic dermatitis, integrates emerging mechanistic and clinical data, and discusses evolving therapeutic strategies aimed at phenotype-driven region-specific management of this complex manifestation of atopic dermatitis.
Additional Links: PMID-42329514
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Citation:
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@article {pmid42329514,
year = {2026},
author = {Navarro-Triviño, FJ and Ruiz-Villaverde, R and Torres, T},
title = {Rethinking Head and Neck Atopic Dermatitis: Pathogenic Axes and Emerging Therapeutic Directions.},
journal = {American journal of clinical dermatology},
volume = {},
number = {},
pages = {},
pmid = {42329514},
issn = {1179-1888},
abstract = {Head and neck atopic dermatitis represents a common and clinically challenging phenotype of atopic dermatitis, characterized by anatomical selectivity, chronicity, and variable therapeutic response. Increasing evidence indicates that head and neck atopic dermatitis is not merely a regional extension of generalized disease, but a distinct phenotype shaped by the convergence of regional barrier fragility, a lipid-rich sebaceous microenvironment, microbiome imbalance, particularly involving Malassezia species, and a mixed immune signature integrating type 2, type 17, and type 22 inflammatory pathways. These factors promote persistent inflammation, psoriasiform features, and relative treatment refractoriness in the head and neck region. The clinical relevance of this phenotype has increased in the era of targeted therapies, as persistent or de novo facial involvement has been reported during biologic treatment, most notably with interleukin-4Rα blockade. Dupilumab-associated head and neck dermatitis exemplifies a pathway shift characterized by suppression of type 2 inflammation alongside exaggerated interleukin-22 and aryl hydrocarbon receptor-driven epithelial stress responses, providing mechanistic insight into paradoxical inflammation and incomplete regional control. Advances in immunobiology are beginning to translate into more tailored therapeutic strategies. Interleukin-13-selective biologics, systemic and topical Janus kinase inhibitors, and emerging agents targeting tissue-resident memory T-cell pathways offer new opportunities to address the dominant inflammatory circuits active in this region. Although comparative data remain limited, these approaches raise the possibility of improved control in selected patients with difficult-to-treat head and neck involvement. This review synthesizes current evidence on the pathogenic hallmarks of head and neck atopic dermatitis, integrates emerging mechanistic and clinical data, and discusses evolving therapeutic strategies aimed at phenotype-driven region-specific management of this complex manifestation of atopic dermatitis.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Unravelling the associations between local environmental factors, soil properties and cultivable root-associated endophytes in dry pea (Pisum sativum L.).
World journal of microbiology & biotechnology, 42(7):.
Endophytic microorganisms in legume roots form an important interface between soil conditions and plant health. However, field-scale evidence remains limited on how cultivable endophytic bacterial and fungal assemblages in pea roots vary with soil and climatic conditions after nodule removal. In this study, 96 healthy pea plants were collected from eight field plots in Palencia, Spain. Cultivable endophytic bacteria and fungi were isolated from surface-disinfected root tissues after nodule removal, and community composition was assessed by Sanger sequencing of 16 S rRNA gene and ITS markers using a 97% OTU workflow. Bacterial communities showed greater compositional variation among plots, although genera such as Pseudomonas, Achromobacter, Peribacillus and Bacillus were repeatedly isolated across sites. In the cultivable fungal fraction, Fusarium was the most frequently isolated genus. Non-metric multidimensional scaling (NMDS)-envfit analysis showed that bacterial community variation was significantly associated with soil silt percentage (r[2] = 0.87, P = 0.007), whereas fungal community variation was significantly associated with exchangeable magnesium (r[2] = 0.67, P = 0.046). No climatic variable showed a significant fit at the study scale. Overall, these results provide a culture-based description of recurrent endophytic taxa in healthy pea roots and their preliminary associations with local soil conditions, offering a basis for future strain-based functional studies and more comprehensive microbiome analyses using culture-independent approaches.
Additional Links: PMID-42329569
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@article {pmid42329569,
year = {2026},
author = {Qu, S and Martín-García, J and Martín-Jiménez, D and Zunzunegui, I and Sánchez-Gómez, T and Santamaría, Ó and Poveda, J},
title = {Unravelling the associations between local environmental factors, soil properties and cultivable root-associated endophytes in dry pea (Pisum sativum L.).},
journal = {World journal of microbiology & biotechnology},
volume = {42},
number = {7},
pages = {},
pmid = {42329569},
issn = {1573-0972},
mesh = {*Pisum sativum/microbiology ; *Soil Microbiology ; *Plant Roots/microbiology ; *Endophytes/classification/isolation & purification/genetics/growth & development ; *Bacteria/classification/isolation & purification/genetics ; RNA, Ribosomal, 16S/genetics ; *Fungi/classification/isolation & purification/genetics ; *Soil/chemistry ; Phylogeny ; Spain ; DNA, Bacterial/genetics ; Sequence Analysis, DNA ; Root Nodules, Plant/microbiology ; DNA, Fungal/genetics ; },
abstract = {Endophytic microorganisms in legume roots form an important interface between soil conditions and plant health. However, field-scale evidence remains limited on how cultivable endophytic bacterial and fungal assemblages in pea roots vary with soil and climatic conditions after nodule removal. In this study, 96 healthy pea plants were collected from eight field plots in Palencia, Spain. Cultivable endophytic bacteria and fungi were isolated from surface-disinfected root tissues after nodule removal, and community composition was assessed by Sanger sequencing of 16 S rRNA gene and ITS markers using a 97% OTU workflow. Bacterial communities showed greater compositional variation among plots, although genera such as Pseudomonas, Achromobacter, Peribacillus and Bacillus were repeatedly isolated across sites. In the cultivable fungal fraction, Fusarium was the most frequently isolated genus. Non-metric multidimensional scaling (NMDS)-envfit analysis showed that bacterial community variation was significantly associated with soil silt percentage (r[2] = 0.87, P = 0.007), whereas fungal community variation was significantly associated with exchangeable magnesium (r[2] = 0.67, P = 0.046). No climatic variable showed a significant fit at the study scale. Overall, these results provide a culture-based description of recurrent endophytic taxa in healthy pea roots and their preliminary associations with local soil conditions, offering a basis for future strain-based functional studies and more comprehensive microbiome analyses using culture-independent approaches.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Pisum sativum/microbiology
*Soil Microbiology
*Plant Roots/microbiology
*Endophytes/classification/isolation & purification/genetics/growth & development
*Bacteria/classification/isolation & purification/genetics
RNA, Ribosomal, 16S/genetics
*Fungi/classification/isolation & purification/genetics
*Soil/chemistry
Phylogeny
Spain
DNA, Bacterial/genetics
Sequence Analysis, DNA
Root Nodules, Plant/microbiology
DNA, Fungal/genetics
RevDate: 2026-06-22
The respiratory microbiome: dynamics from health to disease.
FEMS microbiology ecology pii:8713279 [Epub ahead of print].
Research on the respiratory microbiome has moved beyond the sterile-lung paradigm, but disease-associated microbial patterns are still often described as static signatures. In this mini-review, we synthesize current evidence within a dynamic state-transition framework in which respiratory microbial communities are shaped by microbial immigration, elimination, local growth conditions, and host inflammatory tone. This framework traces the respiratory microbiome from early-life assembly and homeostatic maintenance to perturbation, recovery, or persistence in alternative ecological states. We discuss how barrier integrity, mucociliary clearance, mucus and nutrient landscapes, inflammatory feedback, microbial metabolites, and the gut-lung axis regulate microbial stability and disease susceptibility. Across asthma, chronic obstructive pulmonary disease, cystic fibrosis, bronchiectasis, and respiratory infection, dysbiosis is interpreted not as a set of disease-specific taxa, but as a context-dependent outcome of shared ecological mechanisms. We also highlight methodological and translational priorities, including contamination control in low-biomass samples, longitudinal sampling, multi-omics integration, spatial host profiling, and cautious interpretation of association versus causality. Viewing the respiratory microbiome as an ecological system in motion may better connect microbial dynamics with disease heterogeneity, risk stratification, and future microbiome-directed interventions.
Additional Links: PMID-42329775
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@article {pmid42329775,
year = {2026},
author = {Lin, W and Sun, Z and Chen, J and Huang, S},
title = {The respiratory microbiome: dynamics from health to disease.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag058},
pmid = {42329775},
issn = {1574-6941},
abstract = {Research on the respiratory microbiome has moved beyond the sterile-lung paradigm, but disease-associated microbial patterns are still often described as static signatures. In this mini-review, we synthesize current evidence within a dynamic state-transition framework in which respiratory microbial communities are shaped by microbial immigration, elimination, local growth conditions, and host inflammatory tone. This framework traces the respiratory microbiome from early-life assembly and homeostatic maintenance to perturbation, recovery, or persistence in alternative ecological states. We discuss how barrier integrity, mucociliary clearance, mucus and nutrient landscapes, inflammatory feedback, microbial metabolites, and the gut-lung axis regulate microbial stability and disease susceptibility. Across asthma, chronic obstructive pulmonary disease, cystic fibrosis, bronchiectasis, and respiratory infection, dysbiosis is interpreted not as a set of disease-specific taxa, but as a context-dependent outcome of shared ecological mechanisms. We also highlight methodological and translational priorities, including contamination control in low-biomass samples, longitudinal sampling, multi-omics integration, spatial host profiling, and cautious interpretation of association versus causality. Viewing the respiratory microbiome as an ecological system in motion may better connect microbial dynamics with disease heterogeneity, risk stratification, and future microbiome-directed interventions.},
}
RevDate: 2026-06-22
Applying PCR cycle autonormalization to PacBio full-length 16S rRNA library preparations: impacts on error rates and sequence distributions.
mSphere [Epub ahead of print].
The bacterial 16S rRNA gene is widely used to characterize host-associated and environmental microbiomes, most commonly through sequencing short hypervariable regions. Recent improvements in PacBio sequencing chemistry and concatenation approaches can now enable high-throughput, full-length 16S rRNA gene sequencing with high accuracy and depth. However, errors introduced during library preparation remain a major limitation, particularly during PCR amplification of full-length amplicons, where error accumulation may be elevated due to longer sequence lengths. These challenges are amplified when samples vary widely in microbial biomass, making it difficult to select a single optimal number of PCR cycles. Here, we evaluated PCR cycle autonormalization for PacBio Kinnex full-length 16S rRNA gene sequencing across seven agriculturally relevant specimen types. We compared conventional fixed-cycle PCR protocols (20, 24, and 30 cycles) with an autonormalization approach in which individual reactions were terminated during exponential amplification based on real-time fluorescence thresholds. Under the workflow tested here, autonormalized libraries generally retained a high proportion of sequences following denoising and chimera removal, exhibited low residual error rates (<0.005%), and yielded relatively even read distributions across heterogeneous sample inputs. Overamplified reactions (30 cycles) showed elevated residual error rates and greater sequence loss, particularly in samples with higher microbial biodiversity, whereas low-cycle libraries produced more variable read output among specimens. Importantly, the PCR protocol had relatively minor effects on overall community composition compared with specimen type. These results support PCR cycle autonormalization as a useful workflow strategy for heterogeneous full-length 16S library preparation, while also highlighting the importance of library design, pooling strategy, and downstream processing in shaping technical outcomes.IMPORTANCEAmplicon-based sequencing of the 16S rRNA gene is a foundational tool in microbiome research, yet PCR amplification remains a major source of library-preparation error. This challenge is magnified for full-length 16S rRNA sequencing and for workflows that process specimen types with widely varying microbial biomass. Selecting a single PCR cycle number can underamplify low-biomass samples or overamplify high-titer samples, increasing artifacts and sequence loss during downstream processing. Here, we show that PCR cycle autonormalization can be integrated into a PacBio full-length 16S rRNA workflow and, under the conditions tested, provides low residual error rates and relatively even sample representation across heterogeneous inputs. Autonormalization also enables blind pooling of amplicons without post-PCR quantification or equimolar normalization, reducing hands-on time and sample loss. These benefits make cycle autonormalization particularly valuable for high-throughput and production-scale library preparation applications handling diverse specimen types.
Additional Links: PMID-42330062
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PubMed:
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@article {pmid42330062,
year = {2026},
author = {Mason, CJ and Weaver, M and Kissinger, KR and Johnson, MA and Copeland, DC and Anderson, KE and Geib, SM},
title = {Applying PCR cycle autonormalization to PacBio full-length 16S rRNA library preparations: impacts on error rates and sequence distributions.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0029526},
doi = {10.1128/msphere.00295-26},
pmid = {42330062},
issn = {2379-5042},
abstract = {The bacterial 16S rRNA gene is widely used to characterize host-associated and environmental microbiomes, most commonly through sequencing short hypervariable regions. Recent improvements in PacBio sequencing chemistry and concatenation approaches can now enable high-throughput, full-length 16S rRNA gene sequencing with high accuracy and depth. However, errors introduced during library preparation remain a major limitation, particularly during PCR amplification of full-length amplicons, where error accumulation may be elevated due to longer sequence lengths. These challenges are amplified when samples vary widely in microbial biomass, making it difficult to select a single optimal number of PCR cycles. Here, we evaluated PCR cycle autonormalization for PacBio Kinnex full-length 16S rRNA gene sequencing across seven agriculturally relevant specimen types. We compared conventional fixed-cycle PCR protocols (20, 24, and 30 cycles) with an autonormalization approach in which individual reactions were terminated during exponential amplification based on real-time fluorescence thresholds. Under the workflow tested here, autonormalized libraries generally retained a high proportion of sequences following denoising and chimera removal, exhibited low residual error rates (<0.005%), and yielded relatively even read distributions across heterogeneous sample inputs. Overamplified reactions (30 cycles) showed elevated residual error rates and greater sequence loss, particularly in samples with higher microbial biodiversity, whereas low-cycle libraries produced more variable read output among specimens. Importantly, the PCR protocol had relatively minor effects on overall community composition compared with specimen type. These results support PCR cycle autonormalization as a useful workflow strategy for heterogeneous full-length 16S library preparation, while also highlighting the importance of library design, pooling strategy, and downstream processing in shaping technical outcomes.IMPORTANCEAmplicon-based sequencing of the 16S rRNA gene is a foundational tool in microbiome research, yet PCR amplification remains a major source of library-preparation error. This challenge is magnified for full-length 16S rRNA sequencing and for workflows that process specimen types with widely varying microbial biomass. Selecting a single PCR cycle number can underamplify low-biomass samples or overamplify high-titer samples, increasing artifacts and sequence loss during downstream processing. Here, we show that PCR cycle autonormalization can be integrated into a PacBio full-length 16S rRNA workflow and, under the conditions tested, provides low residual error rates and relatively even sample representation across heterogeneous inputs. Autonormalization also enables blind pooling of amplicons without post-PCR quantification or equimolar normalization, reducing hands-on time and sample loss. These benefits make cycle autonormalization particularly valuable for high-throughput and production-scale library preparation applications handling diverse specimen types.},
}
RevDate: 2026-06-22
CoDaLoMic: An R package for modeling microbiome compositional and longitudinal data.
PLoS computational biology, 22(6):e1014328 pii:PCOMPBIOL-D-25-01429 [Epub ahead of print].
In this paper we present CoDaLoMic, an R package for analyzing longitudinal and compositional microbiome datasets. The CoDaLoMic package implements three models specifically designed for the analysis of microbiome data that are both compositional and longitudinal. Unlike many existing methods that focus solely on pairwise interactions, CoDaLoMic also captures interactions among groups of bacteria, providing a more robust methodological framework for studying microbial relationships at the community level. In addition, the package facilitates the analysis of microbiome variability in relation to host health status and allows for the identification of groups of taxa that exhibit similar temporal dynamics. Working with time series data makes it possible to understand not only the current state of a microbial community but also its dynamics over time, which is essential for identifying patterns of ecological succession, detecting events of dysbiosis or recovery, and inferring potential causal relationships between taxa. On the other hand, focusing on interactions among groups of bacteria, rather than analyzing only pairwise relationships, enables a more integrated and functionally meaningful view of the microbiome. Many key ecological functions are the result of the collective behavior of functionally related groups of taxa. Two datasets have been considered in CoDaLoMic, one real and one simulated. The real dataset contains the information of the genera present in the microbiome of the Blatella germanica cockroach at 105 time points. The simulated dataset is defined taking Lotka-Volterra structure into account. CoDaLoMic is available at CRAN.
Additional Links: PMID-42330077
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PubMed:
Citation:
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@article {pmid42330077,
year = {2026},
author = {Creus-Martí, I and Moya, A and Santonja, FJ},
title = {CoDaLoMic: An R package for modeling microbiome compositional and longitudinal data.},
journal = {PLoS computational biology},
volume = {22},
number = {6},
pages = {e1014328},
doi = {10.1371/journal.pcbi.1014328},
pmid = {42330077},
issn = {1553-7358},
abstract = {In this paper we present CoDaLoMic, an R package for analyzing longitudinal and compositional microbiome datasets. The CoDaLoMic package implements three models specifically designed for the analysis of microbiome data that are both compositional and longitudinal. Unlike many existing methods that focus solely on pairwise interactions, CoDaLoMic also captures interactions among groups of bacteria, providing a more robust methodological framework for studying microbial relationships at the community level. In addition, the package facilitates the analysis of microbiome variability in relation to host health status and allows for the identification of groups of taxa that exhibit similar temporal dynamics. Working with time series data makes it possible to understand not only the current state of a microbial community but also its dynamics over time, which is essential for identifying patterns of ecological succession, detecting events of dysbiosis or recovery, and inferring potential causal relationships between taxa. On the other hand, focusing on interactions among groups of bacteria, rather than analyzing only pairwise relationships, enables a more integrated and functionally meaningful view of the microbiome. Many key ecological functions are the result of the collective behavior of functionally related groups of taxa. Two datasets have been considered in CoDaLoMic, one real and one simulated. The real dataset contains the information of the genera present in the microbiome of the Blatella germanica cockroach at 105 time points. The simulated dataset is defined taking Lotka-Volterra structure into account. CoDaLoMic is available at CRAN.},
}
RevDate: 2026-06-22
Insights into the clinical presentation, imaging, and management of infiltrative keratitis following accelerated corneal collagen cross-linking.
Indian journal of ophthalmology pii:02223307-990000000-00466 [Epub ahead of print].
PURPOSE: To analyze the risk factors, clinical features, visual outcomes, and in-vivo imaging characteristics in cases of keratoconus developing keratitis following accelerated collagen cross-linking (CXL).
METHODS: A retrospective observational case series at a tertiary eye center in India evaluating eyes that underwent accelerated CXL from January 2021 to July 2024.
RESULTS: Of 723 eyes undergoing CXL, 14 eyes developed infiltrative keratitis (1.93%). The majority belonged to the upper middle socioeconomic class and presented in summer and rainy seasons. The relative risk of developing infiltrates in cases ≤16 years was 2.38, and in cases with history of vernal keratoconjunctivitis, it was 0.7. The median area of epithelial defect was 12 mm 2 , and the average resolution time was 18.4 ± 12.9 days. The most common organism that was isolated was coagulase-negative Staphylococcus. The majority of the cases on anterior segment optical coherence tomography showed involvement anterior to the demarcation line. Scheimpflug imaging showed three keratometric patterns: flattening and thinning, flattening and thinning with transient steepening, and minimal to no change.
CONCLUSION: Infiltrative keratitis following accelerated CXL is a rare clinical entity. Early presentation and timely management including use of topical steroids are associated with good visual outcomes.
Additional Links: PMID-42330205
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@article {pmid42330205,
year = {2026},
author = {Bari, A and Sushma, N and Agarwal, T and Shakkarwal, C and Maharana, PK and Dada, T and Sharma, N},
title = {Insights into the clinical presentation, imaging, and management of infiltrative keratitis following accelerated corneal collagen cross-linking.},
journal = {Indian journal of ophthalmology},
volume = {},
number = {},
pages = {},
doi = {10.4103/IJO.IJO_1451_25},
pmid = {42330205},
issn = {1998-3689},
abstract = {PURPOSE: To analyze the risk factors, clinical features, visual outcomes, and in-vivo imaging characteristics in cases of keratoconus developing keratitis following accelerated collagen cross-linking (CXL).
METHODS: A retrospective observational case series at a tertiary eye center in India evaluating eyes that underwent accelerated CXL from January 2021 to July 2024.
RESULTS: Of 723 eyes undergoing CXL, 14 eyes developed infiltrative keratitis (1.93%). The majority belonged to the upper middle socioeconomic class and presented in summer and rainy seasons. The relative risk of developing infiltrates in cases ≤16 years was 2.38, and in cases with history of vernal keratoconjunctivitis, it was 0.7. The median area of epithelial defect was 12 mm 2 , and the average resolution time was 18.4 ± 12.9 days. The most common organism that was isolated was coagulase-negative Staphylococcus. The majority of the cases on anterior segment optical coherence tomography showed involvement anterior to the demarcation line. Scheimpflug imaging showed three keratometric patterns: flattening and thinning, flattening and thinning with transient steepening, and minimal to no change.
CONCLUSION: Infiltrative keratitis following accelerated CXL is a rare clinical entity. Early presentation and timely management including use of topical steroids are associated with good visual outcomes.},
}
RevDate: 2026-06-22
Light-Activated Ruthenium Nanoclusters Reprogram the Metabolic-Quorum Sensing Axis for Precision Periodontitis Therapy.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Periodontitis is a polymicrobial disease driven by metabolic interdependencies, wherein commensal bacteria fuel the virulence of keystone pathogens like Porphyromonas gingivalis (P. gingivalis). In particular, Veillonella parvula (V. parvula) supplies essential nutrients to the keystone pathogen P. gingivalis, enabling its virulence even at low abundance. Therefore, targeting V. parvula nitrate metabolism to deprive P. gingivalis of nutrients and attenuate its virulence represents a promising therapeutic strategy for controlling periodontitis progression. We engineered L-cysteine-capped ruthenium nanoclusters (Ru NCs) that efficiently reduce nitrate to ammonium under 660 nm light. This photocatalytic conversion depleted the bioavailable nitrate pool associated with V. parvula metabolism, disrupting amino acid production and quorum-sensing-related support for P. gingivalis. Consequently, Ru NCs potently reduced biofilm biomass and thickness, suppressed P. gingivalis activity, and downregulated its key virulence genes (RgpA/B, Kgp, FimA). Multiomics analyses supported nitrate-dependent metabolic collapse in V. parvula, which was associated with downstream energy and biosynthetic impairment in P. gingivalis. In a rat periodontitis model, light-activated Ru NCs attenuated alveolar bone loss, preserved collagen, and shifted the local cytokine profile from pro-inflammatory (IL-6) to anti-inflammatory (Arg-1). This work provides a proof-of-concept strategy for targeting defined interspecies metabolic interactions, offering a new paradigm for microbiome-targeted therapy.
Additional Links: PMID-42330329
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@article {pmid42330329,
year = {2026},
author = {Zhou, J and Sun, X and Liu, C and Shi, Y and Li, M and Bo, M and Zhai, J and Li, C and Wu, Z and Bai, X and Wang, L},
title = {Light-Activated Ruthenium Nanoclusters Reprogram the Metabolic-Quorum Sensing Axis for Precision Periodontitis Therapy.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e76245},
doi = {10.1002/advs.76245},
pmid = {42330329},
issn = {2198-3844},
support = {82571148//National Natural Science Foundation of China/ ; YDZJ202401209ZYTS//Natural Science Foundation of Jilin Province/ ; JCSZ2025678-4 -11 -15 -19//Science and Technology Project of Jilin Province Financial Department/ ; 2025JBGS04//Interdisciplinary Innovation Team Project of Norman Bethune Health Science Department Jilin University/ ; },
abstract = {Periodontitis is a polymicrobial disease driven by metabolic interdependencies, wherein commensal bacteria fuel the virulence of keystone pathogens like Porphyromonas gingivalis (P. gingivalis). In particular, Veillonella parvula (V. parvula) supplies essential nutrients to the keystone pathogen P. gingivalis, enabling its virulence even at low abundance. Therefore, targeting V. parvula nitrate metabolism to deprive P. gingivalis of nutrients and attenuate its virulence represents a promising therapeutic strategy for controlling periodontitis progression. We engineered L-cysteine-capped ruthenium nanoclusters (Ru NCs) that efficiently reduce nitrate to ammonium under 660 nm light. This photocatalytic conversion depleted the bioavailable nitrate pool associated with V. parvula metabolism, disrupting amino acid production and quorum-sensing-related support for P. gingivalis. Consequently, Ru NCs potently reduced biofilm biomass and thickness, suppressed P. gingivalis activity, and downregulated its key virulence genes (RgpA/B, Kgp, FimA). Multiomics analyses supported nitrate-dependent metabolic collapse in V. parvula, which was associated with downstream energy and biosynthetic impairment in P. gingivalis. In a rat periodontitis model, light-activated Ru NCs attenuated alveolar bone loss, preserved collagen, and shifted the local cytokine profile from pro-inflammatory (IL-6) to anti-inflammatory (Arg-1). This work provides a proof-of-concept strategy for targeting defined interspecies metabolic interactions, offering a new paradigm for microbiome-targeted therapy.},
}
RevDate: 2026-06-22
Doxycycline post-exposure prophylaxis may dramatically reduce syphilis among gay, bisexual, and other men who have sex with men: a modeling study.
Sexually transmitted diseases pii:00007435-990000000-00704 [Epub ahead of print].
BACKGROUND: Syphilis cases in the United States have surged over the past decade, and cases are highest among gay, bisexual, and other men who have sex with men (GBMSM). The CDC recommends doxycycline post-exposure prophylaxis (doxy PEP) for GBMSM recently diagnosed with bacterial STIs to mitigate this burden. Potential drawbacks include increased antimicrobial resistance and microbiome disruption. Here, we estimate doxy PEP coverage levels required to eliminate sustained community transmission among GBMSM while balancing the drawbacks of doxy PEP.
METHODS: We fit a modified susceptible-infectious-susceptible model of syphilis transmission among GBMSM to syphilis case counts by sex-of-sex-partner. We simulated a range of doxy PEP coverage and adherence levels among GBMSM linked to HIV treatment and prevention over a ten-year period. We tracked syphilis prevalence and incident cases among GBMSM with and without healthcare access.
RESULTS: With a lower bound efficacy estimate (41%) and 10% doxy PEP utilization (coverage × adherence) among GBMSM linked to HIV treatment and prevention, we estimated a 24% [Interquartile Range: 17%-30%] reduction in annual syphilis cases among GBMSM over the next 10 years. Under upper bound efficacy estimates (97%) and 50% utilization, we estimated a 99% [IQR: 88%-100%] reduction in annual syphilis cases among GBMSM over the next 10 years. Our model shows that if sub-populations of GBMSM have reduced access to healthcare, then the elimination of sustained community transmission is unlikely over the next decade.
CONCLUSIONS: Doxy PEP may dramatically reduce syphilis incidence among GBMSM, but barriers to healthcare may impede the elimination of sustained community transmission of syphilis.
Additional Links: PMID-42330441
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@article {pmid42330441,
year = {2026},
author = {Clay, PA and Jackson, DA and Bachmann, LH and Spicknall, IH},
title = {Doxycycline post-exposure prophylaxis may dramatically reduce syphilis among gay, bisexual, and other men who have sex with men: a modeling study.},
journal = {Sexually transmitted diseases},
volume = {},
number = {},
pages = {},
doi = {10.1097/OLQ.0000000000002371},
pmid = {42330441},
issn = {1537-4521},
abstract = {BACKGROUND: Syphilis cases in the United States have surged over the past decade, and cases are highest among gay, bisexual, and other men who have sex with men (GBMSM). The CDC recommends doxycycline post-exposure prophylaxis (doxy PEP) for GBMSM recently diagnosed with bacterial STIs to mitigate this burden. Potential drawbacks include increased antimicrobial resistance and microbiome disruption. Here, we estimate doxy PEP coverage levels required to eliminate sustained community transmission among GBMSM while balancing the drawbacks of doxy PEP.
METHODS: We fit a modified susceptible-infectious-susceptible model of syphilis transmission among GBMSM to syphilis case counts by sex-of-sex-partner. We simulated a range of doxy PEP coverage and adherence levels among GBMSM linked to HIV treatment and prevention over a ten-year period. We tracked syphilis prevalence and incident cases among GBMSM with and without healthcare access.
RESULTS: With a lower bound efficacy estimate (41%) and 10% doxy PEP utilization (coverage × adherence) among GBMSM linked to HIV treatment and prevention, we estimated a 24% [Interquartile Range: 17%-30%] reduction in annual syphilis cases among GBMSM over the next 10 years. Under upper bound efficacy estimates (97%) and 50% utilization, we estimated a 99% [IQR: 88%-100%] reduction in annual syphilis cases among GBMSM over the next 10 years. Our model shows that if sub-populations of GBMSM have reduced access to healthcare, then the elimination of sustained community transmission is unlikely over the next decade.
CONCLUSIONS: Doxy PEP may dramatically reduce syphilis incidence among GBMSM, but barriers to healthcare may impede the elimination of sustained community transmission of syphilis.},
}
RevDate: 2026-06-22
Disruption of intestinal mucosal immunity and microbial homeostasis in Schizothorax davidi under chronic DBP exposure: From functional compensation to transcriptional decompensation.
Aquatic toxicology (Amsterdam, Netherlands), 298:107909 pii:S0166-445X(26)00206-7 [Epub ahead of print].
Di-n‑butyl phthalate (DBP) is a ubiquitous environmental pollutant in the Yangtze River, yet the integrated toxicological mechanisms by which it impairs the microbiota-gut-brain axis to induce behavioral alterations in fish remain poorly understood. As a rare fish endemic to the upper reaches of the Yangtze River and a pivotal ecological indicator, Schizothorax davidi is currently facing severe environmental exposure risks. In this study, Schizothorax davidi was exposed to environmentally relevant concentrations of DBP (3, 30, and 300 μg/L) for 30days. A multidisciplinary approach, integrating YOLOv8-based behavioral tracking with multi-omics, was employed to evaluate its chronic toxicity. Our results revealed a biphasic behavioral response: acute hyperactivity at low doses (T1), acting as a stress-induced escape response, transitioned into significant locomotor suppression at higher doses (T2-T3), indicating non-adaptive neurotoxic impairment. Joint transcriptomic and 16S rRNA analysis demonstrated that the intestine shifted from a state of functional immune compensation to transcriptional decompensation as DBP concentrations increased. Furthermore, DBP exposure dramatically restructured the gut microbiota, identifying Planctomycetota as a keystone functional hub; its decline significantly correlated with the downregulation of host immune-regulatory and mucosal protective genes. In contrast to the intestinal response, transcriptomic interference in the brain intensified with concentration, triggering a TNF-mediated "molecular storm" and activating apoptotic pathways that signify a transition from reversible neuroinflammation to irreversible neural damage. Collectively, these findings demonstrate that DBP exposure compromises both the physical and microbial barriers of the gut, enabling the translocation of systemic inflammatory signals that drive central neurological failure. This research provides crucial mechanistic insights and scientific evidence for the ecological risk assessment of native fish species in the upper Yangtze River.
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@article {pmid42330678,
year = {2026},
author = {Lei, L and Liao, R and Peng, M and Zhou, Y and Xiao, C and Yu, X and Liu, S and Duan, Y and Fu, S and Li, H and Liu, C and Chen, X and Li, L and Zeng, B and Liu, H and Zhou, C},
title = {Disruption of intestinal mucosal immunity and microbial homeostasis in Schizothorax davidi under chronic DBP exposure: From functional compensation to transcriptional decompensation.},
journal = {Aquatic toxicology (Amsterdam, Netherlands)},
volume = {298},
number = {},
pages = {107909},
doi = {10.1016/j.aquatox.2026.107909},
pmid = {42330678},
issn = {1879-1514},
abstract = {Di-n‑butyl phthalate (DBP) is a ubiquitous environmental pollutant in the Yangtze River, yet the integrated toxicological mechanisms by which it impairs the microbiota-gut-brain axis to induce behavioral alterations in fish remain poorly understood. As a rare fish endemic to the upper reaches of the Yangtze River and a pivotal ecological indicator, Schizothorax davidi is currently facing severe environmental exposure risks. In this study, Schizothorax davidi was exposed to environmentally relevant concentrations of DBP (3, 30, and 300 μg/L) for 30days. A multidisciplinary approach, integrating YOLOv8-based behavioral tracking with multi-omics, was employed to evaluate its chronic toxicity. Our results revealed a biphasic behavioral response: acute hyperactivity at low doses (T1), acting as a stress-induced escape response, transitioned into significant locomotor suppression at higher doses (T2-T3), indicating non-adaptive neurotoxic impairment. Joint transcriptomic and 16S rRNA analysis demonstrated that the intestine shifted from a state of functional immune compensation to transcriptional decompensation as DBP concentrations increased. Furthermore, DBP exposure dramatically restructured the gut microbiota, identifying Planctomycetota as a keystone functional hub; its decline significantly correlated with the downregulation of host immune-regulatory and mucosal protective genes. In contrast to the intestinal response, transcriptomic interference in the brain intensified with concentration, triggering a TNF-mediated "molecular storm" and activating apoptotic pathways that signify a transition from reversible neuroinflammation to irreversible neural damage. Collectively, these findings demonstrate that DBP exposure compromises both the physical and microbial barriers of the gut, enabling the translocation of systemic inflammatory signals that drive central neurological failure. This research provides crucial mechanistic insights and scientific evidence for the ecological risk assessment of native fish species in the upper Yangtze River.},
}
RevDate: 2026-06-22
Microbiome-mediated plant immunity: Molecular signalling, community assembly, and emerging intergenerational feedback.
Microbiological research, 311:128591 pii:S0944-5013(26)00155-2 [Epub ahead of print].
Classical pattern-triggered (PTI) and effector-triggered (ETI) immunity, developed in single-pathogen systems, illuminates how plants recognise molecular threats but cannot fully explain immune homeostasis within the dynamic microbial communities plants encounter in nature. The extended plant immune system reframes immunity as a host-microbiome network sculpted by root exudates, yet two dimensions remain insufficiently integrated: the ecological rules translating recruited communities into systemic immune output, and the mechanisms by which holobiont state may carry over across generations. We propose that plant immune homeostasis is best analyzed as a three-node feedback circuit that we hypothesize closes across generations. Node 1 (molecular recruitment) integrates root exudate-mediated cross-kingdom signalling, in which primary and secondary metabolites jointly serve nutritional and immune-informative roles. Node 2 (ecological translation) is governed by dispersal, immune filtering, drift, priority effects, and functional redundancy, which together determine whether recruitment signals translate into immune buffering. Node 3 (intergenerational carry-over) comprises three mechanistically distinct routes-epigenetic reprogramming, seed microbiota transmission, and soil legacy-that range from provisionally established to largely hypothetical and whose field-scale validation remains limited. Treating this circuit, rather than the host or host-microbiome network, as the minimal unit of immune analysis generates testable predictions-linking functional redundancy to immune buffering, soil legacy to next-generation priming, and node-specific failure modes to dissociable signatures. This framing positions the holobiont across time (understood here as an analytical unit rather than an evolutionary one) as a tractable framework for hypothesis-driven plant immunity research.
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PubMed:
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@article {pmid42330748,
year = {2026},
author = {Liu, X and Ao, Z and Liu, X and Fu, X and Chen, L and He, X and Liu, X},
title = {Microbiome-mediated plant immunity: Molecular signalling, community assembly, and emerging intergenerational feedback.},
journal = {Microbiological research},
volume = {311},
number = {},
pages = {128591},
doi = {10.1016/j.micres.2026.128591},
pmid = {42330748},
issn = {1618-0623},
abstract = {Classical pattern-triggered (PTI) and effector-triggered (ETI) immunity, developed in single-pathogen systems, illuminates how plants recognise molecular threats but cannot fully explain immune homeostasis within the dynamic microbial communities plants encounter in nature. The extended plant immune system reframes immunity as a host-microbiome network sculpted by root exudates, yet two dimensions remain insufficiently integrated: the ecological rules translating recruited communities into systemic immune output, and the mechanisms by which holobiont state may carry over across generations. We propose that plant immune homeostasis is best analyzed as a three-node feedback circuit that we hypothesize closes across generations. Node 1 (molecular recruitment) integrates root exudate-mediated cross-kingdom signalling, in which primary and secondary metabolites jointly serve nutritional and immune-informative roles. Node 2 (ecological translation) is governed by dispersal, immune filtering, drift, priority effects, and functional redundancy, which together determine whether recruitment signals translate into immune buffering. Node 3 (intergenerational carry-over) comprises three mechanistically distinct routes-epigenetic reprogramming, seed microbiota transmission, and soil legacy-that range from provisionally established to largely hypothetical and whose field-scale validation remains limited. Treating this circuit, rather than the host or host-microbiome network, as the minimal unit of immune analysis generates testable predictions-linking functional redundancy to immune buffering, soil legacy to next-generation priming, and node-specific failure modes to dissociable signatures. This framing positions the holobiont across time (understood here as an analytical unit rather than an evolutionary one) as a tractable framework for hypothesis-driven plant immunity research.},
}
RevDate: 2026-06-22
Improving plant salt tolerance using the endophytic halophile Vreelandella salis sp. nov.
Plant physiology and biochemistry : PPB, 237:111492 pii:S0981-9428(26)00478-X [Epub ahead of print].
Soil salinity is a pervasive abiotic stress that severely constrains global crop productivity, demanding sustainable biotechnological solutions. This study characterized Vreelandella salis strain PAMB 3232ᵀ, a novel species of halophilic endophytic bacterium isolated from the shoot of the halophyte Suaeda maritima. Polyphasic analyses confirmed the taxonomic delineation of PAMB 3232ᵀ. This strain exhibits remarkable halotolerance, sustaining growth in up to 24% (w/v) NaCl. Genomic analysis revealed an enrichment of genes associated with metabolic resilience, particularly those involved in carbohydrate and amino acid metabolism, as well as cofactor and vitamin biosynthesis. Inoculation with strain PAMB 3232ᵀ significantly enhanced growth in Brassica rapa, increasing the shoot fresh weight by 26% under non-saline conditions and by 17.0% under salinity stress (200 mM NaCl). Physiological analyses further indicated enhanced stress tolerance, reflected by improved K[+]/Na[+] homeostasis and reduced malondialdehyde (MDA) accumulation. Moreover, rhizosphere microbiome profiling revealed that inoculation reshaped the rhizosphere microbial community. Under salinity, the rhizosphere network showed increased connectivity and modularity, with Pseudomonadota serving as key hubs and enrichment of beneficial Bacillota. Collectively, these results indicate that V. salis PAMB 3232ᵀ enhances crop salt tolerance via coordinated physiological and microbiome-mediated effects, supporting its potential as a microbial inoculant for salt-affected agriculture.
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@article {pmid42330784,
year = {2026},
author = {Peng, Y and Lee, J},
title = {Improving plant salt tolerance using the endophytic halophile Vreelandella salis sp. nov.},
journal = {Plant physiology and biochemistry : PPB},
volume = {237},
number = {},
pages = {111492},
doi = {10.1016/j.plaphy.2026.111492},
pmid = {42330784},
issn = {1873-2690},
abstract = {Soil salinity is a pervasive abiotic stress that severely constrains global crop productivity, demanding sustainable biotechnological solutions. This study characterized Vreelandella salis strain PAMB 3232ᵀ, a novel species of halophilic endophytic bacterium isolated from the shoot of the halophyte Suaeda maritima. Polyphasic analyses confirmed the taxonomic delineation of PAMB 3232ᵀ. This strain exhibits remarkable halotolerance, sustaining growth in up to 24% (w/v) NaCl. Genomic analysis revealed an enrichment of genes associated with metabolic resilience, particularly those involved in carbohydrate and amino acid metabolism, as well as cofactor and vitamin biosynthesis. Inoculation with strain PAMB 3232ᵀ significantly enhanced growth in Brassica rapa, increasing the shoot fresh weight by 26% under non-saline conditions and by 17.0% under salinity stress (200 mM NaCl). Physiological analyses further indicated enhanced stress tolerance, reflected by improved K[+]/Na[+] homeostasis and reduced malondialdehyde (MDA) accumulation. Moreover, rhizosphere microbiome profiling revealed that inoculation reshaped the rhizosphere microbial community. Under salinity, the rhizosphere network showed increased connectivity and modularity, with Pseudomonadota serving as key hubs and enrichment of beneficial Bacillota. Collectively, these results indicate that V. salis PAMB 3232ᵀ enhances crop salt tolerance via coordinated physiological and microbiome-mediated effects, supporting its potential as a microbial inoculant for salt-affected agriculture.},
}
RevDate: 2026-06-22
Micron-engineered biochar mitigates antimony and microplastics toxicity by reshaping soil microbiome and plant transcriptomic responses.
Journal of hazardous materials, 514:142705 pii:S0304-3894(26)01684-5 [Epub ahead of print].
Antimony (Sb) and microplastics (MPs) are environmental threats for plants and human health. Antimony is known to impair plant growth, but the combined effects of Sb and MPs on plant and soil traits remain unexplored. This study examined the role of micron-engineered biochar (MBC) in mitigating Sb (250 mg kg[-1]) + MPs (1%) soil contamination. Five treatments were established in a pot experiment: control, Sb + MPs, Sb + MPs + MBC applied at 1%, 1.5% and 2%. MBC counteracted the negative impacts of Sb + MPs on leaf water status, osmo-regulating compounds (average, +57%), antioxidant activities (average, +93%), soil Sb content and plant uptake (both, -31%), soil nutrient (N, P, K) contents and plant uptake (average, +72%), and grain yield (+57%). MBC also increased the abundance of Acidobacteria, Actinobacteria, Bacteriodota, and Proteobacteria as well as antimony degrading genes. Transcriptomic analysis revealed that MBC supply mitigated Sb + MPs toxicity by upregulating the MAPK signaling cascade, ABC transporters, ion export channels, peroxisomes, ascorbic acid, aldehyde, and galactose metabolism. These findings suggest that MBC is a multidimensional resource for remediating co-contaminated soils and enhancing rice productivity.
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PubMed:
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@article {pmid42330898,
year = {2026},
author = {Hassan, MU and Ahmed, W and Barbanti, L and Yuxin, H and Shujian, Z and Altihani, FA and Qitao, S and Guoqin, H},
title = {Micron-engineered biochar mitigates antimony and microplastics toxicity by reshaping soil microbiome and plant transcriptomic responses.},
journal = {Journal of hazardous materials},
volume = {514},
number = {},
pages = {142705},
doi = {10.1016/j.jhazmat.2026.142705},
pmid = {42330898},
issn = {1873-3336},
abstract = {Antimony (Sb) and microplastics (MPs) are environmental threats for plants and human health. Antimony is known to impair plant growth, but the combined effects of Sb and MPs on plant and soil traits remain unexplored. This study examined the role of micron-engineered biochar (MBC) in mitigating Sb (250 mg kg[-1]) + MPs (1%) soil contamination. Five treatments were established in a pot experiment: control, Sb + MPs, Sb + MPs + MBC applied at 1%, 1.5% and 2%. MBC counteracted the negative impacts of Sb + MPs on leaf water status, osmo-regulating compounds (average, +57%), antioxidant activities (average, +93%), soil Sb content and plant uptake (both, -31%), soil nutrient (N, P, K) contents and plant uptake (average, +72%), and grain yield (+57%). MBC also increased the abundance of Acidobacteria, Actinobacteria, Bacteriodota, and Proteobacteria as well as antimony degrading genes. Transcriptomic analysis revealed that MBC supply mitigated Sb + MPs toxicity by upregulating the MAPK signaling cascade, ABC transporters, ion export channels, peroxisomes, ascorbic acid, aldehyde, and galactose metabolism. These findings suggest that MBC is a multidimensional resource for remediating co-contaminated soils and enhancing rice productivity.},
}
RevDate: 2026-06-22
Shoot-root hormonal coordination and cross-sphere microbiome assembly underpin nanomaterial-induced resistance to rare earth elements in lettuce.
Journal of hazardous materials, 514:142728 pii:S0304-3894(26)01707-3 [Epub ahead of print].
Mining-induced rare earth elements (REEs) pollution in agricultural soil threatens food security, necessitating effective remediation strategies. Foliar-applied nanoparticles (NPs) offer a promising approach, while their potential in alleviating REEs-induced stress in crops remains insufficiently understood, particularly the systemic phytohormone-mediated responses and associated microbiome assembly that are crucial for plant resilience. Here, we demonstrated that SiO2-NPs and MnO2-NPs (0.5 and 1.25 mg/day/plant) significantly promoted lettuce growth (up to 3.02-fold) and reduced REEs accumulation (up to 74.0%/91.2% in roots/shoots). Concurrently, plant nutritional status and photosynthesis activity were improved, with SiO2-NPs specifically contributing to enhanced energy homeostasis. Gene set enrichment analysis (GSEA) revealed that NPs treatments activated plant resistance system, with SiO2-NPs specifically promoting the biosynthesis of stress resistance-related compounds and MnO2-NPs tending to regulate phytohormone signal transduction process. Crucially, these transcriptional responses were closely correlated to multiple phytohormones modulated by NPs in both shoots and roots, including auxin and jasmonates, as identified by weighted gene co-expression network analysis (WGCNA). Furthermore, NPs reshaped phyllosphere and rhizosphere microbiomes, such as Pseudomonadota, Cyanobacteriota and Bacillota. Notably, rhizosphere microbiome exhibited a strong correlation with phytohormone levels in shoots and roots, revealing the existence of a hormone-microbiome regulatory network that facilitates whole-plant adaptation to REEs stress. These findings underscore the pivotal role of NPs-induced phytohormonal signaling in coordinating shoot-root stress resistance and modulating microbiome composition under REEs contamination, providing mechanistic insights for developing NPs-based strategies to safeguard food production.
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@article {pmid42330899,
year = {2026},
author = {Xi, Q and Qiu, H and Jiang, X and Wang, L and Yao, Y and He, E},
title = {Shoot-root hormonal coordination and cross-sphere microbiome assembly underpin nanomaterial-induced resistance to rare earth elements in lettuce.},
journal = {Journal of hazardous materials},
volume = {514},
number = {},
pages = {142728},
doi = {10.1016/j.jhazmat.2026.142728},
pmid = {42330899},
issn = {1873-3336},
abstract = {Mining-induced rare earth elements (REEs) pollution in agricultural soil threatens food security, necessitating effective remediation strategies. Foliar-applied nanoparticles (NPs) offer a promising approach, while their potential in alleviating REEs-induced stress in crops remains insufficiently understood, particularly the systemic phytohormone-mediated responses and associated microbiome assembly that are crucial for plant resilience. Here, we demonstrated that SiO2-NPs and MnO2-NPs (0.5 and 1.25 mg/day/plant) significantly promoted lettuce growth (up to 3.02-fold) and reduced REEs accumulation (up to 74.0%/91.2% in roots/shoots). Concurrently, plant nutritional status and photosynthesis activity were improved, with SiO2-NPs specifically contributing to enhanced energy homeostasis. Gene set enrichment analysis (GSEA) revealed that NPs treatments activated plant resistance system, with SiO2-NPs specifically promoting the biosynthesis of stress resistance-related compounds and MnO2-NPs tending to regulate phytohormone signal transduction process. Crucially, these transcriptional responses were closely correlated to multiple phytohormones modulated by NPs in both shoots and roots, including auxin and jasmonates, as identified by weighted gene co-expression network analysis (WGCNA). Furthermore, NPs reshaped phyllosphere and rhizosphere microbiomes, such as Pseudomonadota, Cyanobacteriota and Bacillota. Notably, rhizosphere microbiome exhibited a strong correlation with phytohormone levels in shoots and roots, revealing the existence of a hormone-microbiome regulatory network that facilitates whole-plant adaptation to REEs stress. These findings underscore the pivotal role of NPs-induced phytohormonal signaling in coordinating shoot-root stress resistance and modulating microbiome composition under REEs contamination, providing mechanistic insights for developing NPs-based strategies to safeguard food production.},
}
RevDate: 2026-06-22
Zinc accumulation as a primary contributor to co-exposure toxicity with 6PPD-quinone in earthworms: Multi-level evidence.
Journal of hazardous materials, 514:142749 pii:S0304-3894(26)01729-2 [Epub ahead of print].
Tire and road wear particles introduce complex mixtures of metals and organic additives into soils, yet the primary drivers of their combined toxicity remain poorly resolved. Here, we investigated the individual and combined effects of zinc oxide (ZnO), a major inorganic tire additive, and 6PPD-quinone (6PPD-Q), a toxic transformation product of the tire antioxidant 6PPD, using a soil invertebrate exposure model. A gradient of ZnO concentrations was tested alone and in combination with an environmentally relevant level of 6PPD-Q to simulate co-contaminated soils. While single exposures induced oxidative stress, metabolic perturbation, and gut microbiome alteration, co-exposure under high Zn conditions resulted in increased mortality and growth inhibition relative to single treatments. Chemical analysis revealed enhanced Zn accumulation in organisms under co-exposure, whereas 6PPD-Q bioaccumulation declined at elevated Zn levels, indicating that internal Zn burden was more consistently associated with organism-level impairment than measured internal 6PPD-Q concentration under the tested conditions. Integrated biochemical, histological, and multi-omics analyses showed that co-exposure was associated with enhanced oxidative stress, altered energy metabolism, impaired neuroimmune function, and destabilized gut microbial structure and predicted metabolic potential. Complementary multi-omics analyses revealed coordinated alterations in antioxidant defense, detoxification capacity, and mitochondrial metabolism under high-Zn co-exposure, consistent with a reduced physiological tolerance to chemical stress. Together, these findings support the interpretation that zinc accumulation likely represents a primary contributor to co-exposure toxicity, while 6PPD-quinone may amplify adverse outcomes by constraining organismal stress-buffering capacity. These results highlight the need to consider metal-organic interactions and differential toxic contributions in mixture-based environmental risk assessment of tire-derived contaminants.
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@article {pmid42330910,
year = {2026},
author = {Zhou, H and Li, Z and Wu, Z and Zou, L and Sun, H and Li, H and Wang, X and Wang, Y and Jin, J and Hofmann, T and Tang, J},
title = {Zinc accumulation as a primary contributor to co-exposure toxicity with 6PPD-quinone in earthworms: Multi-level evidence.},
journal = {Journal of hazardous materials},
volume = {514},
number = {},
pages = {142749},
doi = {10.1016/j.jhazmat.2026.142749},
pmid = {42330910},
issn = {1873-3336},
abstract = {Tire and road wear particles introduce complex mixtures of metals and organic additives into soils, yet the primary drivers of their combined toxicity remain poorly resolved. Here, we investigated the individual and combined effects of zinc oxide (ZnO), a major inorganic tire additive, and 6PPD-quinone (6PPD-Q), a toxic transformation product of the tire antioxidant 6PPD, using a soil invertebrate exposure model. A gradient of ZnO concentrations was tested alone and in combination with an environmentally relevant level of 6PPD-Q to simulate co-contaminated soils. While single exposures induced oxidative stress, metabolic perturbation, and gut microbiome alteration, co-exposure under high Zn conditions resulted in increased mortality and growth inhibition relative to single treatments. Chemical analysis revealed enhanced Zn accumulation in organisms under co-exposure, whereas 6PPD-Q bioaccumulation declined at elevated Zn levels, indicating that internal Zn burden was more consistently associated with organism-level impairment than measured internal 6PPD-Q concentration under the tested conditions. Integrated biochemical, histological, and multi-omics analyses showed that co-exposure was associated with enhanced oxidative stress, altered energy metabolism, impaired neuroimmune function, and destabilized gut microbial structure and predicted metabolic potential. Complementary multi-omics analyses revealed coordinated alterations in antioxidant defense, detoxification capacity, and mitochondrial metabolism under high-Zn co-exposure, consistent with a reduced physiological tolerance to chemical stress. Together, these findings support the interpretation that zinc accumulation likely represents a primary contributor to co-exposure toxicity, while 6PPD-quinone may amplify adverse outcomes by constraining organismal stress-buffering capacity. These results highlight the need to consider metal-organic interactions and differential toxic contributions in mixture-based environmental risk assessment of tire-derived contaminants.},
}
RevDate: 2026-06-22
Molecular features of external Auditory Canal cholesteatoma by microbial metagenomic sequencing.
Genomics pii:S0888-7543(26)00090-X [Epub ahead of print].
OBJECTIVE: External auditory canal cholesteatoma (EACC), a rare destructive benign lesion, causes significant hearing loss, recurrent infections, and impaired quality of life. We characterized its microbial profiles to explore associations with disease progression.
METHODS: Cholesteatoma tissues from surgically treated EACC patients (2021-2022) underwent metagenomic sequencing (Illumina MiSeq). Taxonomic composition, functional genes, and antimicrobial resistance (AMR) profiles were systematically analyzed.
RESULTS: We identified 4377 core genes revealing abundance correlations. Dominant taxa included Firmicutes (42.1%), Proteobacteria (28.6%), and Actinobacteria (19.3%), with enriched Staphylococcus (32.4%) and Corynebacterium (21.7%). Hierarchical clustering and PCA/NMDS confirmed significant taxonomic divergence. AMR profiling detected multidrug-resistant genotypes (e.g., blaTEM, mecA).
CONCLUSION: This study defines EACC's microbial complexity and its pathogenic role, advocating microbiome-targeted strategies to mitigate infections.
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@article {pmid42331262,
year = {2026},
author = {He, G and Guo, X and Lu, W and Zou, Y and Zheng, J and Han, X and Hong, Y and Wei, R},
title = {Molecular features of external Auditory Canal cholesteatoma by microbial metagenomic sequencing.},
journal = {Genomics},
volume = {},
number = {},
pages = {111282},
doi = {10.1016/j.ygeno.2026.111282},
pmid = {42331262},
issn = {1089-8646},
abstract = {OBJECTIVE: External auditory canal cholesteatoma (EACC), a rare destructive benign lesion, causes significant hearing loss, recurrent infections, and impaired quality of life. We characterized its microbial profiles to explore associations with disease progression.
METHODS: Cholesteatoma tissues from surgically treated EACC patients (2021-2022) underwent metagenomic sequencing (Illumina MiSeq). Taxonomic composition, functional genes, and antimicrobial resistance (AMR) profiles were systematically analyzed.
RESULTS: We identified 4377 core genes revealing abundance correlations. Dominant taxa included Firmicutes (42.1%), Proteobacteria (28.6%), and Actinobacteria (19.3%), with enriched Staphylococcus (32.4%) and Corynebacterium (21.7%). Hierarchical clustering and PCA/NMDS confirmed significant taxonomic divergence. AMR profiling detected multidrug-resistant genotypes (e.g., blaTEM, mecA).
CONCLUSION: This study defines EACC's microbial complexity and its pathogenic role, advocating microbiome-targeted strategies to mitigate infections.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-23
[Application of salicylic acid in inflammatory skin diseases and the effect on skin microbiome].
Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine], 60(6):988-995.
Emerging evidence underscores the pivotal role of the skin microbiome in the pathogenesis of inflammatory skin diseases. Dysbiosis (an imbalance in microbial composition), significantly drives the onset and exacerbation of these conditions. This article synthesizes current applications of salicylic acid in the management of common inflammatory skin diseases, with a specific focus on its capacity to modulate the skin microbiome. By elucidating the interplay between inflammatory states and microbial ecology, this article aim to offer new perspectives on utilizing salicylic acid novel insights for both therapeutic and preventive strategies.
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@article {pmid42331541,
year = {2026},
author = {Yuan, JH and Wei, AH and Tao, R},
title = {[Application of salicylic acid in inflammatory skin diseases and the effect on skin microbiome].},
journal = {Zhonghua yu fang yi xue za zhi [Chinese journal of preventive medicine]},
volume = {60},
number = {6},
pages = {988-995},
doi = {10.3760/cma.j.cn112150-20250708-00634},
pmid = {42331541},
issn = {0253-9624},
support = {7254317//Beijing Municipal Natural Science Foundation/ ; PYZ24107//Research Cultivation Program of Capital Medical University/ ; 82173447//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Salicylic Acid/therapeutic use ; *Skin Diseases/drug therapy/microbiology ; *Microbiota/drug effects ; Skin Microbiome ; *Skin/microbiology ; },
abstract = {Emerging evidence underscores the pivotal role of the skin microbiome in the pathogenesis of inflammatory skin diseases. Dysbiosis (an imbalance in microbial composition), significantly drives the onset and exacerbation of these conditions. This article synthesizes current applications of salicylic acid in the management of common inflammatory skin diseases, with a specific focus on its capacity to modulate the skin microbiome. By elucidating the interplay between inflammatory states and microbial ecology, this article aim to offer new perspectives on utilizing salicylic acid novel insights for both therapeutic and preventive strategies.},
}
MeSH Terms:
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Humans
*Salicylic Acid/therapeutic use
*Skin Diseases/drug therapy/microbiology
*Microbiota/drug effects
Skin Microbiome
*Skin/microbiology
RevDate: 2026-06-22
Gut microbiome metabolites meet immunometabolism in inflammatory bowel disease.
Trends in immunology pii:S1471-4906(26)00138-9 [Epub ahead of print].
Growing evidence indicates that gut microbiota-derived metabolites are key regulators of immunometabolism in inflammatory bowel disease (IBD). Intestinal epithelial cells and immune cells exhibit profound metabolic alterations in IBD. Microbial metabolites act as intermediates in host-microbe communication, reshaping mitochondrial functions and cellular metabolic pathways, thereby impacting immune functions. Dysbiosis may, therefore, perturb immune homeostasis by rewiring host metabolic circuits. Understanding how microbial metabolites orchestrate immunometabolic crosstalk in the gut and leveraging it to recalibrate host immunometabolic circuits represents promising, underexplored therapeutic avenues. In this review, we highlight emerging concepts on how gut microbiota-derived metabolites shape immune cell immunometabolism and discuss the therapeutic potential of targeting the microbiota-metabolite-immunometabolism axis in IBD.
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@article {pmid42331651,
year = {2026},
author = {Li, Q and de Oliveira Formiga, R and Sokol, H},
title = {Gut microbiome metabolites meet immunometabolism in inflammatory bowel disease.},
journal = {Trends in immunology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.it.2026.06.001},
pmid = {42331651},
issn = {1471-4981},
abstract = {Growing evidence indicates that gut microbiota-derived metabolites are key regulators of immunometabolism in inflammatory bowel disease (IBD). Intestinal epithelial cells and immune cells exhibit profound metabolic alterations in IBD. Microbial metabolites act as intermediates in host-microbe communication, reshaping mitochondrial functions and cellular metabolic pathways, thereby impacting immune functions. Dysbiosis may, therefore, perturb immune homeostasis by rewiring host metabolic circuits. Understanding how microbial metabolites orchestrate immunometabolic crosstalk in the gut and leveraging it to recalibrate host immunometabolic circuits represents promising, underexplored therapeutic avenues. In this review, we highlight emerging concepts on how gut microbiota-derived metabolites shape immune cell immunometabolism and discuss the therapeutic potential of targeting the microbiota-metabolite-immunometabolism axis in IBD.},
}
RevDate: 2026-06-22
Pilot metaproteomic profiling reveals bacterial diversity and potential medical and veterinary relevance of tick microbiomes in northern Algeria.
Scientific reports pii:10.1038/s41598-026-58580-1 [Epub ahead of print].
Ticks are major ectoparasites and vectors of pathogens affecting humans, livestock, and wildlife. They harbor diverse microbial communities that may influence tick biology and interactions with microorganisms; however, functional information on tick-associated microbiomes remains limited, particularly in North Africa. In this pilot study, we applied a metaproteomic approach based on high-resolution tandem mass spectrometry to characterize bacterial communities associated with three tick species collected in Algeria: Rhipicephalus sanguineus sensu lato, Hyalomma aegyptium, and Hyalomma dromedarii. Peptide spectra were assigned to taxa using a two-step database search strategy based on NCBInr, and bacterial composition and relative abundance were compared across tick species and sampling locations. A total of 40 bacterial genera belonging to 32 families and four phyla were identified. Microbiome composition differed significantly between tick genera and collection locations, suggesting an influence of species-specific and geographical factors on microbial community structure. Dominant genera included Streptomyces, Bacillus, Clostridium, Escherichia, Flavobacterium, Paenibacillus, and Providencia. Peptides related to Coxiella spp. were frequently detected, consistent with previous reports of Coxiella-like endosymbionts in ticks. This pilot study provides a first metaproteomic characterization of tick-associated communities in Algeria. The results reveal species- and location-associated differences in microbial composition and highlight the potential of metaproteomics for exploring tick-associated microbiomes in North Africa.
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@article {pmid42331868,
year = {2026},
author = {Kernif, T and Lozano, C and Khardine, FA and Medrouh, B and Hachid, A and Fernandez, B and Eddaikra, N and Delbecq, S and Armengaud, J and Sereno, D and Holzmuller, P},
title = {Pilot metaproteomic profiling reveals bacterial diversity and potential medical and veterinary relevance of tick microbiomes in northern Algeria.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-58580-1},
pmid = {42331868},
issn = {2045-2322},
support = {LeiSHeild-RISE MATI Grant N°778298//Horizon 2020 Framework Programme/ ; },
abstract = {Ticks are major ectoparasites and vectors of pathogens affecting humans, livestock, and wildlife. They harbor diverse microbial communities that may influence tick biology and interactions with microorganisms; however, functional information on tick-associated microbiomes remains limited, particularly in North Africa. In this pilot study, we applied a metaproteomic approach based on high-resolution tandem mass spectrometry to characterize bacterial communities associated with three tick species collected in Algeria: Rhipicephalus sanguineus sensu lato, Hyalomma aegyptium, and Hyalomma dromedarii. Peptide spectra were assigned to taxa using a two-step database search strategy based on NCBInr, and bacterial composition and relative abundance were compared across tick species and sampling locations. A total of 40 bacterial genera belonging to 32 families and four phyla were identified. Microbiome composition differed significantly between tick genera and collection locations, suggesting an influence of species-specific and geographical factors on microbial community structure. Dominant genera included Streptomyces, Bacillus, Clostridium, Escherichia, Flavobacterium, Paenibacillus, and Providencia. Peptides related to Coxiella spp. were frequently detected, consistent with previous reports of Coxiella-like endosymbionts in ticks. This pilot study provides a first metaproteomic characterization of tick-associated communities in Algeria. The results reveal species- and location-associated differences in microbial composition and highlight the potential of metaproteomics for exploring tick-associated microbiomes in North Africa.},
}
RevDate: 2026-06-22
Modelling the role of the microbiome in antimicrobial resistance across scales.
Nature microbiology [Epub ahead of print].
The microbiome actively influences antimicrobial resistance (AMR) dynamics by shaping both ecological and evolutionary processes. However, the extent of its role in resistance emergence, transmission and persistence remains unclear. Traditional AMR research has mainly focused on genetic mechanisms and pathogen-level dynamics. In contrast, the intersection of AMR and the microbiome, including resistance-gene reservoirs, microbial competition and community-mediated selection, remains poorly represented, especially in a modelling context. Here we present a structured framework for incorporating microbiome-AMR interactions into predictive models. We identify key microbiome-mediated processes shaping AMR across different levels of complexity, describe how these can be quantitatively integrated into models, and identify critical data gaps that limit current approaches. By bridging microbiome ecology, AMR biology and mathematical modelling, we set out research priorities and strategies to improve resistance prediction and guide microbiome-targeted interventions.
Additional Links: PMID-42332064
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@article {pmid42332064,
year = {2026},
author = {Pagani, L and León-Sampedro, R and Amicone, M and Tepekule, B and Witzany, C and Brugger, SD and de Vos, MGJ and Mitri, S and Bakkeren, E and Bottery, MJ and Opatowski, L and Leventhal, GE and Faust, K and Böttcher, L and Lehtinen, S and Kouyos, RD and Bonhoeffer, S},
title = {Modelling the role of the microbiome in antimicrobial resistance across scales.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42332064},
issn = {2058-5276},
support = {PCEGP3_181272//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; 51NF40_180575//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; 211422//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; PCEGP3_181272//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; 51NF40_180575//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; },
abstract = {The microbiome actively influences antimicrobial resistance (AMR) dynamics by shaping both ecological and evolutionary processes. However, the extent of its role in resistance emergence, transmission and persistence remains unclear. Traditional AMR research has mainly focused on genetic mechanisms and pathogen-level dynamics. In contrast, the intersection of AMR and the microbiome, including resistance-gene reservoirs, microbial competition and community-mediated selection, remains poorly represented, especially in a modelling context. Here we present a structured framework for incorporating microbiome-AMR interactions into predictive models. We identify key microbiome-mediated processes shaping AMR across different levels of complexity, describe how these can be quantitatively integrated into models, and identify critical data gaps that limit current approaches. By bridging microbiome ecology, AMR biology and mathematical modelling, we set out research priorities and strategies to improve resistance prediction and guide microbiome-targeted interventions.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-23
The importance of meal timing for maintenance of daily rhythms in the gut transcriptome and microbiota.
Npj biological timing and sleep, 3(1):.
Gut function exhibits 24 h (circadian) rhythmicity, in part driven by intrinsic clocks within intestinal epithelial cells (IECs). The gut microbiome also demonstrates circadian rhythms in composition and function, important for maintenance of metabolic, immune and gut health. Here, we determined the influence of feeding behaviour on the 24 h colonic landscape using an interval feeding paradigm, whereby food intake was partitioned equally across the 24 h day. RNAseq analysis revealed that the IEC intrinsic clock persists in the absence of diurnal feeding rhythms; however, a subset of key transcripts loses rhythmicity, demonstrating that cell extrinsic temporal cues contribute significantly to the maintenance of the rhythmic gut transcriptome. Furthermore, interval-fed mice demonstrated a striking loss of rhythms in secretory IgA, a critical regulator of the temporal landscape of the gut microbiome. In keeping, rhythmicity within the microbiota and microbial-derived short chain fatty acids was significantly diminished. This work highlights the importance of daily rhythms in feeding behaviour for the maintenance of rhythmic processes within the gut, with implications for metabolic and immune health.
Additional Links: PMID-42332254
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@article {pmid42332254,
year = {2026},
author = {Hunter, FK and Downton, P and Luengas-Martinez, A and Dickson, SH and Cain, J and Else, KJ and Hepworth, MR and Gibbs, JE},
title = {The importance of meal timing for maintenance of daily rhythms in the gut transcriptome and microbiota.},
journal = {Npj biological timing and sleep},
volume = {3},
number = {1},
pages = {},
pmid = {42332254},
issn = {2948-281X},
support = {105644/Z/14/Z/WT_/Wellcome Trust/United Kingdom ; 22625/VAC_/Versus Arthritis/United Kingdom ; },
abstract = {Gut function exhibits 24 h (circadian) rhythmicity, in part driven by intrinsic clocks within intestinal epithelial cells (IECs). The gut microbiome also demonstrates circadian rhythms in composition and function, important for maintenance of metabolic, immune and gut health. Here, we determined the influence of feeding behaviour on the 24 h colonic landscape using an interval feeding paradigm, whereby food intake was partitioned equally across the 24 h day. RNAseq analysis revealed that the IEC intrinsic clock persists in the absence of diurnal feeding rhythms; however, a subset of key transcripts loses rhythmicity, demonstrating that cell extrinsic temporal cues contribute significantly to the maintenance of the rhythmic gut transcriptome. Furthermore, interval-fed mice demonstrated a striking loss of rhythms in secretory IgA, a critical regulator of the temporal landscape of the gut microbiome. In keeping, rhythmicity within the microbiota and microbial-derived short chain fatty acids was significantly diminished. This work highlights the importance of daily rhythms in feeding behaviour for the maintenance of rhythmic processes within the gut, with implications for metabolic and immune health.},
}
RevDate: 2026-06-22
Hair vs. fabric: substrate-dependent microbiome shifts dictate the accuracy of forensic body-fluid identification.
International journal of legal medicine [Epub ahead of print].
Hair and clothing are among the most frequently recovered evidentiary items at crime scenes. Compared with human soft tissue, they resist environmental degradation and frequently retain perpetrator-derived biological deposits; accurate identification of these traces is therefore pivotal for case qualification and investigation. Microbiome profiling has emerged as a promising forensic tool for body-fluid attribution, yet body fluids like blood and semen contain only a sparse indigenous flora and are highly vulnerable to environmental or substrate-borne microbial overwrite. To date, systematic evaluations of how deposition surface and ambient microbiota influence the reliability of microbe-based fluid identification remain scarce, especially with respect to hair-a substrate that inherently carries the victim's resident microbial community and may obscure fluid-specific markers. In this study, four forensically relevant body fluids (blood, semen, vaginal fluid and saliva) were deposited on hair shafts and cotton fabric and aged for 30 days under indoor conditions. Amplicon sequencing of the V3-V4 hypervariable region of the bacterial 16S rRNA gene revealed that fabric-hosted stains retained a stable, fluid-specific microbiota across all sampling intervals. In contrast, hair-associated traces underwent a rapid and persistent compositional shift toward the native scalp/hair community, resulting in significant loss of fluid-identifying signals. Consequently, the prediction accuracy of our random-forest classifier decreased to 84.2% when hair samples were included. Saliva and vaginal fluid proved exceptional: a subset of oral-associated taxa (Streptococcus, Gemella) and vaginal associated microorganisms (Lactobacillus) remained detectable on both substrates, preserving a degree of fluid specificity. Collectively, these findings demonstrate that substrate-derived microbiota can compromise microbiome-based body-fluid identification, underscoring the necessity of matrix-specific marker panels and cautious extrapolation of signatures derived from pristine laboratory simulations to real-world evidentiary samples.
Additional Links: PMID-42332287
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Citation:
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@article {pmid42332287,
year = {2026},
author = {Li, S and Wang, C and Chen, Z and Wang, X and Liu, S and Yang, C and Luo, G and Zhao, Z and Cai, J and Zhang, Y},
title = {Hair vs. fabric: substrate-dependent microbiome shifts dictate the accuracy of forensic body-fluid identification.},
journal = {International journal of legal medicine},
volume = {},
number = {},
pages = {},
pmid = {42332287},
issn = {1437-1596},
support = {82030058//National Natural Science Foundation of China/ ; },
abstract = {Hair and clothing are among the most frequently recovered evidentiary items at crime scenes. Compared with human soft tissue, they resist environmental degradation and frequently retain perpetrator-derived biological deposits; accurate identification of these traces is therefore pivotal for case qualification and investigation. Microbiome profiling has emerged as a promising forensic tool for body-fluid attribution, yet body fluids like blood and semen contain only a sparse indigenous flora and are highly vulnerable to environmental or substrate-borne microbial overwrite. To date, systematic evaluations of how deposition surface and ambient microbiota influence the reliability of microbe-based fluid identification remain scarce, especially with respect to hair-a substrate that inherently carries the victim's resident microbial community and may obscure fluid-specific markers. In this study, four forensically relevant body fluids (blood, semen, vaginal fluid and saliva) were deposited on hair shafts and cotton fabric and aged for 30 days under indoor conditions. Amplicon sequencing of the V3-V4 hypervariable region of the bacterial 16S rRNA gene revealed that fabric-hosted stains retained a stable, fluid-specific microbiota across all sampling intervals. In contrast, hair-associated traces underwent a rapid and persistent compositional shift toward the native scalp/hair community, resulting in significant loss of fluid-identifying signals. Consequently, the prediction accuracy of our random-forest classifier decreased to 84.2% when hair samples were included. Saliva and vaginal fluid proved exceptional: a subset of oral-associated taxa (Streptococcus, Gemella) and vaginal associated microorganisms (Lactobacillus) remained detectable on both substrates, preserving a degree of fluid specificity. Collectively, these findings demonstrate that substrate-derived microbiota can compromise microbiome-based body-fluid identification, underscoring the necessity of matrix-specific marker panels and cautious extrapolation of signatures derived from pristine laboratory simulations to real-world evidentiary samples.},
}
RevDate: 2026-06-23
CmpDate: 2026-06-23
A two-sample bidirectional Mendelian randomization study on gut microbiota, dental caries, and toothache.
Medicine, 105(25):e48944.
We aimed to evaluate whether gut microbiotas have an effect on caries and toothache and explore whether dental caries and toothache have any impact on the identified significant bacterial genera. We first used genetic instruments of gut microbiota from the MiBioGen consortium to investigate the relationship with toothache and dental caries. The genome-wide association study summary data were from the UK Biobank and the FinnGen consortium, respectively. Mendelian randomization (MR) Egger regression, weighted median, inverse-variance weighted, simple mode, and weighted mode were used in the analysis. MR-PRESSO and Cochrane Q statistics were used to detect pleiotropy and heterogeneity. Furthermore, we performed a bidirectional MR analysis to examine the direction of the relationship. In our study, we identified 22 gut microbiota that were associated with toothache and dental caries. In the reverse MR analysis, the analysis suggested a strong correlation between the gut microbiome (Eubacterium nodatum group) and toothache. Our MR analysis suggested that the gut microbiota influences the occurrence of dental caries and toothache, while dental caries and toothache exert an impact on the identified significant bacterial genera.
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@article {pmid42332442,
year = {2026},
author = {Zhang, L and Zheng, X and Xia, J and Guo, L and Yang, S},
title = {A two-sample bidirectional Mendelian randomization study on gut microbiota, dental caries, and toothache.},
journal = {Medicine},
volume = {105},
number = {25},
pages = {e48944},
pmid = {42332442},
issn = {1536-5964},
mesh = {*Dental Caries/microbiology/genetics ; Humans ; *Mendelian Randomization Analysis ; *Gastrointestinal Microbiome/genetics ; Genome-Wide Association Study ; *Toothache/microbiology/genetics ; },
abstract = {We aimed to evaluate whether gut microbiotas have an effect on caries and toothache and explore whether dental caries and toothache have any impact on the identified significant bacterial genera. We first used genetic instruments of gut microbiota from the MiBioGen consortium to investigate the relationship with toothache and dental caries. The genome-wide association study summary data were from the UK Biobank and the FinnGen consortium, respectively. Mendelian randomization (MR) Egger regression, weighted median, inverse-variance weighted, simple mode, and weighted mode were used in the analysis. MR-PRESSO and Cochrane Q statistics were used to detect pleiotropy and heterogeneity. Furthermore, we performed a bidirectional MR analysis to examine the direction of the relationship. In our study, we identified 22 gut microbiota that were associated with toothache and dental caries. In the reverse MR analysis, the analysis suggested a strong correlation between the gut microbiome (Eubacterium nodatum group) and toothache. Our MR analysis suggested that the gut microbiota influences the occurrence of dental caries and toothache, while dental caries and toothache exert an impact on the identified significant bacterial genera.},
}
MeSH Terms:
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*Dental Caries/microbiology/genetics
Humans
*Mendelian Randomization Analysis
*Gastrointestinal Microbiome/genetics
Genome-Wide Association Study
*Toothache/microbiology/genetics
RevDate: 2026-06-23
Evaluation of periodontal status in gastritis patients with clinical and microbiological parameters.
BMC oral health pii:10.1186/s12903-026-08835-0 [Epub ahead of print].
BACKGROUND: Gastritis is characterized by alterations in the gastric microbiota. This dysbiosis in the stomach may affect immune system regulation as well as influence the oral microbiota. Periodontal disease results from dysbiosis of subgingival microbial communities that cause inflammatory responses in periodontal tissues. The aim of our study is to examine the oral flora profile and dysbiosis status of gastritis patients along with their periodontal status.
METHODS: A total of 30 patients were included in our study, divided into two groups 15 patients diagnosed with gastritis and 15 systemically healthy individuals. Subsequently, the patients were subdivided into subgroups as periodontally healthy, gingivitis, and stage 1 periodontitis based on their periodontal status. Clinical periodontal parameters and saliva samples were collected. Microbial community composition was analyzed using 16 S rRNA gene-based next-generation sequencing. Clinical and microbiological parameters were evaluated using non-parametric statistical methods.
RESULTS: While no differences were observed in any metric in beta diversity analysis across gender groups, study groups, and subgroups, bacterial diversity was found to be higher in women in the Simpson, Shannon and Chao1 metrics in alpha diversity analysis, In the subgroups, a significant increase was observed in the stage 1 periodontitis-gastritis group in the Chao1 metric. Bacterial taxa that showed statistically significant differences between the groups and subgroups were identified using LEfSe analysis.
CONCLUSION: Our study underscore dysbiosis in the oral flora in the context of gastritis while also taking into account the periodontal status. Gastritis with periodontitis may enhance the microbial diversity and abundance. Future research studies are needed to unravel systemic interaction between periodontitits and gastritis.
TRIAL REGISTRATION: This clinical trial was registered at ClinicTrials.gov (NCT07378540) Registration Date: 29/01/2026.
Additional Links: PMID-42332672
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@article {pmid42332672,
year = {2026},
author = {Erdem Altınyürek, E and Öztürk, VÖ},
title = {Evaluation of periodontal status in gastritis patients with clinical and microbiological parameters.},
journal = {BMC oral health},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12903-026-08835-0},
pmid = {42332672},
issn = {1472-6831},
support = {DHF-24004//Aydın Adnan Menderes University Scientific Research Projects Unit/ ; },
abstract = {BACKGROUND: Gastritis is characterized by alterations in the gastric microbiota. This dysbiosis in the stomach may affect immune system regulation as well as influence the oral microbiota. Periodontal disease results from dysbiosis of subgingival microbial communities that cause inflammatory responses in periodontal tissues. The aim of our study is to examine the oral flora profile and dysbiosis status of gastritis patients along with their periodontal status.
METHODS: A total of 30 patients were included in our study, divided into two groups 15 patients diagnosed with gastritis and 15 systemically healthy individuals. Subsequently, the patients were subdivided into subgroups as periodontally healthy, gingivitis, and stage 1 periodontitis based on their periodontal status. Clinical periodontal parameters and saliva samples were collected. Microbial community composition was analyzed using 16 S rRNA gene-based next-generation sequencing. Clinical and microbiological parameters were evaluated using non-parametric statistical methods.
RESULTS: While no differences were observed in any metric in beta diversity analysis across gender groups, study groups, and subgroups, bacterial diversity was found to be higher in women in the Simpson, Shannon and Chao1 metrics in alpha diversity analysis, In the subgroups, a significant increase was observed in the stage 1 periodontitis-gastritis group in the Chao1 metric. Bacterial taxa that showed statistically significant differences between the groups and subgroups were identified using LEfSe analysis.
CONCLUSION: Our study underscore dysbiosis in the oral flora in the context of gastritis while also taking into account the periodontal status. Gastritis with periodontitis may enhance the microbial diversity and abundance. Future research studies are needed to unravel systemic interaction between periodontitits and gastritis.
TRIAL REGISTRATION: This clinical trial was registered at ClinicTrials.gov (NCT07378540) Registration Date: 29/01/2026.},
}
RevDate: 2026-06-23
Widespread adhesion and iron acquisition traits in Escherichia coli strains obtained from irritable bowel syndrome (IBS) patients.
BMC research notes pii:10.1186/s13104-026-07922-3 [Epub ahead of print].
BACKGROUND: The intestinal microbiome is essential for maintaining a balanced and healthy gut environment. Certain Escherichia coli strains can disrupt it through various pathogenic factors and have been linked to gastrointestinal diseases. In this study, E. coli strains were isolated from individuals with irritable bowel syndrome (IBS) and healthy controls. Identification was performed using microbiological and molecular methods. The presence of key virulence factors, including adhesins (iha, lpfA, afaC, sfaDE, papC, focG, aafII), iron acquisition systems (chuA, iroN, fepC, irp2, iutA, ireA), hemolysin (hlyA), microcins and colicins (cva, colY), and multifunctional factors (malX, yajQ), was assessed by polymerase chain reaction.
RESULTS: The genes lpfA, papC, iroN, ireA, cva, and malX were found to be significantly more prevalent in IBS-associated isolates following Bonferroni correction (p < 0.0031). A higher prevalence of sfaDE, focG, chuA, and hlyA was also observed, though these differences were not statistically significant. Conversely, the genes iha and irp2 were significantly more common in E. coli isolates from healthy individuals. Notably, none of the isolates harbored the afaC and aafII genes. This study demonstrates significant differences in the distribution of specific virulence genes between E. coli isolates from IBS patients and healthy individuals. The higher prevalence of specific genes in IBS isolates may contribute to their pathogenic potential, whereas the frequent occurrence of iha and irp2 in healthy individuals may suggest a role in maintaining a balanced gut microbiome. These findings highlight distinct virulence gene profiles, suggesting a potential association between these E. coli factors and IBS disease status.
Additional Links: PMID-42332759
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@article {pmid42332759,
year = {2026},
author = {Khadiv, A and Yazdanmanesh, M and Heidari, H and Yazdani, F and Houri, H and Badakhsh, B and Ghafourian, S and Kazemian, H},
title = {Widespread adhesion and iron acquisition traits in Escherichia coli strains obtained from irritable bowel syndrome (IBS) patients.},
journal = {BMC research notes},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13104-026-07922-3},
pmid = {42332759},
issn = {1756-0500},
abstract = {BACKGROUND: The intestinal microbiome is essential for maintaining a balanced and healthy gut environment. Certain Escherichia coli strains can disrupt it through various pathogenic factors and have been linked to gastrointestinal diseases. In this study, E. coli strains were isolated from individuals with irritable bowel syndrome (IBS) and healthy controls. Identification was performed using microbiological and molecular methods. The presence of key virulence factors, including adhesins (iha, lpfA, afaC, sfaDE, papC, focG, aafII), iron acquisition systems (chuA, iroN, fepC, irp2, iutA, ireA), hemolysin (hlyA), microcins and colicins (cva, colY), and multifunctional factors (malX, yajQ), was assessed by polymerase chain reaction.
RESULTS: The genes lpfA, papC, iroN, ireA, cva, and malX were found to be significantly more prevalent in IBS-associated isolates following Bonferroni correction (p < 0.0031). A higher prevalence of sfaDE, focG, chuA, and hlyA was also observed, though these differences were not statistically significant. Conversely, the genes iha and irp2 were significantly more common in E. coli isolates from healthy individuals. Notably, none of the isolates harbored the afaC and aafII genes. This study demonstrates significant differences in the distribution of specific virulence genes between E. coli isolates from IBS patients and healthy individuals. The higher prevalence of specific genes in IBS isolates may contribute to their pathogenic potential, whereas the frequent occurrence of iha and irp2 in healthy individuals may suggest a role in maintaining a balanced gut microbiome. These findings highlight distinct virulence gene profiles, suggesting a potential association between these E. coli factors and IBS disease status.},
}
RevDate: 2026-06-23
Circulating imidazole propionate and coronary heart disease risk: interplay between histidine intake, fiber, and gut microbiome.
BMC medicine pii:10.1186/s12916-026-05012-6 [Epub ahead of print].
BACKGROUND: Imidazole propionate (ImP), a microbial metabolite of histidine, may impair glucose metabolism, but its relevance to coronary heart disease (CHD) risk and potential diet-microbiota regulations remain unclear. We aimed to examine prospective associations of plasma ImP levels and histidine intake with CHD risk, to identify ImP-predicting gut microbes, and to investigate diet-microbiome interactions influencing ImP levels.
METHODS: Associations of ImP and histidine with CHD risk were evaluated using Cox models in 7,432 participants from Nurses' Health Study (NHS), NHSII, and Health Professionals Follow-up Study. Microbiome-diet interactions influencing ImP levels were assessed using fecal metagenome and 7-day diet record data in 296 men from the Men's Lifestyle Validation Study, with replication in the Mind-Body Study.
RESULTS: Higher plasma ImP was associated with increased CHD risk (HR comparing extreme quintiles = 1.82; 95%CI = 1.17-2.81; p-trend = 0.002), while histidine intake showed a non-significant inverse association. Although histidine intake was not associated with ImP levels, the intake of fiber, especially pectin, emerged as a key negative predictor. We identified 17 distinct ImP-predicting species, including Clostridium and Blautia species. A parametric ImP-microbial score was constructed based on these species to represent the microbial capacity of producing ImP. Further functional characterization uncovered that the microbial urocanate reductase gene urdA was also associated with cardiovascular risk markers. No significant interaction was observed between histidine intake and the microbial score on ImP levels, but ImP levels increased with higher histidine intake and higher microbial score only under low pectin intake (p for 3-way interaction = 0.01). Similar interactions were seen for total fiber (p = 0.09), soluble fiber (p = 0.09), and insoluble fiber (p = 0.11), without statistical significance.
CONCLUSIONS: ImP, but not its dietary precursor histidine, was associated with a higher CHD risk. The gut microbial metabolism of ImP appeared context-dependent, with ImP production from histidine associated with a higher ImP-producing microbial capacity and lower fiber intake. These findings highlight the potential role of dietary fiber and gut microbiome in modulating diet-health associations related to ImP metabolism.
Additional Links: PMID-42332773
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@article {pmid42332773,
year = {2026},
author = {Liang, X and Zhu, L and Li, J and Li, Y and Ivey, KL and Lee, KH and Eliassen, AH and Chan, AT and Huttenhower, C and Zhang, C and Hu, FB and Qi, Q and Hu, Y and Rimm, EB and Sun, Q},
title = {Circulating imidazole propionate and coronary heart disease risk: interplay between histidine intake, fiber, and gut microbiome.},
journal = {BMC medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12916-026-05012-6},
pmid = {42332773},
issn = {1741-7015},
support = {UM1 CA186107/NH/NIH HHS/United States ; HL060712/HL/NHLBI NIH HHS/United States ; DK126698/HL/NHLBI NIH HHS/United States ; HL035464/HL/NHLBI NIH HHS/United States ; DK126698/HL/NHLBI NIH HHS/United States ; DK129670/DK/NIDDK NIH HHS/United States ; DK119268/DK/NIDDK NIH HHS/United States ; DK129670/DK/NIDDK NIH HHS/United States ; ES036206/ES/NIEHS NIH HHS/United States ; ES036206/ES/NIEHS NIH HHS/United States ; U01CA152904/CA/NCI NIH HHS/United States ; DK120870//National Heart, Lung, and Blood Institute (NHLBI)/ ; },
abstract = {BACKGROUND: Imidazole propionate (ImP), a microbial metabolite of histidine, may impair glucose metabolism, but its relevance to coronary heart disease (CHD) risk and potential diet-microbiota regulations remain unclear. We aimed to examine prospective associations of plasma ImP levels and histidine intake with CHD risk, to identify ImP-predicting gut microbes, and to investigate diet-microbiome interactions influencing ImP levels.
METHODS: Associations of ImP and histidine with CHD risk were evaluated using Cox models in 7,432 participants from Nurses' Health Study (NHS), NHSII, and Health Professionals Follow-up Study. Microbiome-diet interactions influencing ImP levels were assessed using fecal metagenome and 7-day diet record data in 296 men from the Men's Lifestyle Validation Study, with replication in the Mind-Body Study.
RESULTS: Higher plasma ImP was associated with increased CHD risk (HR comparing extreme quintiles = 1.82; 95%CI = 1.17-2.81; p-trend = 0.002), while histidine intake showed a non-significant inverse association. Although histidine intake was not associated with ImP levels, the intake of fiber, especially pectin, emerged as a key negative predictor. We identified 17 distinct ImP-predicting species, including Clostridium and Blautia species. A parametric ImP-microbial score was constructed based on these species to represent the microbial capacity of producing ImP. Further functional characterization uncovered that the microbial urocanate reductase gene urdA was also associated with cardiovascular risk markers. No significant interaction was observed between histidine intake and the microbial score on ImP levels, but ImP levels increased with higher histidine intake and higher microbial score only under low pectin intake (p for 3-way interaction = 0.01). Similar interactions were seen for total fiber (p = 0.09), soluble fiber (p = 0.09), and insoluble fiber (p = 0.11), without statistical significance.
CONCLUSIONS: ImP, but not its dietary precursor histidine, was associated with a higher CHD risk. The gut microbial metabolism of ImP appeared context-dependent, with ImP production from histidine associated with a higher ImP-producing microbial capacity and lower fiber intake. These findings highlight the potential role of dietary fiber and gut microbiome in modulating diet-health associations related to ImP metabolism.},
}
RevDate: 2026-06-23
Gestational diabetes mellitus and maternal-infant microbiome axis: mechanistic insights and therapeutic interventions.
Journal of translational medicine pii:10.1186/s12967-026-08491-6 [Epub ahead of print].
BACKGROUND: Gestational diabetes mellitus (GDM) alters maternal metabolism and the gut microbiota, thereby significantly affecting neonatal health. This narrative review synthesizes current clinical and translational evidence on temporal changes in the maternal gut microbiota across the three pregnancy trimesters in women with GDM and examines its subsequent impact on neonatal microbiome composition, immune development, and long-term disease risk.
MAIN BODY: GDM-associated dysbiosis has been reported early in pregnancy, but human evidence remains heterogeneous and does not establish direct vertical transmission; instead, maternal metabolic status and perinatal exposures may jointly shape early neonatal microbial patterns and immune-metabolic trajectories. These microbial alterations are closely associated with immune dysregulation and increased risks of inflammatory and metabolic disorders in offspring. Although diet, obesity, and probiotics influence microbial composition, their clinical efficacy in GDM remains inconsistent. Importantly, the available evidence remains heterogeneous, reflecting differences in cohort characteristics, sequencing methods, and study design, which limits definitive causal interpretation.
CONCLUSIONS: Advances in microbiota-based diagnostics and personalized microbial interventions-including microbiome-guided dietary modulation, targeted probiotic strategies, and metabolite-focused approaches tailored to individual maternal metabolic and microbial profiles-offer promising strategies to mitigate adverse outcomes by targeting the maternal-neonatal microbiome axis, highlighting microbiome-based approaches as an emerging translational direction.
CLINICAL TRIAL NUMBER: Not applicable.
Additional Links: PMID-42332788
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@article {pmid42332788,
year = {2026},
author = {Choi, J and Keum, J and Kwak, MJ and Kim, SH and Hoh, JK and Jeon, BH and Park, HK},
title = {Gestational diabetes mellitus and maternal-infant microbiome axis: mechanistic insights and therapeutic interventions.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08491-6},
pmid = {42332788},
issn = {1479-5876},
support = {HY-202500000002957//Hanyang University/ ; RS-2023-00219983//National Research Foundation of Korea/ ; RS-2026-25497708//National Research Foundation of Korea/ ; 2026-RISE-01-027-01//Seoul RISE Center and ICT/ ; RS-2025-00520940//National Research foundation of Korea/ ; },
abstract = {BACKGROUND: Gestational diabetes mellitus (GDM) alters maternal metabolism and the gut microbiota, thereby significantly affecting neonatal health. This narrative review synthesizes current clinical and translational evidence on temporal changes in the maternal gut microbiota across the three pregnancy trimesters in women with GDM and examines its subsequent impact on neonatal microbiome composition, immune development, and long-term disease risk.
MAIN BODY: GDM-associated dysbiosis has been reported early in pregnancy, but human evidence remains heterogeneous and does not establish direct vertical transmission; instead, maternal metabolic status and perinatal exposures may jointly shape early neonatal microbial patterns and immune-metabolic trajectories. These microbial alterations are closely associated with immune dysregulation and increased risks of inflammatory and metabolic disorders in offspring. Although diet, obesity, and probiotics influence microbial composition, their clinical efficacy in GDM remains inconsistent. Importantly, the available evidence remains heterogeneous, reflecting differences in cohort characteristics, sequencing methods, and study design, which limits definitive causal interpretation.
CONCLUSIONS: Advances in microbiota-based diagnostics and personalized microbial interventions-including microbiome-guided dietary modulation, targeted probiotic strategies, and metabolite-focused approaches tailored to individual maternal metabolic and microbial profiles-offer promising strategies to mitigate adverse outcomes by targeting the maternal-neonatal microbiome axis, highlighting microbiome-based approaches as an emerging translational direction.
CLINICAL TRIAL NUMBER: Not applicable.},
}
RevDate: 2026-06-23
From coexistence to antagonism: nutrient- and temperature-dependent interactions between Bacillus atrophaeus JunSE1L and Pseudomonas chlororaphis O6 with implications for the wheat rhizosphere.
Journal of biological engineering pii:10.1186/s13036-026-00716-y [Epub ahead of print].
BACKGROUND: Interactions between beneficial plant-associated microbes influence microbial community structure and plant health, yet antagonistic relationships among co-occurring beneficial bacteria remain poorly understood. This study examined interactions between Pseudomonas chlororaphis O6 (PcO6), a wheat root-colonizing epiphyte, and JunSE1L, a Bacillus atrophaeus seed-borne endophyte isolated from winter wheat (Triticum aestivum var. Juniper).
RESULTS: For wheat grown in a sterile sand matrix, JunSE1L emerged from seeds and colonized roots; however, when PcO6 was introduced at the bottom of the growth boxes, it migrated and became the dominant rhizoplane colonizer. JunSE1L emerged from both damaged roots and shoots, and produced biosurfactants that lowered the surface tension of water to 30 mN/m. On agar plates at 22 °C PcO6 strongly inhibited JunSE1L growth on minimal medium (MM) and to a limited extent on rich LB medium; inhibition was absent on both media at 37 °C. On MM, JunSE1L colonies adopted dendritic, highly spread morphologies, potentially from biosurfactant release that may have also facilitated PcO6 swarming over established JunSE1L colonies. Whole PcO6 supernatant and a < 3 kDa filtrate each suppressed JunSE1L growth in liquid MM at 22 ˚C. The inhibitory compound(s) was resistant to proteinase K digestion and heat deactivation, exhibiting bacteriostatic activity against JunSE1L.
CONCLUSIONS: PcO6 inhibits JunSE1L in a temperature-, nutrient-, and density-dependent manner: On rich growth media they coexist, while on defined minimal media, PcO6 dominates, suggesting that resource limitation intensifies competitive interactions and favors epiphyte (PcO6) - mediated suppression of endophyte (JunSE1L). While both bacteria comprise the wheat root microbiome, under conditions recapitulating the rhizosphere (defined nutrients, moderate temperature, and PcO6 already present in the soil) PcO6 release of a bacteriostatic agent may repress JunSE1L emergence. To the contrary, JunSE1L release of biosurfactants may facilitate PcO6 migration to the rhizoplane.
Additional Links: PMID-42332808
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@article {pmid42332808,
year = {2026},
author = {Wankhade, A and Clark, A and Britt, DW},
title = {From coexistence to antagonism: nutrient- and temperature-dependent interactions between Bacillus atrophaeus JunSE1L and Pseudomonas chlororaphis O6 with implications for the wheat rhizosphere.},
journal = {Journal of biological engineering},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13036-026-00716-y},
pmid = {42332808},
issn = {1754-1611},
support = {2024-67022-42830//USDA-NIFA/ ; UTAO-1581//Utah Agricultural Experiment Station/ ; },
abstract = {BACKGROUND: Interactions between beneficial plant-associated microbes influence microbial community structure and plant health, yet antagonistic relationships among co-occurring beneficial bacteria remain poorly understood. This study examined interactions between Pseudomonas chlororaphis O6 (PcO6), a wheat root-colonizing epiphyte, and JunSE1L, a Bacillus atrophaeus seed-borne endophyte isolated from winter wheat (Triticum aestivum var. Juniper).
RESULTS: For wheat grown in a sterile sand matrix, JunSE1L emerged from seeds and colonized roots; however, when PcO6 was introduced at the bottom of the growth boxes, it migrated and became the dominant rhizoplane colonizer. JunSE1L emerged from both damaged roots and shoots, and produced biosurfactants that lowered the surface tension of water to 30 mN/m. On agar plates at 22 °C PcO6 strongly inhibited JunSE1L growth on minimal medium (MM) and to a limited extent on rich LB medium; inhibition was absent on both media at 37 °C. On MM, JunSE1L colonies adopted dendritic, highly spread morphologies, potentially from biosurfactant release that may have also facilitated PcO6 swarming over established JunSE1L colonies. Whole PcO6 supernatant and a < 3 kDa filtrate each suppressed JunSE1L growth in liquid MM at 22 ˚C. The inhibitory compound(s) was resistant to proteinase K digestion and heat deactivation, exhibiting bacteriostatic activity against JunSE1L.
CONCLUSIONS: PcO6 inhibits JunSE1L in a temperature-, nutrient-, and density-dependent manner: On rich growth media they coexist, while on defined minimal media, PcO6 dominates, suggesting that resource limitation intensifies competitive interactions and favors epiphyte (PcO6) - mediated suppression of endophyte (JunSE1L). While both bacteria comprise the wheat root microbiome, under conditions recapitulating the rhizosphere (defined nutrients, moderate temperature, and PcO6 already present in the soil) PcO6 release of a bacteriostatic agent may repress JunSE1L emergence. To the contrary, JunSE1L release of biosurfactants may facilitate PcO6 migration to the rhizoplane.},
}
RevDate: 2026-06-23
CmpDate: 2026-06-23
Impacts of dietary patterns on the gut microbiome: comparing a priori dietary indices and a posteriori dietary patterns.
Food science and biotechnology, 35(8):2345-2360.
UNLABELLED: This study examined the associations of a priori dietary indices and a posteriori dietary patterns with gut microbiome diversity and taxonomic composition. Primary stool samples were combined with long-term food purchase data from 142 households collected between 2017 and 2020. A priori indices, including the alternative Mediterranean Diet Score and revised Healthy Purchase Index, were calculated using predefined criteria, while a posteriori patterns were derived using principal component analysis. The revised Healthy Purchase Index and prudent dietary pattern were positively associated with microbial diversity, whereas the alternative Mediterranean Diet Score and overall food consumption intensity were not. At the genus level, the high alternative Mediterranean Diet Score group showed greater abundances of short-chain fatty acid-producing genera, including Anaerostipes, Faecalibacterium, and Roseburia, whereas these differences were not observed for the revised Healthy Purchase Index or prudent dietary pattern. These findings suggest that dietary quality and patterns may contribute to gut microbiome composition.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-026-02186-w.
Additional Links: PMID-42333099
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@article {pmid42333099,
year = {2026},
author = {Kim, N and Eom, H and Lee, H and Moon, J and Jung, Y and Oh, HS and Kim, N and Chun, J and Lee, D},
title = {Impacts of dietary patterns on the gut microbiome: comparing a priori dietary indices and a posteriori dietary patterns.},
journal = {Food science and biotechnology},
volume = {35},
number = {8},
pages = {2345-2360},
pmid = {42333099},
issn = {2092-6456},
abstract = {UNLABELLED: This study examined the associations of a priori dietary indices and a posteriori dietary patterns with gut microbiome diversity and taxonomic composition. Primary stool samples were combined with long-term food purchase data from 142 households collected between 2017 and 2020. A priori indices, including the alternative Mediterranean Diet Score and revised Healthy Purchase Index, were calculated using predefined criteria, while a posteriori patterns were derived using principal component analysis. The revised Healthy Purchase Index and prudent dietary pattern were positively associated with microbial diversity, whereas the alternative Mediterranean Diet Score and overall food consumption intensity were not. At the genus level, the high alternative Mediterranean Diet Score group showed greater abundances of short-chain fatty acid-producing genera, including Anaerostipes, Faecalibacterium, and Roseburia, whereas these differences were not observed for the revised Healthy Purchase Index or prudent dietary pattern. These findings suggest that dietary quality and patterns may contribute to gut microbiome composition.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-026-02186-w.},
}
RevDate: 2026-06-23
CmpDate: 2026-06-23
Solid-state fermentation of wheat bran using tea-derived starters improves dietary fiber composition and whole wheat bread quality.
Food science and biotechnology, 35(8):2165-2177.
UNLABELLED: Wheat bran is an important source of dietary fiber in whole wheat products, yet the high content of insoluble dietary fiber (IDF) drastically impairs dough rheology and bread quality. In this study, solid-state fermentation was applied to wheat bran using ten tea-derived starters. All starters promoted IDF degradation and induced a transient increase in soluble dietary fiber. Among them, QD and FY showed superior modification efficiency, remarkably reducing the crystallinity of cellulose. Consequently, the dough prepared with fermented bran exhibited reduced viscoelastic stiffness and improved flow behavior, while the corresponding breads showed increased specific volume and reduced crumb hardness. Microbiome analysis of QD and FY showed that fermentation markedly reduced bacterial and fungal diversity, selectively enriching the genera of Bacillus and Aspergillus with cellulolytic and xylanolytic potential. Overall, this study provided new insights for modifying wheat bran composition and structure, thereby improving the processing quality of whole wheat bread.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-026-02189-7.
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@article {pmid42333114,
year = {2026},
author = {Chen, J and Peng, Y and Wang, A and Lu, S and Li, H and Wang, J},
title = {Solid-state fermentation of wheat bran using tea-derived starters improves dietary fiber composition and whole wheat bread quality.},
journal = {Food science and biotechnology},
volume = {35},
number = {8},
pages = {2165-2177},
pmid = {42333114},
issn = {2092-6456},
abstract = {UNLABELLED: Wheat bran is an important source of dietary fiber in whole wheat products, yet the high content of insoluble dietary fiber (IDF) drastically impairs dough rheology and bread quality. In this study, solid-state fermentation was applied to wheat bran using ten tea-derived starters. All starters promoted IDF degradation and induced a transient increase in soluble dietary fiber. Among them, QD and FY showed superior modification efficiency, remarkably reducing the crystallinity of cellulose. Consequently, the dough prepared with fermented bran exhibited reduced viscoelastic stiffness and improved flow behavior, while the corresponding breads showed increased specific volume and reduced crumb hardness. Microbiome analysis of QD and FY showed that fermentation markedly reduced bacterial and fungal diversity, selectively enriching the genera of Bacillus and Aspergillus with cellulolytic and xylanolytic potential. Overall, this study provided new insights for modifying wheat bran composition and structure, thereby improving the processing quality of whole wheat bread.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-026-02189-7.},
}
RevDate: 2026-06-23
CmpDate: 2026-06-23
Advances in the detection of antimicrobial resistance in aquatic environments: a methodological perspective.
Biology methods & protocols, 11(1):bpag029.
Antimicrobial resistance (AMR) is a global health and environmental challenge, driven by complex interactions among microbial communities, resistance genes, and selective pressures in various ecological niches. Traditional surveillance procedures often fall short in capturing the full diversity and dynamics of resistance reservoirs in the environment. This review examines the integration of artificial intelligence (AI) and machine learning (ML) with next-generation sequencing (NGS) technologies for comprehensive resistome profiling. We discuss advances in multi-omics approaches, particularly metagenomics, microbiome-based analytics, and metatranscriptomics. We also highlight computational workflows that enable high-resolution mapping of resistance genes, their mobile genetic elements, and host associations. The role of AI/ML in resistome prediction, classification, and source tracking, as well as the incorporation of environmental metadata for contextual interpretation is discussed based on the selected literature. Moreover, we assess current challenges and propose future directions for developing standardized, scalable, and interpretable bioinformatic pipelines in AMR surveillance. This review primarily elucidates the potential of integrated AI-omics platforms to revolutionize aquatic environmental AMR monitoring and inform risk assessment and mitigation strategies.
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@article {pmid42333270,
year = {2026},
author = {Ibitoye, OA and Anyanwu, CN and Agbaje, AB and Fasogbon, IV and Dangana, RS and Akinola, SA and Tibyangye, J and Adam, AA and Aja, PM},
title = {Advances in the detection of antimicrobial resistance in aquatic environments: a methodological perspective.},
journal = {Biology methods & protocols},
volume = {11},
number = {1},
pages = {bpag029},
pmid = {42333270},
issn = {2396-8923},
abstract = {Antimicrobial resistance (AMR) is a global health and environmental challenge, driven by complex interactions among microbial communities, resistance genes, and selective pressures in various ecological niches. Traditional surveillance procedures often fall short in capturing the full diversity and dynamics of resistance reservoirs in the environment. This review examines the integration of artificial intelligence (AI) and machine learning (ML) with next-generation sequencing (NGS) technologies for comprehensive resistome profiling. We discuss advances in multi-omics approaches, particularly metagenomics, microbiome-based analytics, and metatranscriptomics. We also highlight computational workflows that enable high-resolution mapping of resistance genes, their mobile genetic elements, and host associations. The role of AI/ML in resistome prediction, classification, and source tracking, as well as the incorporation of environmental metadata for contextual interpretation is discussed based on the selected literature. Moreover, we assess current challenges and propose future directions for developing standardized, scalable, and interpretable bioinformatic pipelines in AMR surveillance. This review primarily elucidates the potential of integrated AI-omics platforms to revolutionize aquatic environmental AMR monitoring and inform risk assessment and mitigation strategies.},
}
RevDate: 2026-06-23
CmpDate: 2026-06-23
Oral-Systemic Links: A Narrative Review of the Role of Periodontitis in Alzheimer's Disease Development.
Cureus, 18(5):e109402.
Alzheimer's disease (AD) and periodontitis are prevalent chronic conditions that disproportionately affect aging populations and pose substantial public health challenges worldwide. Increasing evidence suggests a potential association between these two diseases, with chronic oral infection and systemic inflammation emerging as key linking mechanisms. Periodontitis is characterized by a dysbiotic oral microbiome and persistent inflammatory responses that can lead to the dissemination of periodontal pathogens and their virulence factors into the systemic circulation. Notably, some studies have reported the detection of pathogens such as Porphyromonas gingivalis and their toxic products in the brains of individuals with AD, implicating a possible role in neuroinflammation and neurodegeneration. However, it should be clarified that detection does not establish causation. This narrative review aims to synthesize the existing evidence from animal studies exploring the link between periodontitis and AD and its related mechanisms, including neuroinflammation, amyloid and tau pathology, blood-brain barrier dysfunction, and systemic interactions. The electronic search in PubMed yielded 585 results. We focused on the past 10 years, thus removing 114 results. A total of 471 studies remained. Of the 471 articles reviewed, 239 studies were excluded based on their titles, abstracts, publication types, and topics because of inappropriate study designs (i.e., designs other than cross-sectional or animal studies). A total of 232 studies were further investigated. In this review, the analysis focused exclusively on animal studies, and the full texts were assessed against predefined eligibility criteria focusing on study design, animal model, periodontal exposure, and AD-related outcomes. Studies that met all inclusion criteria were included, whereas articles with inappropriate study designs or irrelevant outcomes were excluded. After full-text screening, 101 studies remained. Preclinical (animal) evidence supported plausible mechanistic links between periodontitis and AD. Furthermore, oral pathogens appear to mediate this ongoing neuroinflammation.
Additional Links: PMID-42333360
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@article {pmid42333360,
year = {2026},
author = {Spantidakis, N and Zisis, V and Charisi, C and Fytros, F and Poulopoulos, K and Chontos, T and Yiannouras, A and Papadopoulos, P and Katsagkolis, A and Arsoudi, V and Thomaidi, ZM and Poulopoulos, A and Diamanti, S},
title = {Oral-Systemic Links: A Narrative Review of the Role of Periodontitis in Alzheimer's Disease Development.},
journal = {Cureus},
volume = {18},
number = {5},
pages = {e109402},
pmid = {42333360},
issn = {2168-8184},
abstract = {Alzheimer's disease (AD) and periodontitis are prevalent chronic conditions that disproportionately affect aging populations and pose substantial public health challenges worldwide. Increasing evidence suggests a potential association between these two diseases, with chronic oral infection and systemic inflammation emerging as key linking mechanisms. Periodontitis is characterized by a dysbiotic oral microbiome and persistent inflammatory responses that can lead to the dissemination of periodontal pathogens and their virulence factors into the systemic circulation. Notably, some studies have reported the detection of pathogens such as Porphyromonas gingivalis and their toxic products in the brains of individuals with AD, implicating a possible role in neuroinflammation and neurodegeneration. However, it should be clarified that detection does not establish causation. This narrative review aims to synthesize the existing evidence from animal studies exploring the link between periodontitis and AD and its related mechanisms, including neuroinflammation, amyloid and tau pathology, blood-brain barrier dysfunction, and systemic interactions. The electronic search in PubMed yielded 585 results. We focused on the past 10 years, thus removing 114 results. A total of 471 studies remained. Of the 471 articles reviewed, 239 studies were excluded based on their titles, abstracts, publication types, and topics because of inappropriate study designs (i.e., designs other than cross-sectional or animal studies). A total of 232 studies were further investigated. In this review, the analysis focused exclusively on animal studies, and the full texts were assessed against predefined eligibility criteria focusing on study design, animal model, periodontal exposure, and AD-related outcomes. Studies that met all inclusion criteria were included, whereas articles with inappropriate study designs or irrelevant outcomes were excluded. After full-text screening, 101 studies remained. Preclinical (animal) evidence supported plausible mechanistic links between periodontitis and AD. Furthermore, oral pathogens appear to mediate this ongoing neuroinflammation.},
}
RevDate: 2026-06-23
Microbiome-Driven Carcinogenesis and Circulating Microbial Signals in Genitourinary Cancers.
Cancer science [Epub ahead of print].
The microbiome is increasingly recognized as a regulator of carcinogenesis, tumor immunity, and response to immune checkpoint inhibitors (ICIs), but its role in genitourinary cancers remains less clearly defined than in melanoma or colorectal cancer. In this review, we summarize evidence that microbiome-related pathways influence urothelial carcinoma (UC) and renal cell carcinoma (RCC) across the continuum from tumor initiation to immunotherapy outcome. We highlight recent preclinical studies showing that gut microbial environments can causally modify urothelial carcinogenesis through carcinogen metabolism, inflammatory priming, and diet-microbiome interactions in N-butyl-N-(4-hydroxybutyl) nitrosamine-based mouse models, including a newly established upper tract urothelial carcinoma mouse model, as well as emerging clinical data indicating that circulating extracellular vesicle (EV)-associated bacterial DNA is associated with tumor immune phenotypes and ICI outcomes in UC and RCC. Because blood is a low-biomass matrix, we use the term "circulating microbial signals" rather than "blood microbiome" and emphasize the need for contamination-aware analysis, careful EV characterization, and external validation. Current evidence supports a framework in which microbiome-related signals connect intestinal ecology, systemic immune tone, tumor immune contexture, and treatment response, while indicating that circulating EV-associated bacterial DNA remains an exploratory biomarker platform.
Additional Links: PMID-42333742
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@article {pmid42333742,
year = {2026},
author = {Kawashima, A and Jingushi, K and Saito, T and Uemura, T and Yamamoto, A and Sassi, N and Horitani, H and Inoguchi, S and Horibe, Y and Ishizuya, Y and Hayashi, T and Yamamoto, Y and Nonomura, N},
title = {Microbiome-Driven Carcinogenesis and Circulating Microbial Signals in Genitourinary Cancers.},
journal = {Cancer science},
volume = {},
number = {},
pages = {},
doi = {10.1111/cas.70448},
pmid = {42333742},
issn = {1349-7006},
support = {JP2120988//Japan Society for the Promotion of Science/ ; JP22H03213//Japan Society for the Promotion of Science/ ; JP22K09469//Japan Society for the Promotion of Science/ ; },
abstract = {The microbiome is increasingly recognized as a regulator of carcinogenesis, tumor immunity, and response to immune checkpoint inhibitors (ICIs), but its role in genitourinary cancers remains less clearly defined than in melanoma or colorectal cancer. In this review, we summarize evidence that microbiome-related pathways influence urothelial carcinoma (UC) and renal cell carcinoma (RCC) across the continuum from tumor initiation to immunotherapy outcome. We highlight recent preclinical studies showing that gut microbial environments can causally modify urothelial carcinogenesis through carcinogen metabolism, inflammatory priming, and diet-microbiome interactions in N-butyl-N-(4-hydroxybutyl) nitrosamine-based mouse models, including a newly established upper tract urothelial carcinoma mouse model, as well as emerging clinical data indicating that circulating extracellular vesicle (EV)-associated bacterial DNA is associated with tumor immune phenotypes and ICI outcomes in UC and RCC. Because blood is a low-biomass matrix, we use the term "circulating microbial signals" rather than "blood microbiome" and emphasize the need for contamination-aware analysis, careful EV characterization, and external validation. Current evidence supports a framework in which microbiome-related signals connect intestinal ecology, systemic immune tone, tumor immune contexture, and treatment response, while indicating that circulating EV-associated bacterial DNA remains an exploratory biomarker platform.},
}
RevDate: 2026-06-23
Association of Fontan Circulation With Gut Microbiome-Derived Straight and Branched Short-Chain Fatty Acids.
Additional Links: PMID-42334092
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PubMed:
Citation:
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@article {pmid42334092,
year = {2026},
author = {Shahani, A and Lohana, A and Kumar, P and Rasheed, F and Piryanka, and Muhammad Yousuf, Y},
title = {Association of Fontan Circulation With Gut Microbiome-Derived Straight and Branched Short-Chain Fatty Acids.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70525},
pmid = {42334092},
issn = {1440-1746},
}
RevDate: 2026-06-23
Distinct Microbiota and Functional Pathway Profiles Define Success and Failure in Regenerative Endodontic Treatment.
International endodontic journal [Epub ahead of print].
AIM: To characterize the intracanal microbiota and identify key microbial taxa and functional pathways associated with regenerative endodontic treatment (RET) outcomes.
METHODOLOGY: In this observational cohort study, 196 samples were collected at five time points from external tooth surfaces (T1, T4) and root canals (T2, T3, T5). The V3-V4 hypervariable region of 16S rRNA gene was amplified and sequenced on the Illumina MiSeq platform. Sequence data were pre-processed using QIIME2 and DADA2 to generate amplicon sequence variants (ASVs), classified against the eHOMD database. Microbial diversity, differential abundance, and Receiver Operating Characteristic (ROC) analyses were performed using R statistical software. Functional profiles were predicted using PICRUSt2.
RESULTS: RET induced dynamic shifts in the root canal microbiome, with initially predominant phyla including Actinomycetota, Bacillota, Bacteroidota, Fusobacteriota and Pseudomonadota. Cases with treatment failure consistently showed a higher relative abundance of Fusobacteriota than successful cases. Alpha diversity varied across time points, with outcome-specific differences observed only at T3; beta diversity differed significantly by time point but not by treatment outcome. Differential abundance analysis at T5 revealed enrichment of Rothia dentocariosa and Leptothrix sp. in successful cases, whereas failed cases were enriched in Fusobacterium polymorphum, Streptococcus sanguinis, Campylobacter showae, Lachnoanaerobaculum sp. and Selenomonas sp. These taxa demonstrated moderate diagnostic potential, with area under the curve (AUC) values of 0.70-0.82. Persistence analysis showed that F. polymorphum, C. showae and Selenomonas sp. exhibited greater persistence in failed cases across treatment time points. Predicted functional profiling indicated distinct metabolic potentials between successful and failed treatment groups.
CONCLUSIONS: RET alters the intracanal microbiome, with taxa identified following intracanal dressing exhibiting moderate predictive potential as biomarkers for treatment outcome, thereby contributing to early prognosis and informing RET strategies.
Additional Links: PMID-42334102
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PubMed:
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@article {pmid42334102,
year = {2026},
author = {Naorem, LD and Wikström, A and Quach, P and Manoharan, L and Ordinola-Zapata, R and Rakhimova, O and Brundin, M and Vestman, NR},
title = {Distinct Microbiota and Functional Pathway Profiles Define Success and Failure in Regenerative Endodontic Treatment.},
journal = {International endodontic journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/iej.70205},
pmid = {42334102},
issn = {1365-2591},
support = {TUA 977100//Region of Västerbotten (Sweden)/ ; RV-967705//ALF/ ; JCSMK23-0158//Kempestiftelserna Kempe/ ; },
abstract = {AIM: To characterize the intracanal microbiota and identify key microbial taxa and functional pathways associated with regenerative endodontic treatment (RET) outcomes.
METHODOLOGY: In this observational cohort study, 196 samples were collected at five time points from external tooth surfaces (T1, T4) and root canals (T2, T3, T5). The V3-V4 hypervariable region of 16S rRNA gene was amplified and sequenced on the Illumina MiSeq platform. Sequence data were pre-processed using QIIME2 and DADA2 to generate amplicon sequence variants (ASVs), classified against the eHOMD database. Microbial diversity, differential abundance, and Receiver Operating Characteristic (ROC) analyses were performed using R statistical software. Functional profiles were predicted using PICRUSt2.
RESULTS: RET induced dynamic shifts in the root canal microbiome, with initially predominant phyla including Actinomycetota, Bacillota, Bacteroidota, Fusobacteriota and Pseudomonadota. Cases with treatment failure consistently showed a higher relative abundance of Fusobacteriota than successful cases. Alpha diversity varied across time points, with outcome-specific differences observed only at T3; beta diversity differed significantly by time point but not by treatment outcome. Differential abundance analysis at T5 revealed enrichment of Rothia dentocariosa and Leptothrix sp. in successful cases, whereas failed cases were enriched in Fusobacterium polymorphum, Streptococcus sanguinis, Campylobacter showae, Lachnoanaerobaculum sp. and Selenomonas sp. These taxa demonstrated moderate diagnostic potential, with area under the curve (AUC) values of 0.70-0.82. Persistence analysis showed that F. polymorphum, C. showae and Selenomonas sp. exhibited greater persistence in failed cases across treatment time points. Predicted functional profiling indicated distinct metabolic potentials between successful and failed treatment groups.
CONCLUSIONS: RET alters the intracanal microbiome, with taxa identified following intracanal dressing exhibiting moderate predictive potential as biomarkers for treatment outcome, thereby contributing to early prognosis and informing RET strategies.},
}
RevDate: 2026-06-23
Analysis of clinical characteristics and bronchoalveolar lavage fluid microbial community diversity in non-cystic fibrosis bronchiectasis patients with Pseudomonas aeruginosa colonization.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: This study aims to examine the differences in microbial community abundance and species distribution in the bronchoalveolar lavage fluid (BALF) obtained from non-cystic fibrosis bronchiectasis (NCFB) patients between those with and without Pseudomonas aeruginosa (P. aeruginosa) colonization, and to assess the impact of P. aeruginosa colonization on airway microecological imbalance in NCFB. Sixty-four patients were enrolled, grouped into P. aeruginosa-colonized (PA, 29) and non-colonized (NPA, 35) groups. Among patients with NCFB, those with P. aeruginosa colonization had greater disease severity than those without colonization, with significantly higher bronchiectasis severity index (BSI) scores (P < 0.05). The proportions of patients with higher Bhalla and E-FACED scores were also greater in the PA group than in the NPA group (62.1% vs 42.8% and 34.1% vs 20%, respectively). Annual hospitalization frequency was numerically higher in PA (2.14 ± 2.43 vs 1.47 ± 0.86; P = 0.543). The PA group exhibited poorer pulmonary function, with significantly lower FEV1 and FEV1% predicted (both P < 0.01). In addition, NCFB patients in the PA group showed higher proportions of elevated white blood cell counts (31% vs 17.1%) and neutrophil percentages (41.4% vs 31.4%). Microbiota analysis of BALF demonstrated reduced alpha diversity in NCFB patients with P. aeruginosa colonization, with a predominance of Pseudomonas, whereas non-colonized NCFB patients had relatively higher abundances of Streptococcus, Acinetobacter, Rothia, Veillonella, and Prevotella. Overall, P. aeruginosa colonization in NCFB is associated with increased disease severity, heightened inflammation, and impaired lung function, accompanied by decreased microbial diversity, Pseudomonas dominance, and suppression of commensal taxa.
IMPORTANCE: Pseudomonas aeruginosa is a common colonizer in the airways of patients with non-cystic fibrosis bronchiectasis (NCFB), linked to disease severity, but research on its impact on clinical outcomes and airway microbiome diversity remains limited. This study compared P. aeruginosa-colonized (PA group) and non-colonized (NPA group) NCFB patients and found that the PA group had more severe disease (higher exacerbation, severity scores) and reduced bronchoalveolar lavage fluid (BALF) microbial α/β diversity (marked by Pseudomonas dominance and suppressed symbionts like Streptococcus). These findings indicate that P. aeruginosa reshapes the microecology and is associated with airway microbial imbalance. This study confirms that P. aeruginosa colonization is a key factor in NCFB disease progression and airway microecological imbalance, highlighting reduced colonization and restored homeostasis as precision intervention strategies that inform targeted therapies.
Additional Links: PMID-42334217
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PubMed:
Citation:
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@article {pmid42334217,
year = {2026},
author = {Peng, T and Liu, C and Li, P and Xiong, X and Wang, Y and Zhang, P and Li, J and Zhang, Q and Zhang, W and Ying, Y},
title = {Analysis of clinical characteristics and bronchoalveolar lavage fluid microbial community diversity in non-cystic fibrosis bronchiectasis patients with Pseudomonas aeruginosa colonization.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0087126},
doi = {10.1128/spectrum.00871-26},
pmid = {42334217},
issn = {2165-0497},
abstract = {UNLABELLED: This study aims to examine the differences in microbial community abundance and species distribution in the bronchoalveolar lavage fluid (BALF) obtained from non-cystic fibrosis bronchiectasis (NCFB) patients between those with and without Pseudomonas aeruginosa (P. aeruginosa) colonization, and to assess the impact of P. aeruginosa colonization on airway microecological imbalance in NCFB. Sixty-four patients were enrolled, grouped into P. aeruginosa-colonized (PA, 29) and non-colonized (NPA, 35) groups. Among patients with NCFB, those with P. aeruginosa colonization had greater disease severity than those without colonization, with significantly higher bronchiectasis severity index (BSI) scores (P < 0.05). The proportions of patients with higher Bhalla and E-FACED scores were also greater in the PA group than in the NPA group (62.1% vs 42.8% and 34.1% vs 20%, respectively). Annual hospitalization frequency was numerically higher in PA (2.14 ± 2.43 vs 1.47 ± 0.86; P = 0.543). The PA group exhibited poorer pulmonary function, with significantly lower FEV1 and FEV1% predicted (both P < 0.01). In addition, NCFB patients in the PA group showed higher proportions of elevated white blood cell counts (31% vs 17.1%) and neutrophil percentages (41.4% vs 31.4%). Microbiota analysis of BALF demonstrated reduced alpha diversity in NCFB patients with P. aeruginosa colonization, with a predominance of Pseudomonas, whereas non-colonized NCFB patients had relatively higher abundances of Streptococcus, Acinetobacter, Rothia, Veillonella, and Prevotella. Overall, P. aeruginosa colonization in NCFB is associated with increased disease severity, heightened inflammation, and impaired lung function, accompanied by decreased microbial diversity, Pseudomonas dominance, and suppression of commensal taxa.
IMPORTANCE: Pseudomonas aeruginosa is a common colonizer in the airways of patients with non-cystic fibrosis bronchiectasis (NCFB), linked to disease severity, but research on its impact on clinical outcomes and airway microbiome diversity remains limited. This study compared P. aeruginosa-colonized (PA group) and non-colonized (NPA group) NCFB patients and found that the PA group had more severe disease (higher exacerbation, severity scores) and reduced bronchoalveolar lavage fluid (BALF) microbial α/β diversity (marked by Pseudomonas dominance and suppressed symbionts like Streptococcus). These findings indicate that P. aeruginosa reshapes the microecology and is associated with airway microbial imbalance. This study confirms that P. aeruginosa colonization is a key factor in NCFB disease progression and airway microecological imbalance, highlighting reduced colonization and restored homeostasis as precision intervention strategies that inform targeted therapies.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Modeling cancer with bacteria-integrated tumor microenvironments using biomaterials: Emerging concepts and opportunities.
Materials today. Bio, 39:103330.
The tumor microenvironment (TME) is a dynamic and heterogeneous ecosystem in which cancer, stromal, immune, and physicochemical components collectively regulate disease progression and therapeutic response. Recent evidence further indicates that intratumoral bacteria are active contributors to tumor metabolism, immune modulation, and treatment outcomes, revealing a previously underexplored multi-kingdom dimension of solid tumors. However, mechanistic understanding of tumor-microbe interactions remain limited by the absence of experimental platforms that integrate microbial components into physiologically relevant and controllable tumor models. Here, we propose bacteria-integrated tumor microenvironments as an emerging bioengineering framework for modeling cancer as a multi-kingdom system with biomaterials. We first lay out the existence of bacteria in our body and outline key design principles for these systems, including control of microbial localization, nutrient and oxygen gradients, and interkingdom signaling within engineered matrices. We further discuss applications in studying microbial contributions to therapeutic resistance, evaluating engineered bacterial therapies, and developing patient-specific tumor-microbiome models for precision oncology. Finally, we highlight challenges in standardizing multi-kingdom tumor platforms and integrating them with advanced imaging, sequencing, and computational tools. Collectively, bacteria-integrated TME establish a new paradigm for engineering cancer as a multi-kingdom system with translational potential in oncology.
Additional Links: PMID-42326066
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Citation:
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@article {pmid42326066,
year = {2026},
author = {Jeon, K and Kim, U and Ji, CH and Kamaraj, M and Laird, NZ and Wang, Z and Yu, H and Ermis, M and Sullan, RMA and Shen, X and Falcone, N},
title = {Modeling cancer with bacteria-integrated tumor microenvironments using biomaterials: Emerging concepts and opportunities.},
journal = {Materials today. Bio},
volume = {39},
number = {},
pages = {103330},
pmid = {42326066},
issn = {2590-0064},
abstract = {The tumor microenvironment (TME) is a dynamic and heterogeneous ecosystem in which cancer, stromal, immune, and physicochemical components collectively regulate disease progression and therapeutic response. Recent evidence further indicates that intratumoral bacteria are active contributors to tumor metabolism, immune modulation, and treatment outcomes, revealing a previously underexplored multi-kingdom dimension of solid tumors. However, mechanistic understanding of tumor-microbe interactions remain limited by the absence of experimental platforms that integrate microbial components into physiologically relevant and controllable tumor models. Here, we propose bacteria-integrated tumor microenvironments as an emerging bioengineering framework for modeling cancer as a multi-kingdom system with biomaterials. We first lay out the existence of bacteria in our body and outline key design principles for these systems, including control of microbial localization, nutrient and oxygen gradients, and interkingdom signaling within engineered matrices. We further discuss applications in studying microbial contributions to therapeutic resistance, evaluating engineered bacterial therapies, and developing patient-specific tumor-microbiome models for precision oncology. Finally, we highlight challenges in standardizing multi-kingdom tumor platforms and integrating them with advanced imaging, sequencing, and computational tools. Collectively, bacteria-integrated TME establish a new paradigm for engineering cancer as a multi-kingdom system with translational potential in oncology.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Oral Manifestations of Prediabetes: A Narrative Review of an Early Diagnostic Window for Dental Practice.
Cureus, 18(5):e109375.
Prediabetes is a common metabolic condition affecting a substantial proportion of adults worldwide; however, most individuals remain undiagnosed owing to the prolonged asymptomatic phase of this condition. The oral cavity generates a constellation of clinically detectable changes during this intermediate glycemic stage, including periodontal attachment loss, salivary dysfunction, and oral microbiome dysbiosis, all of which can be examined by dental professionals. Periodontal clinical attachment loss and elevated glycated hemoglobin (HbA1c) levels show a dose-dependent relationship in nondiabetic populations, and active matrix metalloproteinase-8 (aMMP-8) in oral fluids correlates independently with prediabetes, even in its early stages. Salivary oxidative stress markers, adipokines, cariogenic bacterial loads, and physicochemical parameters are measurably altered before overt hyperglycemia is established. Oral microbial communities show reduced species richness, altered IgA immune responses, and shifts in keystone taxa in prediabetic individuals compared to those in healthy individuals. Chairside HbA1c measurement, aMMP-8 point-of-care testing, and structured interprofessional referral models have demonstrated high diagnostic yields in real-world dental settings. This narrative review explores the current literature and proposes dental practice as a first-line venue for opportunistic prediabetes detection, with an emphasis on actionable clinical strategies for practicing dentists.
Additional Links: PMID-42326130
PubMed:
Citation:
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@article {pmid42326130,
year = {2026},
author = {Roshan Arbaaz, B and Maheswaran, T and Adalarasan, S and Kavin, T and Sivaguru, K and Jisha, G},
title = {Oral Manifestations of Prediabetes: A Narrative Review of an Early Diagnostic Window for Dental Practice.},
journal = {Cureus},
volume = {18},
number = {5},
pages = {e109375},
pmid = {42326130},
issn = {2168-8184},
abstract = {Prediabetes is a common metabolic condition affecting a substantial proportion of adults worldwide; however, most individuals remain undiagnosed owing to the prolonged asymptomatic phase of this condition. The oral cavity generates a constellation of clinically detectable changes during this intermediate glycemic stage, including periodontal attachment loss, salivary dysfunction, and oral microbiome dysbiosis, all of which can be examined by dental professionals. Periodontal clinical attachment loss and elevated glycated hemoglobin (HbA1c) levels show a dose-dependent relationship in nondiabetic populations, and active matrix metalloproteinase-8 (aMMP-8) in oral fluids correlates independently with prediabetes, even in its early stages. Salivary oxidative stress markers, adipokines, cariogenic bacterial loads, and physicochemical parameters are measurably altered before overt hyperglycemia is established. Oral microbial communities show reduced species richness, altered IgA immune responses, and shifts in keystone taxa in prediabetic individuals compared to those in healthy individuals. Chairside HbA1c measurement, aMMP-8 point-of-care testing, and structured interprofessional referral models have demonstrated high diagnostic yields in real-world dental settings. This narrative review explores the current literature and proposes dental practice as a first-line venue for opportunistic prediabetes detection, with an emphasis on actionable clinical strategies for practicing dentists.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
INTERPOL Review of Forensic Biology and DNA, 2023-2025.
Forensic science international. Synergy, 13:100705.
As a part of the 21st INTERPOL International Forensic Science Managers Symposium, this work explores the latest scientific developments, methodologies, and trends in forensic biology and forensic DNA analysis of biological evidence during the years 2023 to 2025 and builds upon previous INTERPOL DNA reviews. Almost 2000 references covering the three-year time range of this review were located via various online searches including use of Scopus, Web of Science, and PubMed. The scientific articles, which originated from more than 300 different journals, were curated in a Zotero reference manager database (see Supplemental File 1) and sorted into 15 topics and 116 sub-topics (see Supplemental File 2) under sections focused on advances in current practices (Section 3) and emerging technologies and research studies (Section 4). This triennial review describes 24 books or major reports, 20 special issues of journals on aspects of forensic DNA, 292 articles from 2 International Society for Forensic Genetics (ISFG) conference proceedings, and 70 guidance documents from 17 different organizations to assist in quality DNA testing. Publications were evaluated and sorted into 10 topics around advances in current practices and 5 topics related to emerging technologies and research studies. These topics, which are further sub-divided in a compiled list (see Supplemental File 2) included rapid DNA analysis; law enforcement DNA databases and ethics; forensic investigative genetic genealogy (FIGG); forensic biology and body fluid identification; DNA processing; DNA typing with short tandem repeat (STR) markers; DNA interpretation at the source or sub-source level of the hierarchy of propositions along with mixture interpretation using probabilistic genotyping software (PGS); DNA interpretation at the activity level along with aspects of DNA transfer, persistence, prevalence, and recovery (TPPR); statistics and population genetic data; human identification and kinship analysis; next-generation sequencing (NGS) and technology developments; forensic DNA phenotyping (FDP) and methylation; lineage markers (Y-chromosome, mitochondrial DNA, X-chromosome analyses); new markers and approaches (microhaplotypes, insertion/deletion markers, proteomics, microbiome, single-cell analysis, using environmental DNA, and biomarkers for diagnosis of sudden death, molecular autopsy, or post-mortem interval); and non-human DNA testing and wildlife forensics. Artificial intelligence (AI) tools for summarizing references were explored and utilized in performing this review of over 1900 publications.
Additional Links: PMID-42326394
PubMed:
Citation:
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@article {pmid42326394,
year = {2026},
author = {Butler, JM},
title = {INTERPOL Review of Forensic Biology and DNA, 2023-2025.},
journal = {Forensic science international. Synergy},
volume = {13},
number = {},
pages = {100705},
pmid = {42326394},
issn = {2589-871X},
abstract = {As a part of the 21st INTERPOL International Forensic Science Managers Symposium, this work explores the latest scientific developments, methodologies, and trends in forensic biology and forensic DNA analysis of biological evidence during the years 2023 to 2025 and builds upon previous INTERPOL DNA reviews. Almost 2000 references covering the three-year time range of this review were located via various online searches including use of Scopus, Web of Science, and PubMed. The scientific articles, which originated from more than 300 different journals, were curated in a Zotero reference manager database (see Supplemental File 1) and sorted into 15 topics and 116 sub-topics (see Supplemental File 2) under sections focused on advances in current practices (Section 3) and emerging technologies and research studies (Section 4). This triennial review describes 24 books or major reports, 20 special issues of journals on aspects of forensic DNA, 292 articles from 2 International Society for Forensic Genetics (ISFG) conference proceedings, and 70 guidance documents from 17 different organizations to assist in quality DNA testing. Publications were evaluated and sorted into 10 topics around advances in current practices and 5 topics related to emerging technologies and research studies. These topics, which are further sub-divided in a compiled list (see Supplemental File 2) included rapid DNA analysis; law enforcement DNA databases and ethics; forensic investigative genetic genealogy (FIGG); forensic biology and body fluid identification; DNA processing; DNA typing with short tandem repeat (STR) markers; DNA interpretation at the source or sub-source level of the hierarchy of propositions along with mixture interpretation using probabilistic genotyping software (PGS); DNA interpretation at the activity level along with aspects of DNA transfer, persistence, prevalence, and recovery (TPPR); statistics and population genetic data; human identification and kinship analysis; next-generation sequencing (NGS) and technology developments; forensic DNA phenotyping (FDP) and methylation; lineage markers (Y-chromosome, mitochondrial DNA, X-chromosome analyses); new markers and approaches (microhaplotypes, insertion/deletion markers, proteomics, microbiome, single-cell analysis, using environmental DNA, and biomarkers for diagnosis of sudden death, molecular autopsy, or post-mortem interval); and non-human DNA testing and wildlife forensics. Artificial intelligence (AI) tools for summarizing references were explored and utilized in performing this review of over 1900 publications.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Editorial: Assessing the environmental impact of ruminants: mitigation strategies and climate change implications.
Frontiers in microbiology, 17:1883961.
Additional Links: PMID-42326397
PubMed:
Citation:
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@article {pmid42326397,
year = {2026},
author = {Cherdthong, A and Foiklang, S and Altermann, E},
title = {Editorial: Assessing the environmental impact of ruminants: mitigation strategies and climate change implications.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1883961},
pmid = {42326397},
issn = {1664-302X},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
An approach for diagnosis of diarrhea in neonatal piglets based on the core gut microbiota and machine learning.
Frontiers in microbiology, 17:1852304.
Diarrheal diseases, such as yellow dysentery and white dysentery caused by pathogens or viruses, in newborn piglets lead to substantial economic losses in the swine industry worldwide. Gut microbiota dysbiosis is frequently observed in diarrheic piglets and is thought to play a role in disease pathogenesis, although causal relationships remain to be established. However, developing reliable microbiome-based diagnostic tools still poses a significant challenge. This study aimed to develop a diagnostic model for piglet diarrhea by integrating core microbiota analysis with machine learning. Fecal samples from diarrheic and healthy piglets were subjected to metagenomic sequencing to characterize archaeal, bacterial, and fungal communities. We identified diarrhea-associated bacterial biomarkers via LEfSe, DESeq2, and microbial cooccurrence network analysis. These microbial features were used to construct and compare multiple machine learning classifiers. Our results revealed significant disparities in the structure and diversity of the gut microbiota between diarrheic and healthy piglets, with the bacterial community showing the most notable changes. Among the models developed, the decision tree classifier based on bacterial genus-level features achieved the highest prediction accuracy of 91.18%. Furthermore, a simplified model utilizing a panel of 18 core bacterial genera also demonstrated high efficacy, with a support vector machine model achieving 88.24% accuracy. In independent validation using our internal dataset, the random forest model exhibited the best generalizability and stability. This study establishes a robust, microbiota-based diagnostic model for diarrhea in neonatal piglets, highlighting the potential of machine learning in leveraging microbiome data for disease classification and health management in livestock production.
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@article {pmid42326398,
year = {2026},
author = {Zhao, S and Peng, S and Li, H and Yang, G and Gao, X and Xu, K and Shi, L and Yu, H and Qiao, S},
title = {An approach for diagnosis of diarrhea in neonatal piglets based on the core gut microbiota and machine learning.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1852304},
pmid = {42326398},
issn = {1664-302X},
abstract = {Diarrheal diseases, such as yellow dysentery and white dysentery caused by pathogens or viruses, in newborn piglets lead to substantial economic losses in the swine industry worldwide. Gut microbiota dysbiosis is frequently observed in diarrheic piglets and is thought to play a role in disease pathogenesis, although causal relationships remain to be established. However, developing reliable microbiome-based diagnostic tools still poses a significant challenge. This study aimed to develop a diagnostic model for piglet diarrhea by integrating core microbiota analysis with machine learning. Fecal samples from diarrheic and healthy piglets were subjected to metagenomic sequencing to characterize archaeal, bacterial, and fungal communities. We identified diarrhea-associated bacterial biomarkers via LEfSe, DESeq2, and microbial cooccurrence network analysis. These microbial features were used to construct and compare multiple machine learning classifiers. Our results revealed significant disparities in the structure and diversity of the gut microbiota between diarrheic and healthy piglets, with the bacterial community showing the most notable changes. Among the models developed, the decision tree classifier based on bacterial genus-level features achieved the highest prediction accuracy of 91.18%. Furthermore, a simplified model utilizing a panel of 18 core bacterial genera also demonstrated high efficacy, with a support vector machine model achieving 88.24% accuracy. In independent validation using our internal dataset, the random forest model exhibited the best generalizability and stability. This study establishes a robust, microbiota-based diagnostic model for diarrhea in neonatal piglets, highlighting the potential of machine learning in leveraging microbiome data for disease classification and health management in livestock production.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Extremophilic bacteriorhodopsin from hypersaline salt pan: characterization and photoelectrochemical assessment for potential biosensor applications.
Frontiers in microbiology, 17:1805566.
INTRODUCTION: Salt pans host a diverse microbiome, including specialized extremophilic haloarchaea capable of producing industrially valuable biomolecules, yet remains underexplored extreme environment. Photosensitive bacteriorhodopsin (BR) is a naturally occurring seven helix trans-membrane protein with emerging relevance due to its light driven proton pumping activity, photochemical stability and efficient light to electrical energy conversion.
METHODS: In this study, BR was extracted from haloarchaeal strains isolated from the Tuticorin salt pan using the Bead mix method and confirmed by SDS-PAGE. The extracted BR was further characterized using thin-layer chromatography (TLC), reverse-phase high performance liquid chromatography (R-HPLC), and Raman spectroscopy. The Purified BR was evaluated for its photovoltage response and a prototype biosensor was successfully developed.
RESULTS: Haloarchaeal isolate Halostagnicola larsenii (TP6) demonstrated a remarkable production yield of 360 mg/L of BR under native minimal saline medium conditions, the notably highest recorded for this native strain to date. This isolate was used for further optimization of BR production involving different carbon and nitrogen sources. Two different protein extraction methods were evaluated, of which the bead mix method proved to be effective, yielding around 48.4 mg/L of BR with 72.7% yield. We examined the morphological and physiological traits of these isolates and confirmed the presence of a 26 kDa protein using SDS-PAGE.
DISCUSSION: The isolated extremophilic haloarchaea have the potential to produce large amount of BR, and the characteristics were similar to those previously reported BR from native strains. The observed photoresponsive ability highlights the potential of BR as a bio-based functional component for food bio-sensing, optical devices, and photoelectrochemical biosensors. Overall, this highlights the feasibility of naturally occurring BR from haloarchaea as a sustainable source of photoactive biomolecules for emerging food biotechnology and sustainable biosensor development.
Additional Links: PMID-42326399
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Citation:
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@article {pmid42326399,
year = {2026},
author = {Joseph, S and Stanley Abraham, L and Rajendran, T and Gopal, D and Inbakandan, D and Manikandan, S and Thangavel, B and Jones, S and Setyaningrum, R and Cho, H and Mani, RR and Chang, SW and Ravindran, B},
title = {Extremophilic bacteriorhodopsin from hypersaline salt pan: characterization and photoelectrochemical assessment for potential biosensor applications.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1805566},
pmid = {42326399},
issn = {1664-302X},
abstract = {INTRODUCTION: Salt pans host a diverse microbiome, including specialized extremophilic haloarchaea capable of producing industrially valuable biomolecules, yet remains underexplored extreme environment. Photosensitive bacteriorhodopsin (BR) is a naturally occurring seven helix trans-membrane protein with emerging relevance due to its light driven proton pumping activity, photochemical stability and efficient light to electrical energy conversion.
METHODS: In this study, BR was extracted from haloarchaeal strains isolated from the Tuticorin salt pan using the Bead mix method and confirmed by SDS-PAGE. The extracted BR was further characterized using thin-layer chromatography (TLC), reverse-phase high performance liquid chromatography (R-HPLC), and Raman spectroscopy. The Purified BR was evaluated for its photovoltage response and a prototype biosensor was successfully developed.
RESULTS: Haloarchaeal isolate Halostagnicola larsenii (TP6) demonstrated a remarkable production yield of 360 mg/L of BR under native minimal saline medium conditions, the notably highest recorded for this native strain to date. This isolate was used for further optimization of BR production involving different carbon and nitrogen sources. Two different protein extraction methods were evaluated, of which the bead mix method proved to be effective, yielding around 48.4 mg/L of BR with 72.7% yield. We examined the morphological and physiological traits of these isolates and confirmed the presence of a 26 kDa protein using SDS-PAGE.
DISCUSSION: The isolated extremophilic haloarchaea have the potential to produce large amount of BR, and the characteristics were similar to those previously reported BR from native strains. The observed photoresponsive ability highlights the potential of BR as a bio-based functional component for food bio-sensing, optical devices, and photoelectrochemical biosensors. Overall, this highlights the feasibility of naturally occurring BR from haloarchaea as a sustainable source of photoactive biomolecules for emerging food biotechnology and sustainable biosensor development.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Fecal microbiota and microbial community transplantation: a review of current research.
Frontiers in microbiology, 17:1814047.
Homeostasis across diverse ecosystems, ranging from human hosts to environmental matrices, is profoundly governed by microbial communities. Dysbiosis, the disruption of this microbial equilibrium, leads to significant adverse outcomes in medicine, agriculture, aquaculture, and environmental health. This review synthesizes current knowledge on microbial transfusions, defined as the deliberate transfer of microbial communities or their components to restore, reconstitute, or enhance functional capacities across these systems. We explore the historical context and cutting-edge applications, including Fecal Microbiota Transplantation (FMT) for Clostridioides difficile infection, metabolic and neurological disorders, alongside advancements in vaginal microbiota transplantation. In agriculture, we summarize the engineering of soil microbiomes for enhanced plant health, stress adaptation, and bioremediation, as well as transplantation practices in livestock and wild species. Furthermore, we discuss the role of microbiota transplantation in aquaculture for improving fish health and disease resistance, highlighting both natural and synthetic consortia. The application of microbial communities in bioremediation and ecological restoration is explored, addressing challenges such as stability, cost, and ecological impacts. Ultimately, this review integrates these diverse applications within a "One Health" framework, emphasizing the systemic links among human, animal, and environmental microbiomes. We underscore the potential of microbiota transplantation as a sustainable strategy for restoring ecological balance while identifying critical research gaps and future directions regarding standardized methodologies and the long-term functionality of transplanted microbiomes.
Additional Links: PMID-42326403
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@article {pmid42326403,
year = {2026},
author = {Ryazanov, V and Vershinina, I and Inchagova, K and Bukareva, E and Kolpakov, V and Ruchay, A and Kosyan, D and Marinchev, M and Zdorov, A},
title = {Fecal microbiota and microbial community transplantation: a review of current research.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1814047},
pmid = {42326403},
issn = {1664-302X},
abstract = {Homeostasis across diverse ecosystems, ranging from human hosts to environmental matrices, is profoundly governed by microbial communities. Dysbiosis, the disruption of this microbial equilibrium, leads to significant adverse outcomes in medicine, agriculture, aquaculture, and environmental health. This review synthesizes current knowledge on microbial transfusions, defined as the deliberate transfer of microbial communities or their components to restore, reconstitute, or enhance functional capacities across these systems. We explore the historical context and cutting-edge applications, including Fecal Microbiota Transplantation (FMT) for Clostridioides difficile infection, metabolic and neurological disorders, alongside advancements in vaginal microbiota transplantation. In agriculture, we summarize the engineering of soil microbiomes for enhanced plant health, stress adaptation, and bioremediation, as well as transplantation practices in livestock and wild species. Furthermore, we discuss the role of microbiota transplantation in aquaculture for improving fish health and disease resistance, highlighting both natural and synthetic consortia. The application of microbial communities in bioremediation and ecological restoration is explored, addressing challenges such as stability, cost, and ecological impacts. Ultimately, this review integrates these diverse applications within a "One Health" framework, emphasizing the systemic links among human, animal, and environmental microbiomes. We underscore the potential of microbiota transplantation as a sustainable strategy for restoring ecological balance while identifying critical research gaps and future directions regarding standardized methodologies and the long-term functionality of transplanted microbiomes.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
From probiotic depletion to inflammatory cascade: multi-omics reveals the temporal progression of sleep deprivation-induced gut-liver axis disruption in mice.
Frontiers in microbiology, 17:1846136.
INTRODUCTION: Sleep deprivation (SD) is increasingly recognized as a risk factor for metabolic and hepatic disorders, yet the temporal dynamics linking gut dysbiosis to liver injury remain poorly characterized.
METHODS: In this study, we established a platform-based SD model in a total of 24 C57BL/6J mice (n = 4 per group per weekly time point) over 3 weeks and systematically investigated the weekly progression of gut microbiome alterations, hepatic metabolite profiles, and liver injury markers using Accu16S[®] absolute quantification sequencing and untargeted LC-MS/MS metabolomics.
RESULTS: Our results revealed a temporally ordered three-stage cascade of gut-liver axis disruption. In week 1, core probiotics including Bifidobacterium and Dubosiella declined concurrently with protective metabolites such as tryptamine and glycocholic acid, alongside perturbation of primary bile acid biosynthesis. In week 2, concurrent enrichment of a compensatory Lactobacillaceae member (Ligilactobacillus) and an opportunistic pathogen (Streptococcus) was accompanied by reduced microbiota-metabolite correlation density, coinciding with peak serum ALT/AST levels and metabolic pathway remodeling involving nucleotide sugar and tryptophan metabolism. By week 3, synchronous decline of Lactobacillus, Bifidobacterium, and Dubosiella coincided with full-scale activation of arachidonic acid metabolism and inflammatory immune pathways, accompanied by elevated serum LPS levels suggestive of intestinal barrier perturbation. Correlation analyses revealed that the progressive depletion of beneficial bacteria was associated with the sequential loss of protective metabolites, reorganization of the metabolic network, and inflammatory mediator accumulation, although these relationships remain correlational and require causal validation.
DISCUSSION: These findings describe a "protective loss-homeostatic decoupling-inflammatory signature" descriptive model. Because these findings are based on correlation analyses in a mouse model without causal validation, further mechanistic and interventional studies are required before any clinical implications can be drawn.
Additional Links: PMID-42326407
PubMed:
Citation:
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@article {pmid42326407,
year = {2026},
author = {Dai, MK and Kuang, X and Wang, YF and Liu, XX and Jin, YF and Li, YY and Tai, WL},
title = {From probiotic depletion to inflammatory cascade: multi-omics reveals the temporal progression of sleep deprivation-induced gut-liver axis disruption in mice.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1846136},
pmid = {42326407},
issn = {1664-302X},
abstract = {INTRODUCTION: Sleep deprivation (SD) is increasingly recognized as a risk factor for metabolic and hepatic disorders, yet the temporal dynamics linking gut dysbiosis to liver injury remain poorly characterized.
METHODS: In this study, we established a platform-based SD model in a total of 24 C57BL/6J mice (n = 4 per group per weekly time point) over 3 weeks and systematically investigated the weekly progression of gut microbiome alterations, hepatic metabolite profiles, and liver injury markers using Accu16S[®] absolute quantification sequencing and untargeted LC-MS/MS metabolomics.
RESULTS: Our results revealed a temporally ordered three-stage cascade of gut-liver axis disruption. In week 1, core probiotics including Bifidobacterium and Dubosiella declined concurrently with protective metabolites such as tryptamine and glycocholic acid, alongside perturbation of primary bile acid biosynthesis. In week 2, concurrent enrichment of a compensatory Lactobacillaceae member (Ligilactobacillus) and an opportunistic pathogen (Streptococcus) was accompanied by reduced microbiota-metabolite correlation density, coinciding with peak serum ALT/AST levels and metabolic pathway remodeling involving nucleotide sugar and tryptophan metabolism. By week 3, synchronous decline of Lactobacillus, Bifidobacterium, and Dubosiella coincided with full-scale activation of arachidonic acid metabolism and inflammatory immune pathways, accompanied by elevated serum LPS levels suggestive of intestinal barrier perturbation. Correlation analyses revealed that the progressive depletion of beneficial bacteria was associated with the sequential loss of protective metabolites, reorganization of the metabolic network, and inflammatory mediator accumulation, although these relationships remain correlational and require causal validation.
DISCUSSION: These findings describe a "protective loss-homeostatic decoupling-inflammatory signature" descriptive model. Because these findings are based on correlation analyses in a mouse model without causal validation, further mechanistic and interventional studies are required before any clinical implications can be drawn.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Comparative metagenomic analysis of gut microbiomes in Yunnan ponies and Dutch warmblood horses.
Frontiers in microbiology, 17:1807081.
INTRODUCTION: The Yunnan pony is an officially protected pony breed in China. However, its gut microbiome characteristics remain largely unexplored. This study aimed to compare the gut microbiome and antibiotic resistance genes (ARGs) profiles between Yunnan ponies and Dutch warmblood horses.
METHODOLOGY: A total of 14 fresh fecal samples were collected from Yunnan ponies and Dutch warmblood horses. Metagenomic sequencing was employed to comprehensively analyze and compare the gut microbial composition, function, and ARGs profiles between the two breeds.
RESULTS: The results showed no significant differences between the two breeds in core phylum composition or overall microbial diversity. A total of 146 bacterial genera were identified with significant differences at the genus level. Functional analysis revealed that the gut microbiota of Yunnan ponies was significantly enriched in pathways related to carbohydrate metabolism and pectin degradation, which are involved in basic energy acquisition. In contrast, Dutch warmblood horses were more enriched in host immune interaction pathways such as Toll-like receptor signaling. Analysis of ARGs indicated that while there was no difference in the overall diversity of ARGs between the two groups. Their association networks with specific bacterial hosts were markedly distinct, and the dominant ARG subtypes differed.
DISCUSSION: This study provides a descriptive characterization of the gut microbiome of Yunnan ponies, offering baseline data for future research on the conservation of this genetic resource and its health management in breeding.
Additional Links: PMID-42326408
PubMed:
Citation:
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@article {pmid42326408,
year = {2026},
author = {Cha, J and Yang, J and Zhang, Z and Qian, L and Yang, F and Li, S and Li, J and Jian, Z and Cheng, W},
title = {Comparative metagenomic analysis of gut microbiomes in Yunnan ponies and Dutch warmblood horses.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1807081},
pmid = {42326408},
issn = {1664-302X},
abstract = {INTRODUCTION: The Yunnan pony is an officially protected pony breed in China. However, its gut microbiome characteristics remain largely unexplored. This study aimed to compare the gut microbiome and antibiotic resistance genes (ARGs) profiles between Yunnan ponies and Dutch warmblood horses.
METHODOLOGY: A total of 14 fresh fecal samples were collected from Yunnan ponies and Dutch warmblood horses. Metagenomic sequencing was employed to comprehensively analyze and compare the gut microbial composition, function, and ARGs profiles between the two breeds.
RESULTS: The results showed no significant differences between the two breeds in core phylum composition or overall microbial diversity. A total of 146 bacterial genera were identified with significant differences at the genus level. Functional analysis revealed that the gut microbiota of Yunnan ponies was significantly enriched in pathways related to carbohydrate metabolism and pectin degradation, which are involved in basic energy acquisition. In contrast, Dutch warmblood horses were more enriched in host immune interaction pathways such as Toll-like receptor signaling. Analysis of ARGs indicated that while there was no difference in the overall diversity of ARGs between the two groups. Their association networks with specific bacterial hosts were markedly distinct, and the dominant ARG subtypes differed.
DISCUSSION: This study provides a descriptive characterization of the gut microbiome of Yunnan ponies, offering baseline data for future research on the conservation of this genetic resource and its health management in breeding.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Human milk microbiota: origins, determinants, and roles in maternal-infant microbial transmission and infant microbiome assembly.
Frontiers in microbiology, 17:1790225.
Human milk is a complex and dynamic biological fluid that provides essential nutrients and harbors a diverse, functional microbiota, playing a critical role in infant microbial colonization and early life development. The milk microbiota is derived from multiple maternal and environmental sources, including the maternal gut via the entero-mammary pathway, the mammary and skin microbiota, infant oral microbes through retrograde flow, and environmental exposures. Its composition is influenced by a range of factors, such as maternal metabolic and health status, diet, and antibiotic use, as well as delivery mode, lactation stage, infant characteristics, and geographic context. Human milk contributes to the establishment of oral, airway, and gut microbial communities by transferring key taxa such as Bifidobacterium and Lactobacillus, which are commonly detected in milk; however, direct evidence of specific strains establishing in the infant gut remains limited. Breastfeeding may partially compensate for microbiome deficits in cesarean-delivered, preterm, and antibiotic-exposed infants, supporting protection against infections, allergies, asthma, obesity, and other health outcomes. Translational strategies may help modulate the milk microbiota. These include maternal probiotic or prebiotic supplementation, dietary optimization, and approaches targeting microbiota or bioactive milk components. Such strategies offer feasible and cost-effective means to support healthy infant microbiome development. However, methodological constraints including low-biomass contamination, sequencing biases, and limited strain-level resolution remain significant challenges in accurately characterizing the human milk microbiota. Despite substantial advances, the relative contributions of distinct transmission routes, the persistence of maternal strains, and the efficacy of targeted maternal interventions remain incompletely understood. Addressing these gaps will be essential for refining strategies to promote healthy microbiome maturation and improve lifelong health outcomes.
Additional Links: PMID-42326410
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Citation:
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@article {pmid42326410,
year = {2026},
author = {Ma, G and Peng, L and Qin, L and Cai, R and Tan, X and Gao, R},
title = {Human milk microbiota: origins, determinants, and roles in maternal-infant microbial transmission and infant microbiome assembly.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1790225},
pmid = {42326410},
issn = {1664-302X},
abstract = {Human milk is a complex and dynamic biological fluid that provides essential nutrients and harbors a diverse, functional microbiota, playing a critical role in infant microbial colonization and early life development. The milk microbiota is derived from multiple maternal and environmental sources, including the maternal gut via the entero-mammary pathway, the mammary and skin microbiota, infant oral microbes through retrograde flow, and environmental exposures. Its composition is influenced by a range of factors, such as maternal metabolic and health status, diet, and antibiotic use, as well as delivery mode, lactation stage, infant characteristics, and geographic context. Human milk contributes to the establishment of oral, airway, and gut microbial communities by transferring key taxa such as Bifidobacterium and Lactobacillus, which are commonly detected in milk; however, direct evidence of specific strains establishing in the infant gut remains limited. Breastfeeding may partially compensate for microbiome deficits in cesarean-delivered, preterm, and antibiotic-exposed infants, supporting protection against infections, allergies, asthma, obesity, and other health outcomes. Translational strategies may help modulate the milk microbiota. These include maternal probiotic or prebiotic supplementation, dietary optimization, and approaches targeting microbiota or bioactive milk components. Such strategies offer feasible and cost-effective means to support healthy infant microbiome development. However, methodological constraints including low-biomass contamination, sequencing biases, and limited strain-level resolution remain significant challenges in accurately characterizing the human milk microbiota. Despite substantial advances, the relative contributions of distinct transmission routes, the persistence of maternal strains, and the efficacy of targeted maternal interventions remain incompletely understood. Addressing these gaps will be essential for refining strategies to promote healthy microbiome maturation and improve lifelong health outcomes.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Oral microbiome signatures of post-stroke cognitive impairment.
Frontiers in microbiology, 17:1722999.
INTRODUCTION: To investigate the characteristics of oral microbiota in patients with post-stroke cognitive impairment (PSCI) and to evaluate its potential as a noninvasive candidate microbial signature associated with PSCI.
METHODS: This cross-sectional study enrolled 108 participants, including 40 PSCI patients, 40 post-stroke patients with normal cognition (PSNC), and 28 healthy controls (HC). Saliva samples were collected for 16S rRNA sequencing. Diversity analyses, differential taxa identification, and correlation analyses were performed. Candidate microbial signatures were screened using the least absolute shrinkage and selection operator (LASSO) regression and Random Forest (RF), followed by the construction of multiple machine learning models.
RESULTS: Compared with PSNC and HC, patients with PSCI exhibited significantly reduced richness and diversity of the oral microbiota, and beta-diversity analyses suggested group-level differences in community composition. The relative abundances of gram-negative taxa, such as Proteobacteria, Campylobacterota, Gammaproteobacteria, Pseudomonadales, and Alloprevotella were increased in PSCI samples. In contrast, commensal taxa Leptotrichia, and Veillonella were markedly decreased. Significant associations were observed between differential taxa and cognitive scores (MMSE and MoCA). Three key microbial features were ultimately identified. Models based on these features showed favorable exploratory internal discriminatory performance between PSCI and PSNC within this dataset. In the test set, the RF model achieved an AUC of 0.979 and an Average Precision of 0.983. However, these findings should be interpreted cautiously and require validation in larger independent cohorts.
CONCLUSION: Patients with PSCI present with notable oral microbiota dysbiosis, characterized by depletion of commensal taxa and enrichment of Gram-negative bacteria. Oral microbiota-based models showed favorable exploratory internal discriminatory performance within this dataset, but these findings remain hypothesis-generating and require external validation in larger independent cohorts.
Additional Links: PMID-42326411
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Citation:
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@article {pmid42326411,
year = {2026},
author = {Xu, J and Chang, Y and Ma, J and Wang, H and Li, X and Chen, X and Niu, S and An, Y and Zhao, Y},
title = {Oral microbiome signatures of post-stroke cognitive impairment.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1722999},
pmid = {42326411},
issn = {1664-302X},
abstract = {INTRODUCTION: To investigate the characteristics of oral microbiota in patients with post-stroke cognitive impairment (PSCI) and to evaluate its potential as a noninvasive candidate microbial signature associated with PSCI.
METHODS: This cross-sectional study enrolled 108 participants, including 40 PSCI patients, 40 post-stroke patients with normal cognition (PSNC), and 28 healthy controls (HC). Saliva samples were collected for 16S rRNA sequencing. Diversity analyses, differential taxa identification, and correlation analyses were performed. Candidate microbial signatures were screened using the least absolute shrinkage and selection operator (LASSO) regression and Random Forest (RF), followed by the construction of multiple machine learning models.
RESULTS: Compared with PSNC and HC, patients with PSCI exhibited significantly reduced richness and diversity of the oral microbiota, and beta-diversity analyses suggested group-level differences in community composition. The relative abundances of gram-negative taxa, such as Proteobacteria, Campylobacterota, Gammaproteobacteria, Pseudomonadales, and Alloprevotella were increased in PSCI samples. In contrast, commensal taxa Leptotrichia, and Veillonella were markedly decreased. Significant associations were observed between differential taxa and cognitive scores (MMSE and MoCA). Three key microbial features were ultimately identified. Models based on these features showed favorable exploratory internal discriminatory performance between PSCI and PSNC within this dataset. In the test set, the RF model achieved an AUC of 0.979 and an Average Precision of 0.983. However, these findings should be interpreted cautiously and require validation in larger independent cohorts.
CONCLUSION: Patients with PSCI present with notable oral microbiota dysbiosis, characterized by depletion of commensal taxa and enrichment of Gram-negative bacteria. Oral microbiota-based models showed favorable exploratory internal discriminatory performance within this dataset, but these findings remain hypothesis-generating and require external validation in larger independent cohorts.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Antibiotic growth promoter and phytogenic feed additive consistently alter microbial community structure in chicken cecum.
Frontiers in microbiology, 17:1702973.
BACKGROUND: Efforts to replace antibiotic growth promoters (AGPs) in livestock are often hindered by a limited mechanistic understanding of how sub-therapeutic antibiotic doses enhance animal growth. Since AGP concentrations are typically too low to directly suppress pathogens, their effects on the gut microbiome, particularly its ecological dynamics, warrant closer investigation. A critical but underexplored dimension is how these additives influence the structure and stability of microbial communities as interconnected ecosystems.
METHODS: We conducted a comparative network-based analysis to examine the effects of zinc-bactracin, a commonly used AGP, and Digestarom[®], an alternative phytogenic feed additive (PFA) on cecal microbiome dynamics in broiler chickens. Using metagenomic data from a repeated cross-sectional randomized controlled trial of 96 broiler chickens assigned to three dietary groups: Basal (Control), AGP and PFA, we constructed microbial co-occurrence networks using Spearman's correlation for birds raised on basal, AGP-, or PFA-supplemented diets at key developmental stages (Day 3, 14, 21, and 35). We assessed changes in network topology, modular organization and node centrality. We evaluated whether the network-prioritized keystone taxa could discriminate among diets using a Random Forest classifier.
RESULTS: Compared to the Control group, both AGP and PFA treatments induced consistent shifts in network topology, including reduced connectivity, increased modularity, increased percentage of positive interactions, enhanced mucosa connectivity, and improved structural robustness over experiment time. Overall, these treatment-induced changes were more pronounced under AGP than under PFA. Despite these changes, we identified conserved subgraphs with stable interconnections across diets and time points during the experiment. The node centrality analysis revealed condition-specific keystone taxa, but Linear Discriminant Analysis (LDA) and Random Forest (RF) struggled to accurately differentiate between diets using their abundance, particularly between PFA and the two other groups.
CONCLUSION: Our findings reveal that feed additives can reshape gut microbial dynamics without producing marked compositional shifts. The consistent network-level changes observed for both AGP and PFA highlight the value of ecological network analysis in uncovering microbial community responses. These insights improve our understanding of cecal microbiome responses in chickens, highlight potential modes of action of AGPs, and offer a comparative framework for assessing the microbial impacts of alternative feed additives.
Additional Links: PMID-42326413
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@article {pmid42326413,
year = {2026},
author = {Peng, C and Delle Grazie, G and Ghanbari, M and May, A and Abeel, T},
title = {Antibiotic growth promoter and phytogenic feed additive consistently alter microbial community structure in chicken cecum.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1702973},
pmid = {42326413},
issn = {1664-302X},
abstract = {BACKGROUND: Efforts to replace antibiotic growth promoters (AGPs) in livestock are often hindered by a limited mechanistic understanding of how sub-therapeutic antibiotic doses enhance animal growth. Since AGP concentrations are typically too low to directly suppress pathogens, their effects on the gut microbiome, particularly its ecological dynamics, warrant closer investigation. A critical but underexplored dimension is how these additives influence the structure and stability of microbial communities as interconnected ecosystems.
METHODS: We conducted a comparative network-based analysis to examine the effects of zinc-bactracin, a commonly used AGP, and Digestarom[®], an alternative phytogenic feed additive (PFA) on cecal microbiome dynamics in broiler chickens. Using metagenomic data from a repeated cross-sectional randomized controlled trial of 96 broiler chickens assigned to three dietary groups: Basal (Control), AGP and PFA, we constructed microbial co-occurrence networks using Spearman's correlation for birds raised on basal, AGP-, or PFA-supplemented diets at key developmental stages (Day 3, 14, 21, and 35). We assessed changes in network topology, modular organization and node centrality. We evaluated whether the network-prioritized keystone taxa could discriminate among diets using a Random Forest classifier.
RESULTS: Compared to the Control group, both AGP and PFA treatments induced consistent shifts in network topology, including reduced connectivity, increased modularity, increased percentage of positive interactions, enhanced mucosa connectivity, and improved structural robustness over experiment time. Overall, these treatment-induced changes were more pronounced under AGP than under PFA. Despite these changes, we identified conserved subgraphs with stable interconnections across diets and time points during the experiment. The node centrality analysis revealed condition-specific keystone taxa, but Linear Discriminant Analysis (LDA) and Random Forest (RF) struggled to accurately differentiate between diets using their abundance, particularly between PFA and the two other groups.
CONCLUSION: Our findings reveal that feed additives can reshape gut microbial dynamics without producing marked compositional shifts. The consistent network-level changes observed for both AGP and PFA highlight the value of ecological network analysis in uncovering microbial community responses. These insights improve our understanding of cecal microbiome responses in chickens, highlight potential modes of action of AGPs, and offer a comparative framework for assessing the microbial impacts of alternative feed additives.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Editorial: Women in infectious agents and disease: 2025.
Frontiers in microbiology, 17:1884772.
Additional Links: PMID-42326416
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@article {pmid42326416,
year = {2026},
author = {Alva-Murillo, N and Khaiboullina, S and Tarashi, S},
title = {Editorial: Women in infectious agents and disease: 2025.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1884772},
pmid = {42326416},
issn = {1664-302X},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Gut microbiota dysbiosis in endometriosis: mechanistic insights and gut microbiota-targeted therapeutic strategies.
Frontiers in microbiology, 17:1776574.
Endometriosis (EMs) is a prevalent, estrogen-dependent gynecological disorder characterized by the ectopic implantation and proliferation of endometrial-like tissue outside the uterine cavity, affecting approximately 10% of reproductive-aged women globally. Despite its high incidence, the exact pathogenesis of EMs remains incompletely elucidated, and current clinical treatments are often limited by suboptimal efficacy and adverse effects. Accumulating evidence over the past decade has revealed a strong observational association between gut microbiota dysbiosis and EMs development, suggesting that the gut microbiota may serve as a novel potential target for understanding and managing this disease. This review systematically summarizes the potential mechanistic links underlying the interplay between gut microbiota dysbiosis and EMs progression, focusing on three core pathways: intestinal barrier dysfunction and microbial translocation, immune dysregulation and ectopic lesion immune escape, and estrogen metabolism disorder mediated by microbial enzymes and metabolites. In addition, this review stratifies gut microbiome profiles by EMs clinical subtypes (peritoneal, ovarian, deep infiltrating), clarifies anatomical correlations of the gut-lesion axis, and discusses confounding factors and causal inference methodologies. Beyond mechanistic insights, this review also discusses emerging gut microbiota-targeted therapeutic strategies for EMs, including probiotic supplementation, prebiotic intervention, fecal microbiota transplantation (FMT), and dietary modulation, with supplementary ethical considerations for FMT. Collectively, this review provides a comprehensive overview of the gut microbiota-EMs axis, highlighting current evidence levels and offering perspectives for the development of innovative, effective, and safe therapeutic approaches for EMs patients.
Additional Links: PMID-42326424
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Citation:
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@article {pmid42326424,
year = {2026},
author = {Liang, L and Min, L and Liu, J and Liu, Y and Cheng, W},
title = {Gut microbiota dysbiosis in endometriosis: mechanistic insights and gut microbiota-targeted therapeutic strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1776574},
pmid = {42326424},
issn = {1664-302X},
abstract = {Endometriosis (EMs) is a prevalent, estrogen-dependent gynecological disorder characterized by the ectopic implantation and proliferation of endometrial-like tissue outside the uterine cavity, affecting approximately 10% of reproductive-aged women globally. Despite its high incidence, the exact pathogenesis of EMs remains incompletely elucidated, and current clinical treatments are often limited by suboptimal efficacy and adverse effects. Accumulating evidence over the past decade has revealed a strong observational association between gut microbiota dysbiosis and EMs development, suggesting that the gut microbiota may serve as a novel potential target for understanding and managing this disease. This review systematically summarizes the potential mechanistic links underlying the interplay between gut microbiota dysbiosis and EMs progression, focusing on three core pathways: intestinal barrier dysfunction and microbial translocation, immune dysregulation and ectopic lesion immune escape, and estrogen metabolism disorder mediated by microbial enzymes and metabolites. In addition, this review stratifies gut microbiome profiles by EMs clinical subtypes (peritoneal, ovarian, deep infiltrating), clarifies anatomical correlations of the gut-lesion axis, and discusses confounding factors and causal inference methodologies. Beyond mechanistic insights, this review also discusses emerging gut microbiota-targeted therapeutic strategies for EMs, including probiotic supplementation, prebiotic intervention, fecal microbiota transplantation (FMT), and dietary modulation, with supplementary ethical considerations for FMT. Collectively, this review provides a comprehensive overview of the gut microbiota-EMs axis, highlighting current evidence levels and offering perspectives for the development of innovative, effective, and safe therapeutic approaches for EMs patients.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Sludge compost: a double-edged sword for depleted soil restoration revealed by integrated multi-omics analysis.
Frontiers in microbiology, 17:1731456.
The prospective use of sludge compost for restoring depleted soils requires balancing its agronomic benefits against potential ecological risks. This study employed an integrated metagenomic and metabolomic approach to evaluate the dose-dependent effects of sludge compost on soil properties, maize growth, and rhizosphere microbial communities. Results showed that moderate compost application (≤15% w/w) enhanced soil nutrient availability, promoted root development, and enriched beneficial microbial taxa (Streptomyces, Mesorhizobium, Flavisolibacter), while upregulating plant stress-response metabolites (terpenoids, flavonoids). Conversely, excessive application (>20%) induced salinity stress, impaired root growth, and altered the microbial community, favoring thermophilic and xenobiotic-metabolizing taxa. Critically, high application rates led to the accumulation of residual pharmaceuticals (anti-neoplastic and anti-epileptic agents) and pesticides (insecticides and rodenticides), which correlated with the enrichment of microbial pathways associated with human diseases, highlighting a significant ecological risk. In addition, root integrity was the primary determinant of a sustainable plant-microbe feedback loop. These findings underscore the necessity for tailored application strategies to harness the soil-restorative potential of sludge compost while mitigating contaminant-driven risks, providing a framework for its safe use in sustainable agriculture.
Additional Links: PMID-42326431
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@article {pmid42326431,
year = {2026},
author = {Mei, X and Wu, W and Fang, N and Guo, Y and Dai, X},
title = {Sludge compost: a double-edged sword for depleted soil restoration revealed by integrated multi-omics analysis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1731456},
pmid = {42326431},
issn = {1664-302X},
abstract = {The prospective use of sludge compost for restoring depleted soils requires balancing its agronomic benefits against potential ecological risks. This study employed an integrated metagenomic and metabolomic approach to evaluate the dose-dependent effects of sludge compost on soil properties, maize growth, and rhizosphere microbial communities. Results showed that moderate compost application (≤15% w/w) enhanced soil nutrient availability, promoted root development, and enriched beneficial microbial taxa (Streptomyces, Mesorhizobium, Flavisolibacter), while upregulating plant stress-response metabolites (terpenoids, flavonoids). Conversely, excessive application (>20%) induced salinity stress, impaired root growth, and altered the microbial community, favoring thermophilic and xenobiotic-metabolizing taxa. Critically, high application rates led to the accumulation of residual pharmaceuticals (anti-neoplastic and anti-epileptic agents) and pesticides (insecticides and rodenticides), which correlated with the enrichment of microbial pathways associated with human diseases, highlighting a significant ecological risk. In addition, root integrity was the primary determinant of a sustainable plant-microbe feedback loop. These findings underscore the necessity for tailored application strategies to harness the soil-restorative potential of sludge compost while mitigating contaminant-driven risks, providing a framework for its safe use in sustainable agriculture.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
The Cervical Microbiome in Hispanic Populations in Texas and Puerto Rico with and without Cervical Dysplasia.
Research square pii:rs.3.rs-8002153.
Within the United States, Hispanic women, especially those in Puerto Rico, face an increased risk of cervical cancer development. The objective of this study was to explore the cervical microbiota of Hispanic women at high risk of developing HPV-induced cervical dysplasia or with cervical dysplasia treated in Texas and Puerto Rico. Cervical swab samples were collected from 296 participants (N = 80 Texan Non-Hispanic White, N = 98 Texan Hispanic, and N = 118 Puerto Rican Hispanic) during each patient's initial visit and subjected to 16S V4 rRNA gene sequencing for microbiome profiling. HPV types were grouped as HPV 16, other high-risk HPV types, and other using HPV genotyping. Among participants, 71% (N = 211) were classified as high-risk normal, and 29% (N = 85) had cervical dysplasia. HPV 16 was detected in 15% (N = 45), other high-risk HPV types in 33% (N = 98), while 52% (N = 152) of patients were classified as "other". Comparative analysis of microbial community structures across locations revealed distinct compositions, with Texan Hispanic women showing higher alpha diversity for two alpha diversity metrics (Pielou evenness and Shannon Diversity Index). The prevalence of CSTs varied across locations and disease states, with CSTs III and IV-B being among the most common in the study cohorts. Overall, this descriptive study provides a better understanding of cervical microbiome in Hispanic women across multiple geographic locations, in order to guide future interventions.
Additional Links: PMID-42326495
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@article {pmid42326495,
year = {2026},
author = {Walters, D and Alam, MBE and Harris, T and Lo, D and Diaz, JSG and Napravnik, TC and Lynn, EJ and Boatright, LD and Figueroa, DN and Judge, A and Bhaskar, CCJ and Fontillas, A and Ehsan, SF and Wang, R and Aref, SNJ and Ajami, NJ and Sastry, J and Sims, TT and Romaguera, J and Dorta-Estremera, S and Klopp, A and Godoy-Vitorino, F and Colbert, LE},
title = {The Cervical Microbiome in Hispanic Populations in Texas and Puerto Rico with and without Cervical Dysplasia.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-8002153/v1},
pmid = {42326495},
issn = {2693-5015},
abstract = {Within the United States, Hispanic women, especially those in Puerto Rico, face an increased risk of cervical cancer development. The objective of this study was to explore the cervical microbiota of Hispanic women at high risk of developing HPV-induced cervical dysplasia or with cervical dysplasia treated in Texas and Puerto Rico. Cervical swab samples were collected from 296 participants (N = 80 Texan Non-Hispanic White, N = 98 Texan Hispanic, and N = 118 Puerto Rican Hispanic) during each patient's initial visit and subjected to 16S V4 rRNA gene sequencing for microbiome profiling. HPV types were grouped as HPV 16, other high-risk HPV types, and other using HPV genotyping. Among participants, 71% (N = 211) were classified as high-risk normal, and 29% (N = 85) had cervical dysplasia. HPV 16 was detected in 15% (N = 45), other high-risk HPV types in 33% (N = 98), while 52% (N = 152) of patients were classified as "other". Comparative analysis of microbial community structures across locations revealed distinct compositions, with Texan Hispanic women showing higher alpha diversity for two alpha diversity metrics (Pielou evenness and Shannon Diversity Index). The prevalence of CSTs varied across locations and disease states, with CSTs III and IV-B being among the most common in the study cohorts. Overall, this descriptive study provides a better understanding of cervical microbiome in Hispanic women across multiple geographic locations, in order to guide future interventions.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Bacterial topography of the respiratory tract, including pulmonary site-of-disease, in people with active tuberculosis: a case-control study.
Research square pii:rs.3.rs-9956587.
BACKGROUND: No comprehensive characterization of the respiratory tract (RT) microbiota has been done in people with tuberculosis (TB), a leading global cause of death.
METHODS: 16S rRNA gene sequencing was done on upper RT (URT; oral-washes, naso- and oro-pharyngeal swabs, supraglottic fluid), sputum and lower RT [LRT; bronchoalveolar lavage fluid (BALF) and protected specimen brushings] specimens from HIV-negative people with Xpert MTB/RIF-confirmed TB (cases; n=17) and healthy controls (n=11). In addition to their diseased lobe, cases had their non-diseased lobe sampled.
RESULTS: The LRT had the lowest α-diversity and β-diversity differed compared to other respiratory compartments. In cases, Mycobacterium relative abundance was highest in the diseased lobe 1.537% (CI 0-3.114), followed by the nasopharynx 0.059% (0.012-0.105), non-diseased lobe 0.054% (0-1.620), oropharynx 0.003% (0-0.010) and sputum 0.002% (0-0.004). Compared to the URT and sputum, cases' LRTs were Mycobacterium- and Moraxella -enriched (Erythromicrobium -enriched versus sputum only). In paired comparisons of diseased versus non-diseased lobes in cases, the only differential taxon was Mycobacterium . Amongst non-diseased lobes, those of cases versus controls had reduced α-diversity with Mycoplasma -enrichment and Moraxella- and Klebsiella- depletion.
CONCLUSION: Compared to healthy people, those with TB have a less diverse LRT microbiota, characterized by Mycobacterium -enrichment (within the diseased lobe and surprisingly least so in sputum) and depletion of taxa associated with healthy people. In people with TB, most microbial DNA is not mycobacterial within the diseased lobe and even the non-diseased lobes of cases are microbially distinct from controls. These findings provide a foundation for understanding respiratory tract host-microbiome interactions in TB.
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@article {pmid42326511,
year = {2026},
author = {Chiyaka, TL and Moodley, S and Simon, D and Shaw, JA and Malherbe, ST and Li, Y and Warren, RM and Clemente, JC and Segal, LN and Chegou, NN and Theron, G and Marsh, CC},
title = {Bacterial topography of the respiratory tract, including pulmonary site-of-disease, in people with active tuberculosis: a case-control study.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-9956587/v1},
pmid = {42326511},
issn = {2693-5015},
abstract = {BACKGROUND: No comprehensive characterization of the respiratory tract (RT) microbiota has been done in people with tuberculosis (TB), a leading global cause of death.
METHODS: 16S rRNA gene sequencing was done on upper RT (URT; oral-washes, naso- and oro-pharyngeal swabs, supraglottic fluid), sputum and lower RT [LRT; bronchoalveolar lavage fluid (BALF) and protected specimen brushings] specimens from HIV-negative people with Xpert MTB/RIF-confirmed TB (cases; n=17) and healthy controls (n=11). In addition to their diseased lobe, cases had their non-diseased lobe sampled.
RESULTS: The LRT had the lowest α-diversity and β-diversity differed compared to other respiratory compartments. In cases, Mycobacterium relative abundance was highest in the diseased lobe 1.537% (CI 0-3.114), followed by the nasopharynx 0.059% (0.012-0.105), non-diseased lobe 0.054% (0-1.620), oropharynx 0.003% (0-0.010) and sputum 0.002% (0-0.004). Compared to the URT and sputum, cases' LRTs were Mycobacterium- and Moraxella -enriched (Erythromicrobium -enriched versus sputum only). In paired comparisons of diseased versus non-diseased lobes in cases, the only differential taxon was Mycobacterium . Amongst non-diseased lobes, those of cases versus controls had reduced α-diversity with Mycoplasma -enrichment and Moraxella- and Klebsiella- depletion.
CONCLUSION: Compared to healthy people, those with TB have a less diverse LRT microbiota, characterized by Mycobacterium -enrichment (within the diseased lobe and surprisingly least so in sputum) and depletion of taxa associated with healthy people. In people with TB, most microbial DNA is not mycobacterial within the diseased lobe and even the non-diseased lobes of cases are microbially distinct from controls. These findings provide a foundation for understanding respiratory tract host-microbiome interactions in TB.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Interconnected influences of diet, gut microbiome, and metabolome on cognition across three metabolomics platforms.
Research square pii:rs.3.rs-9917711.
Cognitive impairment is increasing with global aging, yet mechanisms linking diet, the gut microbiome, and metabolism to cognitive function remain unclear. To investigate a diet-microbiome-metabolome axis associated with cognition, we integrated fecal metagenomics, diet, and multi-platform plasma metabolomics in 505 older adults from four ADRCs. Several microbes broadly associated with circulating metabolites were also linked to multiple measures of cognitive performance. These taxa exhibited coordinated metabolic signatures, with cognition-positive microbes associated with antioxidant, lipid, and microbial-host co-metabolites, and microbes negatively associated with cognition were linked to inflammatory and aromatic amino acid-derived metabolites. Dietary patterns, particularly the Healthy Eating Index Greens and Beans component, were associated with microbial composition and metabolomic structure. Mediation analyses supported a diet-microbe-metabolite-cognition pathway, while metabolites remained associated with cognition after accounting for microbial features. These findings highlight the metabolome as a central integrator of diet, microbial activity, and cognitive function.
Additional Links: PMID-42326513
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@article {pmid42326513,
year = {2026},
author = {Knight, R and Khatib, L and Patel, L and MahmoudianDehkordi, S and Labus, J and Agongo, J and Borkowski, K and Ambre, M and Brydges, C and Schimmel, L and Blach, C and Consortium, AGMP and Karu, N and Taylor, M and Diaz, E and Brosch, J and Bendlin, B and Swerdlow, R and Henderson, V and Chen, D and Saykin, A and Craft, S and Brewer, J and Wisniewski, T and Roberson, E and Dorrestein, PC and Kaddurah-Daouk, R},
title = {Interconnected influences of diet, gut microbiome, and metabolome on cognition across three metabolomics platforms.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-9917711/v1},
pmid = {42326513},
issn = {2693-5015},
abstract = {Cognitive impairment is increasing with global aging, yet mechanisms linking diet, the gut microbiome, and metabolism to cognitive function remain unclear. To investigate a diet-microbiome-metabolome axis associated with cognition, we integrated fecal metagenomics, diet, and multi-platform plasma metabolomics in 505 older adults from four ADRCs. Several microbes broadly associated with circulating metabolites were also linked to multiple measures of cognitive performance. These taxa exhibited coordinated metabolic signatures, with cognition-positive microbes associated with antioxidant, lipid, and microbial-host co-metabolites, and microbes negatively associated with cognition were linked to inflammatory and aromatic amino acid-derived metabolites. Dietary patterns, particularly the Healthy Eating Index Greens and Beans component, were associated with microbial composition and metabolomic structure. Mediation analyses supported a diet-microbe-metabolite-cognition pathway, while metabolites remained associated with cognition after accounting for microbial features. These findings highlight the metabolome as a central integrator of diet, microbial activity, and cognitive function.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Exploratory Pilot Multi-Omics Profiling of Gut Microbiota and Metabolic Features in Patients with Prolactinoma.
Cancer management and research, 18:608026.
BACKGROUND: Growing evidence suggests a potential role of the gut microbiota in pituitary neuroendocrine tumors (PitNETs). This exploratory study focused on prolactinoma, the most prevalent PitNET subtype, to preliminarily characterize gut microbial and metabolic features associated with the disease.
MATERIALS AND METHODS: Fecal samples were collected from five patients with hyperprolactinemic prolactinoma and five patients with nonfunctioning (NF) PitNETs. Exploratory metagenomic and metabolomic analyses were performed to profile gut microbiota composition and metabolic alterations.
RESULTS: Compared with NF PitNET controls, prolactinoma patients showed distinct trends in gut microbial composition, including increased abundances of Bacteroides and Eubacterium and decreased abundances of Blautia and Clostridium. Metabolomic profiling identified differential metabolic features, including elevated fatty acid esters of hydroxy fatty acids (FAHFAs) and palmitoleic acid, which were mainly associated with glucose and lipid metabolism pathways.
CONCLUSION: This pilot multi-omics analysis provides preliminary evidence of altered gut microbiome-metabolite profiles in prolactinoma. These findings are hypothesis-generating and may support further investigation of gut-pituitary axis interactions in larger, well-powered cohorts.
Additional Links: PMID-42326540
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@article {pmid42326540,
year = {2026},
author = {Yang, J and Nie, D and Zhang, Y and Li, C},
title = {Exploratory Pilot Multi-Omics Profiling of Gut Microbiota and Metabolic Features in Patients with Prolactinoma.},
journal = {Cancer management and research},
volume = {18},
number = {},
pages = {608026},
pmid = {42326540},
issn = {1179-1322},
abstract = {BACKGROUND: Growing evidence suggests a potential role of the gut microbiota in pituitary neuroendocrine tumors (PitNETs). This exploratory study focused on prolactinoma, the most prevalent PitNET subtype, to preliminarily characterize gut microbial and metabolic features associated with the disease.
MATERIALS AND METHODS: Fecal samples were collected from five patients with hyperprolactinemic prolactinoma and five patients with nonfunctioning (NF) PitNETs. Exploratory metagenomic and metabolomic analyses were performed to profile gut microbiota composition and metabolic alterations.
RESULTS: Compared with NF PitNET controls, prolactinoma patients showed distinct trends in gut microbial composition, including increased abundances of Bacteroides and Eubacterium and decreased abundances of Blautia and Clostridium. Metabolomic profiling identified differential metabolic features, including elevated fatty acid esters of hydroxy fatty acids (FAHFAs) and palmitoleic acid, which were mainly associated with glucose and lipid metabolism pathways.
CONCLUSION: This pilot multi-omics analysis provides preliminary evidence of altered gut microbiome-metabolite profiles in prolactinoma. These findings are hypothesis-generating and may support further investigation of gut-pituitary axis interactions in larger, well-powered cohorts.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Precision Rehabilitation in Spinal Cord Injury: A Systematic Review of Omics Applications for Intervention Monitoring in Spinal Cord Injury.
Archives of rehabilitation research and clinical translation, 8(2):100598.
OBJECTIVE: To systematically evaluate the application and utility of omics technologies, high-throughput methods measuring the complete or targeted set of molecules inside a biological system at a certain timepoint, in monitoring and optimizing rehabilitation interventions in traumatic spinal cord injury.
DATA SOURCES: Embase, Medline/Ovid, and Web of Science were searched from inception to November 27, 2024.
STUDY SELECTION: Eligible studies included adults (≥18 years) with spinal cord injury undergoing rehabilitation interventions assessed using omics technologies (genomics, epigenomics, transcriptomics, proteomics, metabolomics, or metagenomics).
DATA EXTRACTION: Following PRISMA guidelines, independent screening, data extraction, and risk of bias (RoB) assessment (National Institutes of Health Quality Assessment Tools) were performed by 2 investigators. Based on RoB assessment, studies were classified from level 1 (most reliable) to level 4 (least reliable).
DATA SYNTHESIS: Twenty-three trials were included: 8 randomized controlled trials, 5 non-randomized controlled trials, and 10 pre-post trials. Twenty-two studies (96%) exhibit a moderate RoB due to small sample size and heterogeneity. Omics technologies were primarily applied to exercise and electrical muscle stimulation interventions (65%), followed by hormonal and cellular therapies (22%), and diet (13%). Transcriptomic analyses revealed consistent molecular adaptations, including increased mitochondrial biogenesis (proliferator-activated receptor gamma coactivator 1-alpha) and reduced muscle atrophy gene expression (myostatin), correlating with enhanced insulin sensitivity and improved aerobic capacity. Metagenomics consistently identified microbiome shifts, such as decreased inflammatory taxa and increased beneficial taxa, associated with improved metabolic profiles and bowel function. Proteomics and metabolomics highlighted systemic changes related to neurorecovery, immune modulation, and sperm motility, linking molecular signatures directly to clinical outcomes.
CONCLUSIONS: Omics technologies enable early identification of molecular alterations. However, given small sample sizes and heterogeneity of the current studies, these findings should be interpreted with caution. Gradual integration of omics, particularly epigenomics which may capture long-term, injury-related changes holds promise for developing personalized rehabilitation protocols and monitoring clinical progression in spinal cord injury.
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@article {pmid42326568,
year = {2026},
author = {Stacul, A and Valido, E and Nyfeler, N and Bertolo, A and Zeh, RM and Fontana, AO and Pannek, J and Krebs, J and Leichtle, A and Glisic, M and Stoyanov, J},
title = {Precision Rehabilitation in Spinal Cord Injury: A Systematic Review of Omics Applications for Intervention Monitoring in Spinal Cord Injury.},
journal = {Archives of rehabilitation research and clinical translation},
volume = {8},
number = {2},
pages = {100598},
pmid = {42326568},
issn = {2590-1095},
abstract = {OBJECTIVE: To systematically evaluate the application and utility of omics technologies, high-throughput methods measuring the complete or targeted set of molecules inside a biological system at a certain timepoint, in monitoring and optimizing rehabilitation interventions in traumatic spinal cord injury.
DATA SOURCES: Embase, Medline/Ovid, and Web of Science were searched from inception to November 27, 2024.
STUDY SELECTION: Eligible studies included adults (≥18 years) with spinal cord injury undergoing rehabilitation interventions assessed using omics technologies (genomics, epigenomics, transcriptomics, proteomics, metabolomics, or metagenomics).
DATA EXTRACTION: Following PRISMA guidelines, independent screening, data extraction, and risk of bias (RoB) assessment (National Institutes of Health Quality Assessment Tools) were performed by 2 investigators. Based on RoB assessment, studies were classified from level 1 (most reliable) to level 4 (least reliable).
DATA SYNTHESIS: Twenty-three trials were included: 8 randomized controlled trials, 5 non-randomized controlled trials, and 10 pre-post trials. Twenty-two studies (96%) exhibit a moderate RoB due to small sample size and heterogeneity. Omics technologies were primarily applied to exercise and electrical muscle stimulation interventions (65%), followed by hormonal and cellular therapies (22%), and diet (13%). Transcriptomic analyses revealed consistent molecular adaptations, including increased mitochondrial biogenesis (proliferator-activated receptor gamma coactivator 1-alpha) and reduced muscle atrophy gene expression (myostatin), correlating with enhanced insulin sensitivity and improved aerobic capacity. Metagenomics consistently identified microbiome shifts, such as decreased inflammatory taxa and increased beneficial taxa, associated with improved metabolic profiles and bowel function. Proteomics and metabolomics highlighted systemic changes related to neurorecovery, immune modulation, and sperm motility, linking molecular signatures directly to clinical outcomes.
CONCLUSIONS: Omics technologies enable early identification of molecular alterations. However, given small sample sizes and heterogeneity of the current studies, these findings should be interpreted with caution. Gradual integration of omics, particularly epigenomics which may capture long-term, injury-related changes holds promise for developing personalized rehabilitation protocols and monitoring clinical progression in spinal cord injury.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Beyond Urease: New Potential Enzymatic Targets in Helicobacter pylori.
ACS omega, 11(23):33320-33332.
H. pylori infection remains one of the most widespread bacterial diseases globally and a leading risk factor for peptic ulcer disease and gastric cancer. Despite decades of research, the treatment of H. pylori still depends on multidrug antibiotic regimens, whose efficacy is waning due to the rise in antimicrobial resistance. Although significant progress has been made in understanding H. pylori pathogenesis, most studies targeting bacterial enzymes have focused almost exclusively on urease, a well-characterized virulence factor, while other metabolic and structural pathways remain comparatively underexplored. Targeting essential enzymes involved in bacterial metabolism and structural integrity may disrupt vital processes, potentially reducing off-target effects on the host microbiota and overcoming resistance mechanisms. To address this gap, this systematic review, conducted according to PRISMA 2020 guidelines, synthesized experimental studies published between 2014 and 2024 that investigated enzyme-targeted compounds against H. pylori, excluding those focused on urease. Literature searches in PubMed and the Web of Science identified 49 eligible studies exploring enzymes across multiple metabolic pathways. The main pathways identified included purine metabolism, the shikimate and futalosine pathways, and nitrogen metabolism, along with several other enzymatic systems, such as thioredoxin, thymidylate, and peptidoglycan biosynthesis, all of which represent promising targets for selective inhibition in H. pylori. The reported inhibitors exhibited micromolar to submicromolar activity and, in some cases, demonstrated potent antibacterial effects with minimal cytotoxicity. However, most studies remained limited to in vitro assays, and only three included animal tests. These findings highlight enzymatic inhibition as a promising approach for the rational design of narrow-spectrum microbiome-sparing agents. Advancing these discoveries through in vivo validation and druggability assessment will be essential to translating enzyme-based inhibition into effective therapeutic options against H. pylori.
Additional Links: PMID-42326627
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@article {pmid42326627,
year = {2026},
author = {Camini, AM and Cogo, LR and Delawi, ME and Anton, DB and Koakovski Acosta, J and de Lima, JC and Saraiva Macedo Timmers, LF},
title = {Beyond Urease: New Potential Enzymatic Targets in Helicobacter pylori.},
journal = {ACS omega},
volume = {11},
number = {23},
pages = {33320-33332},
pmid = {42326627},
issn = {2470-1343},
abstract = {H. pylori infection remains one of the most widespread bacterial diseases globally and a leading risk factor for peptic ulcer disease and gastric cancer. Despite decades of research, the treatment of H. pylori still depends on multidrug antibiotic regimens, whose efficacy is waning due to the rise in antimicrobial resistance. Although significant progress has been made in understanding H. pylori pathogenesis, most studies targeting bacterial enzymes have focused almost exclusively on urease, a well-characterized virulence factor, while other metabolic and structural pathways remain comparatively underexplored. Targeting essential enzymes involved in bacterial metabolism and structural integrity may disrupt vital processes, potentially reducing off-target effects on the host microbiota and overcoming resistance mechanisms. To address this gap, this systematic review, conducted according to PRISMA 2020 guidelines, synthesized experimental studies published between 2014 and 2024 that investigated enzyme-targeted compounds against H. pylori, excluding those focused on urease. Literature searches in PubMed and the Web of Science identified 49 eligible studies exploring enzymes across multiple metabolic pathways. The main pathways identified included purine metabolism, the shikimate and futalosine pathways, and nitrogen metabolism, along with several other enzymatic systems, such as thioredoxin, thymidylate, and peptidoglycan biosynthesis, all of which represent promising targets for selective inhibition in H. pylori. The reported inhibitors exhibited micromolar to submicromolar activity and, in some cases, demonstrated potent antibacterial effects with minimal cytotoxicity. However, most studies remained limited to in vitro assays, and only three included animal tests. These findings highlight enzymatic inhibition as a promising approach for the rational design of narrow-spectrum microbiome-sparing agents. Advancing these discoveries through in vivo validation and druggability assessment will be essential to translating enzyme-based inhibition into effective therapeutic options against H. pylori.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Machine learning-based classification of COVID-19 severity using respiratory microbiome profiles from shotgun metagenomic sequencing.
Frontiers in bioinformatics, 6:1801685.
Accurate clinical triage is critical for optimizing decision-making and resource allocation during infectious disease outbreaks such as COVID-19. In this study, we present an AI-driven decision-support tool for the triage of COVID-19 patients based on respiratory microbiome profiles derived from shotgun metagenomic sequencing. We analyzed 477 shotgun respiratory metagenomes from three independent public cohorts and generated genus-level taxonomic profiles, which were integrated with minimal clinical metadata (age, sex, and antibiotic exposure) to train supervised machine-learning models, including Random Forest, Support Vector Machine, and XGBoost. Model performance was evaluated using standard classification metrics, cross-validation, and particle swarm optimization for hyperparameter tuning. Across cohorts, we observed a consistent transition from microbiomes dominated by commensal taxa to dysbiotic states enriched in opportunistic and clinically relevant genera, particularly Acinetobacter and Staphylococcus, in severe and deceased patients. Among the evaluated models, XGBoost consistently achieved the best performance, reaching up to 96.1% accuracy, 97.6% F1-score, and 98.2% ROC-AUC in individual cohorts. When trained on the integrated dataset, XGBoost maintained robust performance (95.1% accuracy, 97.2% F1-score, 94.3% ROC-AUC) and demonstrated greater stability and lower variance compared to alternative models. Feature-importance analyses identified a compact and interpretable set of recurrent microbial predictors, and reduced-feature models retained substantial discriminative power when augmented with key clinical variables. These results support the respiratory microbiome as a valuable source of information for outcome-oriented clinical triage and position microbiome-informed machine learning as a scalable and interpretable decision-support approach for managing COVID-19 and future infectious disease scenarios.
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@article {pmid42326740,
year = {2026},
author = {Avina-Bravo, EG and García-Lorenzo, I and Alfaro-Ponce, M and Breton-Deval, L},
title = {Machine learning-based classification of COVID-19 severity using respiratory microbiome profiles from shotgun metagenomic sequencing.},
journal = {Frontiers in bioinformatics},
volume = {6},
number = {},
pages = {1801685},
pmid = {42326740},
issn = {2673-7647},
abstract = {Accurate clinical triage is critical for optimizing decision-making and resource allocation during infectious disease outbreaks such as COVID-19. In this study, we present an AI-driven decision-support tool for the triage of COVID-19 patients based on respiratory microbiome profiles derived from shotgun metagenomic sequencing. We analyzed 477 shotgun respiratory metagenomes from three independent public cohorts and generated genus-level taxonomic profiles, which were integrated with minimal clinical metadata (age, sex, and antibiotic exposure) to train supervised machine-learning models, including Random Forest, Support Vector Machine, and XGBoost. Model performance was evaluated using standard classification metrics, cross-validation, and particle swarm optimization for hyperparameter tuning. Across cohorts, we observed a consistent transition from microbiomes dominated by commensal taxa to dysbiotic states enriched in opportunistic and clinically relevant genera, particularly Acinetobacter and Staphylococcus, in severe and deceased patients. Among the evaluated models, XGBoost consistently achieved the best performance, reaching up to 96.1% accuracy, 97.6% F1-score, and 98.2% ROC-AUC in individual cohorts. When trained on the integrated dataset, XGBoost maintained robust performance (95.1% accuracy, 97.2% F1-score, 94.3% ROC-AUC) and demonstrated greater stability and lower variance compared to alternative models. Feature-importance analyses identified a compact and interpretable set of recurrent microbial predictors, and reduced-feature models retained substantial discriminative power when augmented with key clinical variables. These results support the respiratory microbiome as a valuable source of information for outcome-oriented clinical triage and position microbiome-informed machine learning as a scalable and interpretable decision-support approach for managing COVID-19 and future infectious disease scenarios.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Ig-microbiota binding patterns in mothers and infants: a scoping review.
Gut microbiome (Cambridge, England), 7:e12.
Studies characterising the immunoglobulin (Ig)-bound microbiota apply varying methodologies, making comparisons difficult. This scoping review synthesised evidence on Ig-microbiota binding patterns in maternal and infant contexts, identified recurrent Ig-bound and -unbound bacteria across studies, and highlighted knowledge gaps for further study. Nine articles investigating Ig-microbiota binding patterns in stool or breastmilk samples in mothers or infants were included. Ig-microbiota associations were influenced by sample type, Ig-subclass, genetics, and diet. The most important antibody was IgA, with partial functional redundancy with IgM, while IgG appeared more selective for pathobionts. Ig-bound taxa in early life included important commensals and pathobionts, with high levels of individuality. Ig-microbiota associations shifted with microbiome maturation, environmental and host factors, resembling adults at around 2 years of age. Transfer of Ig-bound Bifidobacterium through breastmilk may contribute to vertical transmission from mother to infant. Ig-microbiota associations also differed between health and disease states, beyond the overall microbiota. Results were limited by study numbers and a lack of methodological consistency. We propose the standardised term "Ig-Seq" in referring to the technique to study Ig-microbiota binding patterns, and suggest standardisation of laboratory protocols, bioinformatic pipelines, and statistical analyses to improve consistency in Ig-Seq.
Additional Links: PMID-42326836
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@article {pmid42326836,
year = {2026},
author = {Yi Jia, AT and Peacock, CS and Dye, DE and Christophersen, CT},
title = {Ig-microbiota binding patterns in mothers and infants: a scoping review.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e12},
pmid = {42326836},
issn = {2632-2897},
abstract = {Studies characterising the immunoglobulin (Ig)-bound microbiota apply varying methodologies, making comparisons difficult. This scoping review synthesised evidence on Ig-microbiota binding patterns in maternal and infant contexts, identified recurrent Ig-bound and -unbound bacteria across studies, and highlighted knowledge gaps for further study. Nine articles investigating Ig-microbiota binding patterns in stool or breastmilk samples in mothers or infants were included. Ig-microbiota associations were influenced by sample type, Ig-subclass, genetics, and diet. The most important antibody was IgA, with partial functional redundancy with IgM, while IgG appeared more selective for pathobionts. Ig-bound taxa in early life included important commensals and pathobionts, with high levels of individuality. Ig-microbiota associations shifted with microbiome maturation, environmental and host factors, resembling adults at around 2 years of age. Transfer of Ig-bound Bifidobacterium through breastmilk may contribute to vertical transmission from mother to infant. Ig-microbiota associations also differed between health and disease states, beyond the overall microbiota. Results were limited by study numbers and a lack of methodological consistency. We propose the standardised term "Ig-Seq" in referring to the technique to study Ig-microbiota binding patterns, and suggest standardisation of laboratory protocols, bioinformatic pipelines, and statistical analyses to improve consistency in Ig-Seq.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Associations between gut microbiome and 24-hour blood pressure variability: a cross-sectional study highlighting sex differences and potential therapeutic targets.
Gut microbiome (Cambridge, England), 7:e9.
Blood pressure (BP) variability is an independent risk factor for cardiovascular disease. Gut microbiome (GM) regulates BP, but its association with BP variability remains unclear. We examined the association of GM, determined by stool shotgun metagenomic sequencing, with 24-hour BP average real variability (ARV) assessed by ambulatory BP monitoring in 235 community-dwelling adults from Hong Kong (111 men and 124 women, mean age 54 ± 6 years) using covariate-adjusted statistical models. The GM alpha diversity was negatively associated with systolic BP (SBP) ARV in the full cohort, driven by women. In men, beta diversity of both GM species and function was associated with SBP ARV, while Bacteroides nordii and the steroid hormone biosynthesis pathway had a positive association with SBP ARV. Bacteroides nordii emerged as the key species driving the significant positive association of steroid hormone biosynthesis and other pro-pathogenic pathways with SBP ARV, including lipopolysaccharide biosynthesis, phenylalanine, and sulfur metabolism in men, warranting further investigation for its causal role. We demonstrated distinct signatures of GM dysbiosis, composition, and function with minimal overlap between men and women with increased 24-hour SBP variability. Our work suggests that sex differences should be an important consideration in mechanistic and therapeutic investigations of GM-mediated BP variability.
Additional Links: PMID-42326837
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@article {pmid42326837,
year = {2026},
author = {Virwani, PD and Qian, G and Cheung, CN and Pijarnvanit, TKKTS and Hsu, MSS and Chow, YH and Tang, LK and Tse, YH and Xian, JW and Lam, SS and Lee, CPI and Lo, CCW and Liu, RKC and Ho, TL and Chow, BY and Leung, KS and Lo, EKK and Yuen, MF and Leung, SY and Hung, IF and Louie, JCY and Teo, KC and El-Nezami, H and Ho, JWK and Lau, KK},
title = {Associations between gut microbiome and 24-hour blood pressure variability: a cross-sectional study highlighting sex differences and potential therapeutic targets.},
journal = {Gut microbiome (Cambridge, England)},
volume = {7},
number = {},
pages = {e9},
pmid = {42326837},
issn = {2632-2897},
abstract = {Blood pressure (BP) variability is an independent risk factor for cardiovascular disease. Gut microbiome (GM) regulates BP, but its association with BP variability remains unclear. We examined the association of GM, determined by stool shotgun metagenomic sequencing, with 24-hour BP average real variability (ARV) assessed by ambulatory BP monitoring in 235 community-dwelling adults from Hong Kong (111 men and 124 women, mean age 54 ± 6 years) using covariate-adjusted statistical models. The GM alpha diversity was negatively associated with systolic BP (SBP) ARV in the full cohort, driven by women. In men, beta diversity of both GM species and function was associated with SBP ARV, while Bacteroides nordii and the steroid hormone biosynthesis pathway had a positive association with SBP ARV. Bacteroides nordii emerged as the key species driving the significant positive association of steroid hormone biosynthesis and other pro-pathogenic pathways with SBP ARV, including lipopolysaccharide biosynthesis, phenylalanine, and sulfur metabolism in men, warranting further investigation for its causal role. We demonstrated distinct signatures of GM dysbiosis, composition, and function with minimal overlap between men and women with increased 24-hour SBP variability. Our work suggests that sex differences should be an important consideration in mechanistic and therapeutic investigations of GM-mediated BP variability.},
}
RevDate: 2026-06-22
Rewilding reshapes gut microbiomes and parasite exposure in European bison: a 17‑month release from Wilder Blean.
Journal for nature conservation, 92:None.
Reintroductions can restore lost ecological processes, but managers require practical health indicators to track the acclimation of released animals. We longitudinally profiled the gut microbiomes of European bison (European bison bonasus) released to the Wilder Blean area (Kent, UK), sampling three adult females before and after release, and a post‑release male and calf. Using V3-V4 16S rRNA gene sequencing, we quantified alpha‑ and beta‑diversity, identified differentially abundant taxa, and screened faeces for Cryptosporidium, Enterocytozoon bieneusi and Blastocystis. Post‑release, adult microbiomes shifted significantly (PERMANOVA P = 0.001) and consistently across all examined animals. Calf microbiome profiles transitioned from early‑life communities to an adult‑like state concurrent with weaning. Parasite screening via separate PCR and qPCR showed that Cryptosporidium positivity declined in females from 36% pre‑release to 13% post‑release, whereas E. bieneusi emerged only after release (∼10% of samples), with multiple genotypes detected. These patterns are consistent with dietary and environmental turnover following release, and they highlight opportunities for using microbiome and parasite metrics as complementary, non‑invasive indicators of rewilding progress. We recommend reporting simple, management‑relevant indicators, archiving sequence data, and documenting soft‑release design and supplementary feeding info to aid interpretation. Integrating routine faecal microbiome and parasite monitoring into rewilding programmes can support adaptive management, inform supplementary feeding decisions, and strengthen biosecurity risk assessments.
Additional Links: PMID-42326879
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@article {pmid42326879,
year = {2026},
author = {Edwards, WJ and Salman Al-Adilee, YM and Denoyelle, C and Mackins, H and Griffiths, RA and Tsaousis, AD},
title = {Rewilding reshapes gut microbiomes and parasite exposure in European bison: a 17‑month release from Wilder Blean.},
journal = {Journal for nature conservation},
volume = {92},
number = {},
pages = {None},
pmid = {42326879},
issn = {1617-1381},
abstract = {Reintroductions can restore lost ecological processes, but managers require practical health indicators to track the acclimation of released animals. We longitudinally profiled the gut microbiomes of European bison (European bison bonasus) released to the Wilder Blean area (Kent, UK), sampling three adult females before and after release, and a post‑release male and calf. Using V3-V4 16S rRNA gene sequencing, we quantified alpha‑ and beta‑diversity, identified differentially abundant taxa, and screened faeces for Cryptosporidium, Enterocytozoon bieneusi and Blastocystis. Post‑release, adult microbiomes shifted significantly (PERMANOVA P = 0.001) and consistently across all examined animals. Calf microbiome profiles transitioned from early‑life communities to an adult‑like state concurrent with weaning. Parasite screening via separate PCR and qPCR showed that Cryptosporidium positivity declined in females from 36% pre‑release to 13% post‑release, whereas E. bieneusi emerged only after release (∼10% of samples), with multiple genotypes detected. These patterns are consistent with dietary and environmental turnover following release, and they highlight opportunities for using microbiome and parasite metrics as complementary, non‑invasive indicators of rewilding progress. We recommend reporting simple, management‑relevant indicators, archiving sequence data, and documenting soft‑release design and supplementary feeding info to aid interpretation. Integrating routine faecal microbiome and parasite monitoring into rewilding programmes can support adaptive management, inform supplementary feeding decisions, and strengthen biosecurity risk assessments.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Sex-linked Lung Estrobolome May Contribute to Pulmonary Hypertension Penetrance of Bmpr2 R899X Mutation via an ET-1 [high] Endoregulatory Macrophage Phenotype.
bioRxiv : the preprint server for biology pii:2026.06.08.729693.
Mutations in the bone morphogenetic protein receptor 2 (BMPR2) are a major genetic driver of pulmonary arterial hypertension (PAH), yet their penetrance is strikingly sex-biased: females are disproportionately affected, while males experience poorer outcomes. While hormonal and chromosomal factors have been implicated, the biological basis for this disparity remains not fully understood. Here, we investigated the role of the lung microbiome in sex-linked PAH pathogenesis. We hypothesized that increased BMPR2 mutation penetrance in females is partly driven by the accumulation of potent vasoactive molecules, such as endothelin-1 (ET-1), in response to lung microbiome dysbiosis. Using humanized Bmpr2 [+/R899X] mice, we integrate lung metagenomics with basic functional immune profiling to show that females develop a distinct microbiome profile, characterized by increased microbial-derived lipopolysaccharide (LPS), potentially fueling the pathogenic effects of the estrogen metabolite 16α-hydroxyestrone (16α-OHE). These signals converge on macrophages, where co-exposure led to a hyperactivated state characterized by enhanced phagocytosis and ET-1 secretion. Tissue-level analyses confirmed immune cell infiltration and spatial association with elevated ET-1, providing evidence that these factors may contribute to the onset of sex-linked PAH. Taken together, these findings identify a previously unrecognized microbiome-estrogen-immune axis that amplifies BMPR2 dysfunction and provides a mechanistic basis for female-biased disease penetrance.
Additional Links: PMID-42327082
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@article {pmid42327082,
year = {2026},
author = {Loya, O and Villarreal, ES and Carneiro, A and Agarwal, S and Fraidenburg, D and Sun, J and de Jesus Perez, V and Lahm, T and Oliveira, SD},
title = {Sex-linked Lung Estrobolome May Contribute to Pulmonary Hypertension Penetrance of Bmpr2 R899X Mutation via an ET-1 [high] Endoregulatory Macrophage Phenotype.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.08.729693},
pmid = {42327082},
issn = {2692-8205},
abstract = {Mutations in the bone morphogenetic protein receptor 2 (BMPR2) are a major genetic driver of pulmonary arterial hypertension (PAH), yet their penetrance is strikingly sex-biased: females are disproportionately affected, while males experience poorer outcomes. While hormonal and chromosomal factors have been implicated, the biological basis for this disparity remains not fully understood. Here, we investigated the role of the lung microbiome in sex-linked PAH pathogenesis. We hypothesized that increased BMPR2 mutation penetrance in females is partly driven by the accumulation of potent vasoactive molecules, such as endothelin-1 (ET-1), in response to lung microbiome dysbiosis. Using humanized Bmpr2 [+/R899X] mice, we integrate lung metagenomics with basic functional immune profiling to show that females develop a distinct microbiome profile, characterized by increased microbial-derived lipopolysaccharide (LPS), potentially fueling the pathogenic effects of the estrogen metabolite 16α-hydroxyestrone (16α-OHE). These signals converge on macrophages, where co-exposure led to a hyperactivated state characterized by enhanced phagocytosis and ET-1 secretion. Tissue-level analyses confirmed immune cell infiltration and spatial association with elevated ET-1, providing evidence that these factors may contribute to the onset of sex-linked PAH. Taken together, these findings identify a previously unrecognized microbiome-estrogen-immune axis that amplifies BMPR2 dysfunction and provides a mechanistic basis for female-biased disease penetrance.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Identification of the complete pathway for conversion of bilirubin to urobilinogen by human gut bacteria.
bioRxiv : the preprint server for biology pii:2026.06.10.731317.
Bilirubin, the predominant product of heme catabolism in mammals, enters the intestine via the hepatobiliary system and subsequently is metabolized by the gut microbiome. This process consumes bilirubin and generates multiple downstream derivatives, such as urobilinogen and stercobilinogen. Levels of bilirubin and its derivatives are associated with susceptibility to inflammatory and metabolic disorders, but the microbial species and enzymes that metabolize bilirubin have remained largely unknown. Here, demonstrate that metabolism of bilirubin to urobilinogen requires two separate reactions that can occur in either order and identify novel enzymes and pathway intermediates required for conversion. We find that bilirubin reductase (BilR), an enzyme that was recently discovered and proposed to convert bilirubin to urobilinogen, is specific for reducing the methine bridges of bilinoids, converting bilirubin to the novel intermediate divinylurobilinogen and mesobilirubin to urobilinogen. Using transcriptomic profiling, we identify the bilinoid vinyl reductase (BilV) responsible for reducing the vinyl groups of bilirubin and divinylurobilinogen. BilV is a flavin-dependent oxidoreductase of the Old Yellow Enzyme (OYE) superfamily with a broad distribution across human gut bacteria that overlaps with but does not completely mirror the distribution of BilR. These findings establish the complete pathway for bacterial conversion of bilirubin to urobilinogen, enabling defined studies to interrogate how this metabolism contributes to human health and disease.
Additional Links: PMID-42327170
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@article {pmid42327170,
year = {2026},
author = {Russell, BJ and Hasenoehrl, E and Marando, VM and Lu, J and Chen, JM and James, MJ and Goyal, M and Walker, S and Rakoff-Nahoum, S and Jost, M},
title = {Identification of the complete pathway for conversion of bilirubin to urobilinogen by human gut bacteria.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.10.731317},
pmid = {42327170},
issn = {2692-8205},
abstract = {Bilirubin, the predominant product of heme catabolism in mammals, enters the intestine via the hepatobiliary system and subsequently is metabolized by the gut microbiome. This process consumes bilirubin and generates multiple downstream derivatives, such as urobilinogen and stercobilinogen. Levels of bilirubin and its derivatives are associated with susceptibility to inflammatory and metabolic disorders, but the microbial species and enzymes that metabolize bilirubin have remained largely unknown. Here, demonstrate that metabolism of bilirubin to urobilinogen requires two separate reactions that can occur in either order and identify novel enzymes and pathway intermediates required for conversion. We find that bilirubin reductase (BilR), an enzyme that was recently discovered and proposed to convert bilirubin to urobilinogen, is specific for reducing the methine bridges of bilinoids, converting bilirubin to the novel intermediate divinylurobilinogen and mesobilirubin to urobilinogen. Using transcriptomic profiling, we identify the bilinoid vinyl reductase (BilV) responsible for reducing the vinyl groups of bilirubin and divinylurobilinogen. BilV is a flavin-dependent oxidoreductase of the Old Yellow Enzyme (OYE) superfamily with a broad distribution across human gut bacteria that overlaps with but does not completely mirror the distribution of BilR. These findings establish the complete pathway for bacterial conversion of bilirubin to urobilinogen, enabling defined studies to interrogate how this metabolism contributes to human health and disease.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Phylogenetic coherence in microbiome composition across environmental gradients.
bioRxiv : the preprint server for biology pii:2026.06.07.730742.
Global surveys of microbial communities across biomes have shown that environmental variables such as depth and pH are strong determinants of community composition. However, we do not understand how the traits of individual taxa, and their evolutionary conservation, conspire to give rise to these patterns. Exploiting large-scale surveys of top soil and marine microbiomes, we use canonical correlation analysis (CCA) to concurrently infer directions of environmental variation and the associated compositional changes. We find that the primary canonical direction, capturing the dominant environmental gradient, exhibits a strong phylogenetic signal: individual species' responses to environmental shifts along this direction are similar among taxa with shared evolutionary history. In contrast, secondary canonical directions show weak or no phylogenetic structure. Together, these results suggest a two-scale view of microbial community assembly. Deeply evolutionarily conserved traits govern community reorganization along the main environmental driver of community composition. Additional environmentally driven changes in community composition then reflect traits that are more evolutionarily labile.
Additional Links: PMID-42327301
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@article {pmid42327301,
year = {2026},
author = {Chakraverti-Wuerthwein, MS and Domenig, A and Kuehn, S},
title = {Phylogenetic coherence in microbiome composition across environmental gradients.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.07.730742},
pmid = {42327301},
issn = {2692-8205},
abstract = {Global surveys of microbial communities across biomes have shown that environmental variables such as depth and pH are strong determinants of community composition. However, we do not understand how the traits of individual taxa, and their evolutionary conservation, conspire to give rise to these patterns. Exploiting large-scale surveys of top soil and marine microbiomes, we use canonical correlation analysis (CCA) to concurrently infer directions of environmental variation and the associated compositional changes. We find that the primary canonical direction, capturing the dominant environmental gradient, exhibits a strong phylogenetic signal: individual species' responses to environmental shifts along this direction are similar among taxa with shared evolutionary history. In contrast, secondary canonical directions show weak or no phylogenetic structure. Together, these results suggest a two-scale view of microbial community assembly. Deeply evolutionarily conserved traits govern community reorganization along the main environmental driver of community composition. Additional environmentally driven changes in community composition then reflect traits that are more evolutionarily labile.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Multi-Omic Profiling of Gut Microbiota and Fecal Metabolites in Patients With Polycystic Ovary Syndrome: A Cross-Sectional Study.
Health science reports, 9(6):e72593.
BACKGROUND AND AIM: Intestinal flora composition in polycystic ovary syndrome (PCOS) varies, and the relationship between intestinal flora, fecal metabolites, clinical characteristics, and PCOS pathogenesis remains unclear. This study aimed to elucidate the gut microbiota characteristics of patients with PCOS, focusing on changes in normal-weight individuals, to provide new insights into its pathogenesis.
METHODS: We combined 16S rRNA gene sequencing re-analysis with metagenomics and metabolomics to investigate gut microbiota and fecal metabolome alterations in PCOS. We re-analyzed our previous data on normal-weight women with PCOS (PCOS, n = 24; healthy controls [HC], n = 12) and the public databases (PCOS, n = 98; HC, n = 71) to further investigate the structure and function of the PCOS intestinal flora. Subsequently, from our previous study samples, we selected 10 patients residing in the Kaifu district, and their fecal samples (normal-weight PCOS group, n = 6; HC group, n = 4) were analyzed using metagenomic sequencing and non-targeted fecal metabolomics. Finally, the correlations among intestinal flora, fecal metabolites, and clinical indicators were evaluated.
RESULTS: Based on the 16S rRNA data reanalysis, there were no significant differences in beta and alpha diversity between PCOS and normal controls. However, the PCOS group displayed a significantly higher relative abundance of Ruminococcus, Lachnospiraceae, and Escherichia-Shigella (p < 0.05) but a significantly lower relative abundance of Prevotella (p < 0.05) compared with the HC group. Subsequent metagenomics and metabolomics analyses revealed functional alterations, particularly in pathways related to secondary bile acid and lipid metabolism. Furthermore, Ruminococcus and Roseburia were positively correlated with Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and negatively correlated with high-density lipoprotein (HDL) in patients with normal-weight PCOS.
CONCLUSIONS: This study highlights gut microbial dysbiosis as a key feature of PCOS. Reanalysis of 16S rRNA data revealed specific taxonomic shifts without altering overall diversity, notably an enrichment of Ruminococcus and a depletion of Prevotella. Furthermore, our metagenomics study identified functional reprogramming in pathways related to secondary bile acid and lipid metabolism. Crucially, even in normal-weight PCOS patients, these microbial alterations significantly correlated with adverse metabolic profiles (heightened insulin resistance and lower HDL levels), highlighting the microbiome as a potential therapeutic target.
ETHICAL REVIEW NO: CHiECRT1900028223.
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@article {pmid42327471,
year = {2026},
author = {Li, YM and He, FF and Donge-Liu, and Bin-Xu, and Shuyi-Li, },
title = {Multi-Omic Profiling of Gut Microbiota and Fecal Metabolites in Patients With Polycystic Ovary Syndrome: A Cross-Sectional Study.},
journal = {Health science reports},
volume = {9},
number = {6},
pages = {e72593},
pmid = {42327471},
issn = {2398-8835},
abstract = {BACKGROUND AND AIM: Intestinal flora composition in polycystic ovary syndrome (PCOS) varies, and the relationship between intestinal flora, fecal metabolites, clinical characteristics, and PCOS pathogenesis remains unclear. This study aimed to elucidate the gut microbiota characteristics of patients with PCOS, focusing on changes in normal-weight individuals, to provide new insights into its pathogenesis.
METHODS: We combined 16S rRNA gene sequencing re-analysis with metagenomics and metabolomics to investigate gut microbiota and fecal metabolome alterations in PCOS. We re-analyzed our previous data on normal-weight women with PCOS (PCOS, n = 24; healthy controls [HC], n = 12) and the public databases (PCOS, n = 98; HC, n = 71) to further investigate the structure and function of the PCOS intestinal flora. Subsequently, from our previous study samples, we selected 10 patients residing in the Kaifu district, and their fecal samples (normal-weight PCOS group, n = 6; HC group, n = 4) were analyzed using metagenomic sequencing and non-targeted fecal metabolomics. Finally, the correlations among intestinal flora, fecal metabolites, and clinical indicators were evaluated.
RESULTS: Based on the 16S rRNA data reanalysis, there were no significant differences in beta and alpha diversity between PCOS and normal controls. However, the PCOS group displayed a significantly higher relative abundance of Ruminococcus, Lachnospiraceae, and Escherichia-Shigella (p < 0.05) but a significantly lower relative abundance of Prevotella (p < 0.05) compared with the HC group. Subsequent metagenomics and metabolomics analyses revealed functional alterations, particularly in pathways related to secondary bile acid and lipid metabolism. Furthermore, Ruminococcus and Roseburia were positively correlated with Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) and negatively correlated with high-density lipoprotein (HDL) in patients with normal-weight PCOS.
CONCLUSIONS: This study highlights gut microbial dysbiosis as a key feature of PCOS. Reanalysis of 16S rRNA data revealed specific taxonomic shifts without altering overall diversity, notably an enrichment of Ruminococcus and a depletion of Prevotella. Furthermore, our metagenomics study identified functional reprogramming in pathways related to secondary bile acid and lipid metabolism. Crucially, even in normal-weight PCOS patients, these microbial alterations significantly correlated with adverse metabolic profiles (heightened insulin resistance and lower HDL levels), highlighting the microbiome as a potential therapeutic target.
ETHICAL REVIEW NO: CHiECRT1900028223.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
The impact of freeze-dried food on gut microbiota composition: a preliminary study.
Current research in food science, 13:101470.
Freeze-dried food is widely used during space expeditions or flights. However, evidence on how this affects the gut microbiota is limited. This study aimed to assess changes in the composition of gut microbiota in volunteers subjected to a 14-day stay in a controlled space-analogue habitat. Five adults provided stool samples at baseline and after two weeks. Meals were freeze-dried and standardized for portion size and composition. Meals were served according to a daily schedule with no additional snacks allowed. Coffee and tea were permitted. Compliance was monitored by returning and verifying the packaging. Bacterial community profiles were assessed using shallow shotgun metagenomics and analyzed using paired statistical methods, including alpha diversity indices and beta diversity ordination with permutation-based testing. Differential abundance analyses were performed to identify taxa showing trends toward change during the intervention. Overall gut bacterial diversity and community structure were essentially stable over 14 days among all participants. No statistically significant changes in alpha diversity were observed, and global beta diversity patterns did not indicate a consistent separation of the entire community between baseline and day 14. Exploratory analyses suggested small changes within individuals in the relative abundance of selected taxa; however, inter-individual variability prevailed, and the small sample size limited statistical power. It appears that a diet consisting entirely of freeze-dried foods, consumed for 14 days, did not significantly affect the overall diversity of the gut microbiota or the structure of its communities. However, these studies are preliminary in nature and provide hypotheses for use in larger, controlled studies aimed at elucidating the microbiome's response to dietary regimens based on freeze-dried products.
Additional Links: PMID-42327630
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@article {pmid42327630,
year = {2026},
author = {Katarzyna, BS and Danuta, CL and Wiktoria, K and Małgorzata, T and Natalia, K and Dominika, MM and Karina, R and Joanna, P and Karina, K and Barbara, G and Danuta, LK and Helena, G and Wiśniewska, M and Karolina, SŻ and Stachowska, E},
title = {The impact of freeze-dried food on gut microbiota composition: a preliminary study.},
journal = {Current research in food science},
volume = {13},
number = {},
pages = {101470},
pmid = {42327630},
issn = {2665-9271},
abstract = {Freeze-dried food is widely used during space expeditions or flights. However, evidence on how this affects the gut microbiota is limited. This study aimed to assess changes in the composition of gut microbiota in volunteers subjected to a 14-day stay in a controlled space-analogue habitat. Five adults provided stool samples at baseline and after two weeks. Meals were freeze-dried and standardized for portion size and composition. Meals were served according to a daily schedule with no additional snacks allowed. Coffee and tea were permitted. Compliance was monitored by returning and verifying the packaging. Bacterial community profiles were assessed using shallow shotgun metagenomics and analyzed using paired statistical methods, including alpha diversity indices and beta diversity ordination with permutation-based testing. Differential abundance analyses were performed to identify taxa showing trends toward change during the intervention. Overall gut bacterial diversity and community structure were essentially stable over 14 days among all participants. No statistically significant changes in alpha diversity were observed, and global beta diversity patterns did not indicate a consistent separation of the entire community between baseline and day 14. Exploratory analyses suggested small changes within individuals in the relative abundance of selected taxa; however, inter-individual variability prevailed, and the small sample size limited statistical power. It appears that a diet consisting entirely of freeze-dried foods, consumed for 14 days, did not significantly affect the overall diversity of the gut microbiota or the structure of its communities. However, these studies are preliminary in nature and provide hypotheses for use in larger, controlled studies aimed at elucidating the microbiome's response to dietary regimens based on freeze-dried products.},
}
RevDate: 2026-06-22
Microbiome Hype Meets Epilepsy: Signal, Noise, and Mechanism.
Epilepsy currents [Epub ahead of print].
Additional Links: PMID-42327664
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@article {pmid42327664,
year = {2026},
author = {Antoine, MW},
title = {Microbiome Hype Meets Epilepsy: Signal, Noise, and Mechanism.},
journal = {Epilepsy currents},
volume = {},
number = {},
pages = {15357597261459806},
pmid = {42327664},
issn = {1535-7597},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Predictive modeling for cervical cancer: existing AI approaches and the emerging role of vaginal microbiome.
Frontiers in network physiology, 6:1799486.
Cervical cancer remains a major global health burden, yet current screening tools lack precision in identifying which women with high-risk human papillomavirus (HPV) infection will progress to high-grade lesions or cancer. Within a network-physiology framework, cervical carcinogenesis is viewed as emerging from dynamic interactions between viral dynamics, host immunity, vaginal ecology, vaccination status and behaviour rather than from isolated risk factors. This perspective review examines artificial intelligence (AI) approaches for cervical cancer prediction and evaluates the emerging role of the vaginal microbiome as a complementary biomarker within these interconnected physiological networks. The review synthesises evidence linking non-Lactobacillus-dominated or Lactobacillus iners-rich vaginal communities with increased HPV persistence and cervical intraepithelial neoplasia, contrasted with protective Lactobacillus crispatus-dominant communities, and outlines how these ecological signatures could be combined with HPV genotype and clinical factors in multi-modal models. A structured narrative synthesis of published AI tools demonstrates that current prognostic, diagnostic and screening algorithms rely mainly on demographic, clinical or imaging variables, with no validated models yet integrating vaginal microbiome profiles into cervical cancer risk calculators. The manuscript proposes a technical framework for microbiome-enabled modelling, covering feature engineering from community state types, algorithm selection, handling of high-dimensional omics data, and staged validation in NHS-relevant populations. Finally, it outlines a translational pathway for embedding microbiome-informed risk models into cervical screening using self-collected tampon sampling, AI-driven triage and digital decision support, and identifies key unmet needs, including longitudinal multi-omic cohorts, international consortia and robust bias auditing.
Additional Links: PMID-42327708
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@article {pmid42327708,
year = {2026},
author = {Gomes, M and Li, Z and Olaitan, A and Gentry-Maharaj, A},
title = {Predictive modeling for cervical cancer: existing AI approaches and the emerging role of vaginal microbiome.},
journal = {Frontiers in network physiology},
volume = {6},
number = {},
pages = {1799486},
pmid = {42327708},
issn = {2674-0109},
abstract = {Cervical cancer remains a major global health burden, yet current screening tools lack precision in identifying which women with high-risk human papillomavirus (HPV) infection will progress to high-grade lesions or cancer. Within a network-physiology framework, cervical carcinogenesis is viewed as emerging from dynamic interactions between viral dynamics, host immunity, vaginal ecology, vaccination status and behaviour rather than from isolated risk factors. This perspective review examines artificial intelligence (AI) approaches for cervical cancer prediction and evaluates the emerging role of the vaginal microbiome as a complementary biomarker within these interconnected physiological networks. The review synthesises evidence linking non-Lactobacillus-dominated or Lactobacillus iners-rich vaginal communities with increased HPV persistence and cervical intraepithelial neoplasia, contrasted with protective Lactobacillus crispatus-dominant communities, and outlines how these ecological signatures could be combined with HPV genotype and clinical factors in multi-modal models. A structured narrative synthesis of published AI tools demonstrates that current prognostic, diagnostic and screening algorithms rely mainly on demographic, clinical or imaging variables, with no validated models yet integrating vaginal microbiome profiles into cervical cancer risk calculators. The manuscript proposes a technical framework for microbiome-enabled modelling, covering feature engineering from community state types, algorithm selection, handling of high-dimensional omics data, and staged validation in NHS-relevant populations. Finally, it outlines a translational pathway for embedding microbiome-informed risk models into cervical screening using self-collected tampon sampling, AI-driven triage and digital decision support, and identifies key unmet needs, including longitudinal multi-omic cohorts, international consortia and robust bias auditing.},
}
RevDate: 2026-06-22
CmpDate: 2026-06-22
Oral and gut microbiota dysbiosis with strengthened oral-gut connectivity in post-stroke cognitive impairment.
Frontiers in immunology, 17:1851811.
BACKGROUND: Microbiome studies in post-stroke cognitive impairment (PSCI) have focused on the gut, while upstream oral dysbiosis and oral-gut axis signatures remain undercharacterized. We profiled paired oral and gut microbiota in PSCI to assess coordinated alterations and cross-site associations.
METHODS: This single-center cross-sectional study enrolled 133 post-stroke participants (64 PSCI). Paired tongue-coating and fecal samples underwent 16S rRNA gene sequencing. We compared α/β diversity, taxonomic composition, and predicted functional pathways at both sites, quantified within-individual oral-gut dissimilarity and the gut fraction of oral-gut shared microbiota, and adapted an oral enrichment score (OES) to index gut "oralization". Differential microbiota, predicted pathways, and MMSE/MoCA scores were integrated into a multi-layer association framework. Machine-learning models were built using oral features, gut features, and combined oral-gut features, with SHAP for interpretability.
RESULTS: PSCI showed reduced oral richness (ACE/Chao1) and reduced gut diversity/evenness (Shannon/Simpson), with significant β-diversity differences at both sites. Oral commensals (Leptotrichia, Neisseria) were depleted, whereas opportunistic taxa (Pseudomonas, Alloprevotella, Streptococcus) were enriched. In the gut, SCFA-associated microbiota (Coprococcus, Faecalibacterium, Ruminococcus) decreased, while Gram-negative potential pathogens (Enterobacter, Pseudomonas, Klebsiella) increased. Tax4Fun2-based inference suggested predicted gut functional alterations involving lipopolysaccharide biosynthesis potential and tryptophan metabolism-related pathways. Oral-gut metrics supported stronger oral-gut association in PSCI, including lower paired dissimilarity, a higher shared-genera fraction, and elevated OES (median 0.0368 vs 0.0142), mainly driven by oral-dominant microbiota (Streptococcus, Fusobacterium, Veillonella and Haemophilus). Combined oral-gut features showed the most favorable exploratory test-set performance (XGBoost AUC 0.945; average precision 0.943).
CONCLUSIONS: PSCI was associated with coordinated oral and gut dysbiosis, characterized by loss of commensals, enrichment of opportunistic or Gram-negative taxa, and a stronger gut oralization signal reflected by reduced oral-gut dissimilarity and elevated OES. Tax4Fun2 suggested predicted functional potential related to lipopolysaccharide biosynthesis and tryptophan metabolism, while combined oral-gut features showed favorable exploratory internal discrimination of PSCI. These findings require validation in larger longitudinal multi-omics cohorts.
Additional Links: PMID-42327718
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@article {pmid42327718,
year = {2026},
author = {Zhang, X and Chen, F and Yang, J and Ma, J and Li, X and Wang, H and Li, Q and Zhao, Y and Xu, J},
title = {Oral and gut microbiota dysbiosis with strengthened oral-gut connectivity in post-stroke cognitive impairment.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1851811},
pmid = {42327718},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Dysbiosis/microbiology ; Female ; *Stroke/complications/microbiology ; Male ; *Cognitive Dysfunction/microbiology/etiology ; Cross-Sectional Studies ; RNA, Ribosomal, 16S/genetics ; Aged ; *Mouth/microbiology ; Feces/microbiology ; Bacteria/classification/genetics ; },
abstract = {BACKGROUND: Microbiome studies in post-stroke cognitive impairment (PSCI) have focused on the gut, while upstream oral dysbiosis and oral-gut axis signatures remain undercharacterized. We profiled paired oral and gut microbiota in PSCI to assess coordinated alterations and cross-site associations.
METHODS: This single-center cross-sectional study enrolled 133 post-stroke participants (64 PSCI). Paired tongue-coating and fecal samples underwent 16S rRNA gene sequencing. We compared α/β diversity, taxonomic composition, and predicted functional pathways at both sites, quantified within-individual oral-gut dissimilarity and the gut fraction of oral-gut shared microbiota, and adapted an oral enrichment score (OES) to index gut "oralization". Differential microbiota, predicted pathways, and MMSE/MoCA scores were integrated into a multi-layer association framework. Machine-learning models were built using oral features, gut features, and combined oral-gut features, with SHAP for interpretability.
RESULTS: PSCI showed reduced oral richness (ACE/Chao1) and reduced gut diversity/evenness (Shannon/Simpson), with significant β-diversity differences at both sites. Oral commensals (Leptotrichia, Neisseria) were depleted, whereas opportunistic taxa (Pseudomonas, Alloprevotella, Streptococcus) were enriched. In the gut, SCFA-associated microbiota (Coprococcus, Faecalibacterium, Ruminococcus) decreased, while Gram-negative potential pathogens (Enterobacter, Pseudomonas, Klebsiella) increased. Tax4Fun2-based inference suggested predicted gut functional alterations involving lipopolysaccharide biosynthesis potential and tryptophan metabolism-related pathways. Oral-gut metrics supported stronger oral-gut association in PSCI, including lower paired dissimilarity, a higher shared-genera fraction, and elevated OES (median 0.0368 vs 0.0142), mainly driven by oral-dominant microbiota (Streptococcus, Fusobacterium, Veillonella and Haemophilus). Combined oral-gut features showed the most favorable exploratory test-set performance (XGBoost AUC 0.945; average precision 0.943).
CONCLUSIONS: PSCI was associated with coordinated oral and gut dysbiosis, characterized by loss of commensals, enrichment of opportunistic or Gram-negative taxa, and a stronger gut oralization signal reflected by reduced oral-gut dissimilarity and elevated OES. Tax4Fun2 suggested predicted functional potential related to lipopolysaccharide biosynthesis and tryptophan metabolism, while combined oral-gut features showed favorable exploratory internal discrimination of PSCI. These findings require validation in larger longitudinal multi-omics cohorts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
*Dysbiosis/microbiology
Female
*Stroke/complications/microbiology
Male
*Cognitive Dysfunction/microbiology/etiology
Cross-Sectional Studies
RNA, Ribosomal, 16S/genetics
Aged
*Mouth/microbiology
Feces/microbiology
Bacteria/classification/genetics
RevDate: 2026-06-22
CmpDate: 2026-06-22
Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.
Frontiers in immunology, 17:1846280.
The presentation of mood disorders that involve agitation and anxiety in patients with cognitive loss represent significant challenges for the care of patients with Alzheimer's disease (AD). Additional concerns rest with the rising lifespan and aging of the global population with expectations that over the next two decades more than 50 percent of the elderly population will suffer from mental health disease and at least 30 million of these individuals will also succumb to cognitive loss with AD. Although current treatments for mood disorders and cognitive loss can have a multi-modal approach with behavioral therapy, cognitive training sessions, physical exercise, nutritional care, environmental changes, and disease modifying agents, these therapies are primarily symptomatic in nature that do not halt disease progression and possess risks for further nervous system insults. Given these consideration, novel work that addresses the shared underlying pathways for mood disorders and cognitive loss with autophagy and related mechanisms of programmed cell death, aging and cellular senescence, perivascular system dysfunction, inflammatory microglial cell dynamics, oxidative stress, metabolic pathways that involve diabetes mellitus and apolipoprotein E, the gut microbiota, glucagon-like peptide-1 receptor agonism, innovative diagnostic strategies, artificial intelligence, and machine learning can offer rewarding avenues for the innovative development of therapeutic strategies that address disease onset and progression of these disorders. These pathways that oversee mood disorders and cognitive are both critical and complex in their intimate relationships and warrant in-depth knowledge of the mechanisms that can influence biological outcome for clinical translation.
Additional Links: PMID-42327728
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@article {pmid42327728,
year = {2026},
author = {Maiese, K},
title = {Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1846280},
pmid = {42327728},
issn = {1664-3224},
mesh = {Humans ; *Alzheimer Disease/metabolism/therapy/psychology/etiology ; *Aging ; *Autophagy ; *Gastrointestinal Microbiome ; Animals ; *Artificial Intelligence ; },
abstract = {The presentation of mood disorders that involve agitation and anxiety in patients with cognitive loss represent significant challenges for the care of patients with Alzheimer's disease (AD). Additional concerns rest with the rising lifespan and aging of the global population with expectations that over the next two decades more than 50 percent of the elderly population will suffer from mental health disease and at least 30 million of these individuals will also succumb to cognitive loss with AD. Although current treatments for mood disorders and cognitive loss can have a multi-modal approach with behavioral therapy, cognitive training sessions, physical exercise, nutritional care, environmental changes, and disease modifying agents, these therapies are primarily symptomatic in nature that do not halt disease progression and possess risks for further nervous system insults. Given these consideration, novel work that addresses the shared underlying pathways for mood disorders and cognitive loss with autophagy and related mechanisms of programmed cell death, aging and cellular senescence, perivascular system dysfunction, inflammatory microglial cell dynamics, oxidative stress, metabolic pathways that involve diabetes mellitus and apolipoprotein E, the gut microbiota, glucagon-like peptide-1 receptor agonism, innovative diagnostic strategies, artificial intelligence, and machine learning can offer rewarding avenues for the innovative development of therapeutic strategies that address disease onset and progression of these disorders. These pathways that oversee mood disorders and cognitive are both critical and complex in their intimate relationships and warrant in-depth knowledge of the mechanisms that can influence biological outcome for clinical translation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Alzheimer Disease/metabolism/therapy/psychology/etiology
*Aging
*Autophagy
*Gastrointestinal Microbiome
Animals
*Artificial Intelligence
RevDate: 2026-06-22
CmpDate: 2026-06-22
The intratumoral microbiome: a review of the tumor microenvironment's fourth axis shaping anti-tumor immunity, cancer prognosis, and therapeutic response.
Frontiers in immunology, 17:1820477.
The tumor microenvironment (TME) is a well-documented, complex, and dynamic ecosystem traditionally considered among three major axes: 1) malignant cells, 2) stromal cells, and 3) infiltrating immune cells; all whose interactions have been assumed to shape tumor growth, progression, and therapeutic response. Specific TME profiles are strongly associated with cancer prognosis, especially those characterized by distinct immune cell populations. Within the TME, less-studied populations of various microorganisms constitute the intratumoral microbiome. While the systemic microbiome is well-established as a regulator of overall health, disease progression, and cancer prognosis, the role of microorganisms residing directly within tumors remains largely underexplored and often overlooked. As evidence on the intratumoral microbiome continues to emerge, it is increasingly apparent that, in addition to the previously characterized components of the TME, these tumor-resident microbes may significantly impact the TME through complex interactions, effectively constituting a fourth component that must be considered alongside malignant, immune, and stromal cells. We therefore propose a framework in which the TME is defined across four axes: malignant cells, stromal cells, infiltrating immune cells, and intratumoral microbes. Herein, we review the effects of intratumoral microbes on various immune cell types commonly studied within the TME, their effects on specific cancers, and subsequent therapeutic insights that arise from understanding the intratumoral microbiome.
Additional Links: PMID-42327767
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Citation:
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@article {pmid42327767,
year = {2026},
author = {Hunter, JGL and Roach, A and Nieves, L and Islas, A and Islas, A and DiPalma, M},
title = {The intratumoral microbiome: a review of the tumor microenvironment's fourth axis shaping anti-tumor immunity, cancer prognosis, and therapeutic response.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1820477},
pmid = {42327767},
issn = {1664-3224},
mesh = {Humans ; *Tumor Microenvironment/immunology ; *Microbiota/immunology ; Prognosis ; *Neoplasms/immunology/therapy/microbiology ; Animals ; },
abstract = {The tumor microenvironment (TME) is a well-documented, complex, and dynamic ecosystem traditionally considered among three major axes: 1) malignant cells, 2) stromal cells, and 3) infiltrating immune cells; all whose interactions have been assumed to shape tumor growth, progression, and therapeutic response. Specific TME profiles are strongly associated with cancer prognosis, especially those characterized by distinct immune cell populations. Within the TME, less-studied populations of various microorganisms constitute the intratumoral microbiome. While the systemic microbiome is well-established as a regulator of overall health, disease progression, and cancer prognosis, the role of microorganisms residing directly within tumors remains largely underexplored and often overlooked. As evidence on the intratumoral microbiome continues to emerge, it is increasingly apparent that, in addition to the previously characterized components of the TME, these tumor-resident microbes may significantly impact the TME through complex interactions, effectively constituting a fourth component that must be considered alongside malignant, immune, and stromal cells. We therefore propose a framework in which the TME is defined across four axes: malignant cells, stromal cells, infiltrating immune cells, and intratumoral microbes. Herein, we review the effects of intratumoral microbes on various immune cell types commonly studied within the TME, their effects on specific cancers, and subsequent therapeutic insights that arise from understanding the intratumoral microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Tumor Microenvironment/immunology
*Microbiota/immunology
Prognosis
*Neoplasms/immunology/therapy/microbiology
Animals
RevDate: 2026-06-22
CmpDate: 2026-06-22
The association between atopic dermatitis and rosacea: a comprehensive review from comorbidities to pathogenic mechanisms.
Frontiers in immunology, 17:1837198.
OBJECTIVE: Atopic dermatitis (AD) and rosacea have traditionally been regarded as two distinct inflammatory skin disorders with divergent pathophysiology. However, emerging evidence has progressively revealed unexpected convergences between these conditions in clinical manifestations, comorbidity profiles and pathogenic mechanisms-raising the question of whether the apparent mechanistic overlaps represent true pathophysiological convergence-sharing common upstream drivers-or merely parallel, non- specific innate immune responses triggered by entirely distinct microbial and genetic factors? This distinction carries profound implications for the design of shared versus disease-specific therapeutic strategies. this review aims not simply to enumerate similarities but to critically evaluate whether the observed convergences represent true mechanistic overlap, or parallel but independent responses.
METHODS: Literature search strategy: A comprehensive literature search was conducted in PubMed, Embase and Scopus, the Cochrane Library between April, 2016 and April, 2026. The search strategy combined controlled vocabulary and free-text terms, including " rosacea", " atopic dermatitis", " mast cells", " comorbidity", " microbiome", " innate immunity", " adaptive immunity", and " neurovascular". Reference lists of relevant articles were also manually screened to identify additional eligible studies.
Studies were included if they: (1) focused on atopic dermatitis and/or rosacea; (2) investigated relevant immunological mechanisms, comorbidities, or pathophysiological pathways; and (3) provided sufficient data to support qualitative synthesis. Both original research articles and high- quality reviews or meta-analyses were considered. Studies were excluded if they: (1) were duplicate publications; (2) lacked sufficient methodological detail or extractable data; or (3) were not directly relevant to the objectives of this review.
Study selection and data extraction were performed independently by two reviewers. Titles and abstracts were initially screened, followed by full-text assessment for eligibility. Any discrepancies were resolved through discussion, and when necessary, a third reviewer was consulted to reach consensus.
STUDY SELECTION PROCESS: A total of 5381records were identified through database searching, with an additional 83 records identified through manual reference screening. After removal of duplicates, 3185records remained for title and abstract screening, of which 2864 were excluded due to irrelevance. A total of 321 full-text articles were assessed for eligibility, and 216 were further excluded for the following reasons: lack of relevance (n =117), insufficient data (n =53), or low methodological quality/non-original articles (n = 46). Ultimately, 105 studies were included in the qualitative synthesis. The study selection process is summarized in a PRISMA-style flow diagram (Graphical Abstract, below). Given the narrative nature of this review, no formal risk-of-bias assessment was performed.
RESULTS: Critical appraisal of the evidence reveals that both diseases share an upstream innate immune activation platform' encompassing TLR2/TLR4 signaling, NLRP3 inflammasome activation, mast cell degranulation and neurovascular dysregulation via the CGRP/SP/VEGF/TRP axis. However, they diverge at the level of adaptive immune polarization: AD is dominated by Th2/ILC2 skewing with IgE sensitization and deficient antimicrobial peptide responses, while rosacea is characterized by Th 1/Th17 involvement with autonomous LL-37 overproduction as its primary amplification loop. Intriguingly, dupilumab-induced rosacea-like dermatitis suggests that these polarization states may not merely differ but actively compete, raising questions about the nature and limits of mechanistic overlap between the two conditions. This duality may challenge simplistic models of mechanistic overlap and has direct implications for differential clinical management. Future research should employ multi-omics approaches and prospective comorbidity cohorts to clarify causal pathways and translate mechanistic insights into optimized therapeutic strategies.
Additional Links: PMID-42327780
PubMed:
Citation:
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@article {pmid42327780,
year = {2026},
author = {Zeng, Y and Feng, Y},
title = {The association between atopic dermatitis and rosacea: a comprehensive review from comorbidities to pathogenic mechanisms.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1837198},
pmid = {42327780},
issn = {1664-3224},
mesh = {Humans ; *Rosacea/immunology/epidemiology ; *Dermatitis, Atopic/immunology/epidemiology ; Immunity, Innate ; Comorbidity ; Animals ; Skin/immunology ; Skin Microbiome ; Adaptive Immunity ; },
abstract = {OBJECTIVE: Atopic dermatitis (AD) and rosacea have traditionally been regarded as two distinct inflammatory skin disorders with divergent pathophysiology. However, emerging evidence has progressively revealed unexpected convergences between these conditions in clinical manifestations, comorbidity profiles and pathogenic mechanisms-raising the question of whether the apparent mechanistic overlaps represent true pathophysiological convergence-sharing common upstream drivers-or merely parallel, non- specific innate immune responses triggered by entirely distinct microbial and genetic factors? This distinction carries profound implications for the design of shared versus disease-specific therapeutic strategies. this review aims not simply to enumerate similarities but to critically evaluate whether the observed convergences represent true mechanistic overlap, or parallel but independent responses.
METHODS: Literature search strategy: A comprehensive literature search was conducted in PubMed, Embase and Scopus, the Cochrane Library between April, 2016 and April, 2026. The search strategy combined controlled vocabulary and free-text terms, including " rosacea", " atopic dermatitis", " mast cells", " comorbidity", " microbiome", " innate immunity", " adaptive immunity", and " neurovascular". Reference lists of relevant articles were also manually screened to identify additional eligible studies.
Studies were included if they: (1) focused on atopic dermatitis and/or rosacea; (2) investigated relevant immunological mechanisms, comorbidities, or pathophysiological pathways; and (3) provided sufficient data to support qualitative synthesis. Both original research articles and high- quality reviews or meta-analyses were considered. Studies were excluded if they: (1) were duplicate publications; (2) lacked sufficient methodological detail or extractable data; or (3) were not directly relevant to the objectives of this review.
Study selection and data extraction were performed independently by two reviewers. Titles and abstracts were initially screened, followed by full-text assessment for eligibility. Any discrepancies were resolved through discussion, and when necessary, a third reviewer was consulted to reach consensus.
STUDY SELECTION PROCESS: A total of 5381records were identified through database searching, with an additional 83 records identified through manual reference screening. After removal of duplicates, 3185records remained for title and abstract screening, of which 2864 were excluded due to irrelevance. A total of 321 full-text articles were assessed for eligibility, and 216 were further excluded for the following reasons: lack of relevance (n =117), insufficient data (n =53), or low methodological quality/non-original articles (n = 46). Ultimately, 105 studies were included in the qualitative synthesis. The study selection process is summarized in a PRISMA-style flow diagram (Graphical Abstract, below). Given the narrative nature of this review, no formal risk-of-bias assessment was performed.
RESULTS: Critical appraisal of the evidence reveals that both diseases share an upstream innate immune activation platform' encompassing TLR2/TLR4 signaling, NLRP3 inflammasome activation, mast cell degranulation and neurovascular dysregulation via the CGRP/SP/VEGF/TRP axis. However, they diverge at the level of adaptive immune polarization: AD is dominated by Th2/ILC2 skewing with IgE sensitization and deficient antimicrobial peptide responses, while rosacea is characterized by Th 1/Th17 involvement with autonomous LL-37 overproduction as its primary amplification loop. Intriguingly, dupilumab-induced rosacea-like dermatitis suggests that these polarization states may not merely differ but actively compete, raising questions about the nature and limits of mechanistic overlap between the two conditions. This duality may challenge simplistic models of mechanistic overlap and has direct implications for differential clinical management. Future research should employ multi-omics approaches and prospective comorbidity cohorts to clarify causal pathways and translate mechanistic insights into optimized therapeutic strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Rosacea/immunology/epidemiology
*Dermatitis, Atopic/immunology/epidemiology
Immunity, Innate
Comorbidity
Animals
Skin/immunology
Skin Microbiome
Adaptive Immunity
RevDate: 2026-06-22
CmpDate: 2026-06-22
Vaginal dysbiosis and inflammatory signatures in preterm labor: an integrated model for predicting preterm birth.
Frontiers in immunology, 17:1809046.
BACKGROUND: Preterm birth (PTB) is a major cause of neonatal morbidity and mortality, with vaginal microbiome dysbiosis and local immune responses implicated in its pathogenesis. However, the role of vaginal immune and extracellular matrix (ECM) remodeling factors in the progression from preterm labor (PTL) to PTB remains unclear. This study examines the associations between microbiome composition and immune and ECM-related protein composition in PTL patients to identify key factors and predictive models associated with the risk of PTB.
METHODS: This prospective study included 136 pregnant women classified into three groups: Control (Term Birth, TB), PTL-TB (Preterm Labor with Term Birth), and PTL-PTB (Preterm Labor with Preterm Birth). Vaginal microbiome composition was analyzed using 16S rRNA sequencing and categorized by dysbiosis status and community state types (CST). Cytokines (IL-1β, IFN-γ, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70) and ECM remodeling enzymes (MMP-1, MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MMP-13, IGFBP-1) were quantified in vaginal secretions using the Luminex[®] Assay multiplex kit. A multivariable logistic regression model was constructed to predict preterm birth, using significant microbiome, cytokine, and MMP variables, with performance evaluated by ROC analysis.
RESULTS: Dysbiosis and CST IV were more prevalent in the PTL-PTB group. IL-1β was highest in CST III, while MMP-9 and other MMPs were elevated in CST IV. CVF MMP-9 was consistently increased across PTL-PTB cases, dysbiosis, and CST IV. However, IGFBP-1, MMP-8, and MMP-13 were significantly different by clinical outcome but not correlated with microbiome composition. A logistic regression model incorporating non-Lactobacillus fraction, IGFBP-1, MMP-9, MMP-13, and TNF-α demonstrated excellent predictive performance (AUC = 0.910) for PTB.
CONCLUSIONS: Distinct microbial and immune profiles are associated with the progression from PTL to PTB. MMP-9 may serve as a key effector linking dysbiosis to extracellular matrix remodeling and PTB. Integrative biomarker models may support early risk stratification in women with PTL.
Additional Links: PMID-42327783
PubMed:
Citation:
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@article {pmid42327783,
year = {2026},
author = {Hong, S and Um, GS and Kang, BS and Kim, O and Lee, SU and Ko, HS and Nam, S and Lee, S and Park, IY and Shin, S},
title = {Vaginal dysbiosis and inflammatory signatures in preterm labor: an integrated model for predicting preterm birth.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1809046},
pmid = {42327783},
issn = {1664-3224},
mesh = {Humans ; Female ; *Dysbiosis/microbiology/immunology ; Pregnancy ; *Obstetric Labor, Premature/microbiology/immunology/metabolism ; *Vagina/microbiology/immunology ; *Premature Birth/microbiology/immunology/diagnosis/etiology ; Adult ; Cytokines/metabolism ; Microbiota ; Prospective Studies ; Biomarkers ; RNA, Ribosomal, 16S/genetics ; },
abstract = {BACKGROUND: Preterm birth (PTB) is a major cause of neonatal morbidity and mortality, with vaginal microbiome dysbiosis and local immune responses implicated in its pathogenesis. However, the role of vaginal immune and extracellular matrix (ECM) remodeling factors in the progression from preterm labor (PTL) to PTB remains unclear. This study examines the associations between microbiome composition and immune and ECM-related protein composition in PTL patients to identify key factors and predictive models associated with the risk of PTB.
METHODS: This prospective study included 136 pregnant women classified into three groups: Control (Term Birth, TB), PTL-TB (Preterm Labor with Term Birth), and PTL-PTB (Preterm Labor with Preterm Birth). Vaginal microbiome composition was analyzed using 16S rRNA sequencing and categorized by dysbiosis status and community state types (CST). Cytokines (IL-1β, IFN-γ, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p70) and ECM remodeling enzymes (MMP-1, MMP-2, MMP-3, MMP-7, MMP-8, MMP-9, MMP-12, MMP-13, IGFBP-1) were quantified in vaginal secretions using the Luminex[®] Assay multiplex kit. A multivariable logistic regression model was constructed to predict preterm birth, using significant microbiome, cytokine, and MMP variables, with performance evaluated by ROC analysis.
RESULTS: Dysbiosis and CST IV were more prevalent in the PTL-PTB group. IL-1β was highest in CST III, while MMP-9 and other MMPs were elevated in CST IV. CVF MMP-9 was consistently increased across PTL-PTB cases, dysbiosis, and CST IV. However, IGFBP-1, MMP-8, and MMP-13 were significantly different by clinical outcome but not correlated with microbiome composition. A logistic regression model incorporating non-Lactobacillus fraction, IGFBP-1, MMP-9, MMP-13, and TNF-α demonstrated excellent predictive performance (AUC = 0.910) for PTB.
CONCLUSIONS: Distinct microbial and immune profiles are associated with the progression from PTL to PTB. MMP-9 may serve as a key effector linking dysbiosis to extracellular matrix remodeling and PTB. Integrative biomarker models may support early risk stratification in women with PTL.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Female
*Dysbiosis/microbiology/immunology
Pregnancy
*Obstetric Labor, Premature/microbiology/immunology/metabolism
*Vagina/microbiology/immunology
*Premature Birth/microbiology/immunology/diagnosis/etiology
Adult
Cytokines/metabolism
Microbiota
Prospective Studies
Biomarkers
RNA, Ribosomal, 16S/genetics
RevDate: 2026-06-22
CmpDate: 2026-06-22
Staphylococcus aureus serine protease-like protein B elicits a type 1/type 2 immune response in atopic dermatitis patients.
Frontiers in immunology, 17:1798583.
INTRODUCTION: Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by type-2-mediated inflammation, along with the detection of type-1 and type-3 cytokines in lesional skin. The skin microbiome of lesional skin is dominated by the pathogen Staphylococcus aureus, which can aggravate the disease via pathogenicity factors. To elucidate the impact of the adaptive immune response on inflammation in AD, this study focused on staphylococcal serine-like proteases (Spl) of S. aureus, a family of secreted pathogenicity factors with the potential to induce type-2 responses.
METHODS: Specific serum IgE against Spl family members was quantified, and SplB-specific CD4[+] T cells were identified by surface expression of CD154 after in vitro stimulation with recombinant SplB. Immunodominant epitopes within the SplB primary structure were predicted to generate MHC multimers for staining, sorting, and cytokine analysis of SplB-specific T cells. TCRB sequencing was applied to identify SplB-specific T cells in AD skin lesions.
RESULTS: We observed significantly elevated levels of IgE antibodies specific for Spl family proteins in patients with AD compared to healthy controls. In vitro, recombinant SplB was sufficient to induce T cell activation and cytokine secretion in PBMCs from patients with AD and healthy controls. SplB-specific T helper cells, which were cell-sorted from patients' blood by MHC-II multimers, showed the capacity to produce IFN-γ and IL-13 ex vivo. Clonal propagation of specific T cells was confirmed by TCR sequencing, and SplB-specific TCR sequences were re-identified in autologous lesional skin biopsy material.
DISCUSSION: The presence of clonally propagated SplB-specific T cells in the skin of patients with AD strongly suggests an impact on inflammation. This type of cellular immune response, which is not exclusively polarized towards type 2, reflects the AD phenotype. This suggests that the adaptive immune response to S. aureus contributes to this phenotype.
Additional Links: PMID-42327791
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Citation:
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@article {pmid42327791,
year = {2026},
author = {Pospich, R and Abdurrahman, G and Honstein, T and Nordengrün, M and Traidl, S and Begemann, G and Kienlin, P and Werfel, T and Bröker, BM and Roesner, LM},
title = {Staphylococcus aureus serine protease-like protein B elicits a type 1/type 2 immune response in atopic dermatitis patients.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1798583},
pmid = {42327791},
issn = {1664-3224},
mesh = {Humans ; *Dermatitis, Atopic/immunology/microbiology ; *Staphylococcus aureus/immunology/enzymology ; Male ; Female ; Immunoglobulin E/blood/immunology ; *Bacterial Proteins/immunology ; *Serine Proteases/immunology ; Cytokines/metabolism ; Adult ; *Th2 Cells/immunology ; Lymphocyte Activation/immunology ; *Th1 Cells/immunology ; Skin/immunology ; Young Adult ; Middle Aged ; Adaptive Immunity ; },
abstract = {INTRODUCTION: Atopic dermatitis (AD), a common chronic inflammatory skin disease, is characterized by type-2-mediated inflammation, along with the detection of type-1 and type-3 cytokines in lesional skin. The skin microbiome of lesional skin is dominated by the pathogen Staphylococcus aureus, which can aggravate the disease via pathogenicity factors. To elucidate the impact of the adaptive immune response on inflammation in AD, this study focused on staphylococcal serine-like proteases (Spl) of S. aureus, a family of secreted pathogenicity factors with the potential to induce type-2 responses.
METHODS: Specific serum IgE against Spl family members was quantified, and SplB-specific CD4[+] T cells were identified by surface expression of CD154 after in vitro stimulation with recombinant SplB. Immunodominant epitopes within the SplB primary structure were predicted to generate MHC multimers for staining, sorting, and cytokine analysis of SplB-specific T cells. TCRB sequencing was applied to identify SplB-specific T cells in AD skin lesions.
RESULTS: We observed significantly elevated levels of IgE antibodies specific for Spl family proteins in patients with AD compared to healthy controls. In vitro, recombinant SplB was sufficient to induce T cell activation and cytokine secretion in PBMCs from patients with AD and healthy controls. SplB-specific T helper cells, which were cell-sorted from patients' blood by MHC-II multimers, showed the capacity to produce IFN-γ and IL-13 ex vivo. Clonal propagation of specific T cells was confirmed by TCR sequencing, and SplB-specific TCR sequences were re-identified in autologous lesional skin biopsy material.
DISCUSSION: The presence of clonally propagated SplB-specific T cells in the skin of patients with AD strongly suggests an impact on inflammation. This type of cellular immune response, which is not exclusively polarized towards type 2, reflects the AD phenotype. This suggests that the adaptive immune response to S. aureus contributes to this phenotype.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dermatitis, Atopic/immunology/microbiology
*Staphylococcus aureus/immunology/enzymology
Male
Female
Immunoglobulin E/blood/immunology
*Bacterial Proteins/immunology
*Serine Proteases/immunology
Cytokines/metabolism
Adult
*Th2 Cells/immunology
Lymphocyte Activation/immunology
*Th1 Cells/immunology
Skin/immunology
Young Adult
Middle Aged
Adaptive Immunity
RevDate: 2026-06-22
CmpDate: 2026-06-22
Non-invasive detection of pediatric atopic dermatitis based on fecal microbiota and metabolite profiles: a diagnostic approach.
Frontiers in immunology, 17:1836716.
BACKGROUND: Atopic dermatitis (AD) is a common chronic skin inflammation, which affects 15-20% of children worldwide. Gut microbiota and its metabolites are crucial modulators of the "gut-skin axis" in atopic dermatogenesis. However, systematic investigations integrating microbiome and metabolome profiling in mild-to-moderate pediatric AD remain limited.
OBJECTIVES: To characterize gut microbiota and metabolic profiles in children with mild-to-moderate AD versus healthy controls, and to identify potential biomarkers and mechanistic pathways involved in disease pathogenesis.
METHODS: This single-center case-control study investigated 53 children diagnosed with AD and 16 healthy participants, and collected their fecal samples for microbial and metabonomic analysis.
RESULTS: Mild-moderate pediatric AD patients exhibited significantly increased gut microbial richness and distinct β-diversity compared to controls (PERMANOVA, R²=0.025, P = 0.017). Bacteroidota was enriched while Actinomycetota was depleted in AD patients (P < 0.05). At genus level, Parabacteroides and Klebsiella increased, whereas Bifidobacterium decreased in AD. Species-level analysis revealed enrichment of bacteroides_plebeius, bacteroides_thetaiotaomicron, bacteroides_xylanisolvens, and parabacteroides_merdae in AD. A combined biomarker panel (Bacteroidota, Parabacteroides, and four key species) demonstrated promising exploratory diagnostic potential (AUC = 0.941, accuracy 84.6%), although these results require external validation in larger independent cohorts. Spearman analysis showed correlations between gut microbiome and clinical severity indicators. Thermodesulfobacteriota, Actinomycetota, Bifidobacterium, and specific ruminococcus strains positively correlated with the severity of AD. Metabolomics identified 68 differentially accumulated metabolites, primarily involved in lipid metabolism and nucleotide metabolism. Bacteroides species showed significant positive correlations with isovaleric acid levels in microbiota-metabolite analyses.
CONCLUSION: Mild-to-moderate pediatric AD is characterized by distinct gut microbiota dysbiosis and metabolic alterations involving lipid metabolism. Cross-sectionally identified microbial features show exploratory associations with AD status, but causal inference is not possible. These hypothesis-generating findings support further investigation of the gut-skin axis in AD development and provide a rationale for future interventional studies targeting the microbiome and metabolome.
Additional Links: PMID-42327796
PubMed:
Citation:
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@article {pmid42327796,
year = {2026},
author = {Peng, J and Li, Z and Wu, W and Sun, N and Yang, X and Liu, Q and Li, H},
title = {Non-invasive detection of pediatric atopic dermatitis based on fecal microbiota and metabolite profiles: a diagnostic approach.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1836716},
pmid = {42327796},
issn = {1664-3224},
mesh = {Humans ; *Dermatitis, Atopic/diagnosis/microbiology/metabolism ; Female ; *Feces/microbiology ; Male ; *Metabolome ; Child ; Case-Control Studies ; Biomarkers ; *Gastrointestinal Microbiome ; Child, Preschool ; Metabolomics/methods ; Bacteria/classification/genetics ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) is a common chronic skin inflammation, which affects 15-20% of children worldwide. Gut microbiota and its metabolites are crucial modulators of the "gut-skin axis" in atopic dermatogenesis. However, systematic investigations integrating microbiome and metabolome profiling in mild-to-moderate pediatric AD remain limited.
OBJECTIVES: To characterize gut microbiota and metabolic profiles in children with mild-to-moderate AD versus healthy controls, and to identify potential biomarkers and mechanistic pathways involved in disease pathogenesis.
METHODS: This single-center case-control study investigated 53 children diagnosed with AD and 16 healthy participants, and collected their fecal samples for microbial and metabonomic analysis.
RESULTS: Mild-moderate pediatric AD patients exhibited significantly increased gut microbial richness and distinct β-diversity compared to controls (PERMANOVA, R²=0.025, P = 0.017). Bacteroidota was enriched while Actinomycetota was depleted in AD patients (P < 0.05). At genus level, Parabacteroides and Klebsiella increased, whereas Bifidobacterium decreased in AD. Species-level analysis revealed enrichment of bacteroides_plebeius, bacteroides_thetaiotaomicron, bacteroides_xylanisolvens, and parabacteroides_merdae in AD. A combined biomarker panel (Bacteroidota, Parabacteroides, and four key species) demonstrated promising exploratory diagnostic potential (AUC = 0.941, accuracy 84.6%), although these results require external validation in larger independent cohorts. Spearman analysis showed correlations between gut microbiome and clinical severity indicators. Thermodesulfobacteriota, Actinomycetota, Bifidobacterium, and specific ruminococcus strains positively correlated with the severity of AD. Metabolomics identified 68 differentially accumulated metabolites, primarily involved in lipid metabolism and nucleotide metabolism. Bacteroides species showed significant positive correlations with isovaleric acid levels in microbiota-metabolite analyses.
CONCLUSION: Mild-to-moderate pediatric AD is characterized by distinct gut microbiota dysbiosis and metabolic alterations involving lipid metabolism. Cross-sectionally identified microbial features show exploratory associations with AD status, but causal inference is not possible. These hypothesis-generating findings support further investigation of the gut-skin axis in AD development and provide a rationale for future interventional studies targeting the microbiome and metabolome.},
}
MeSH Terms:
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Humans
*Dermatitis, Atopic/diagnosis/microbiology/metabolism
Female
*Feces/microbiology
Male
*Metabolome
Child
Case-Control Studies
Biomarkers
*Gastrointestinal Microbiome
Child, Preschool
Metabolomics/methods
Bacteria/classification/genetics
RevDate: 2026-06-22
CmpDate: 2026-06-22
ZipStrain Enables Rapid and Precise Strain-Resolved Metagenomics.
bioRxiv : the preprint server for biology.
Strain-resolved metagenomics characterizes microbial communities at nucleotide-level resolution, enabling researchers to differentiate identical from closely related organisms and characterize population structure and gene content variation. Here we introduce ZipStrain, a program that performs highly accurate strain-resolved metagenomics over 500× faster than available methods while offering superior RAM management. Applied to a dataset of 2,754 samples spanning human populations, we identify a strain-sharing gradient across social relationships, reveal striking variation in clonal structure across bacteria and bacteriophage, and pinpoint genes whose nucleotide identity deviates from genome-wide expectations. ZipStrain is distributed as an open-source Python package and accompanying Nextflow pipeline at https://github.com/OlmLab/ZipStrain.
Additional Links: PMID-42239166
PubMed:
Citation:
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@article {pmid42239166,
year = {2026},
author = {Ghadermazi, P and Emerson, JB and Olm, MR},
title = {ZipStrain Enables Rapid and Precise Strain-Resolved Metagenomics.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {42239166},
issn = {2692-8205},
abstract = {Strain-resolved metagenomics characterizes microbial communities at nucleotide-level resolution, enabling researchers to differentiate identical from closely related organisms and characterize population structure and gene content variation. Here we introduce ZipStrain, a program that performs highly accurate strain-resolved metagenomics over 500× faster than available methods while offering superior RAM management. Applied to a dataset of 2,754 samples spanning human populations, we identify a strain-sharing gradient across social relationships, reveal striking variation in clonal structure across bacteria and bacteriophage, and pinpoint genes whose nucleotide identity deviates from genome-wide expectations. ZipStrain is distributed as an open-source Python package and accompanying Nextflow pipeline at https://github.com/OlmLab/ZipStrain.},
}
RevDate: 2026-06-19
Gut dysbiosis associated with neonatal respiratory distress syndrome and biological plausibility of disease-specific probiotic intervention: a translational study.
Journal of translational medicine pii:10.1186/s12967-026-08462-x [Epub ahead of print].
BACKGROUND: Neonatal respiratory distress syndrome (RDS) is among the most prevalent morbidities in late preterm and term infants. Although the gut-lung axis has been implicated in neonatal respiratory disease, the relationship between RDS and early gut microbiome composition remains poorly characterized. This study aimed to characterize gut microbiome alterations associated with RDS and surfactant replacement therapy (SRT), and to evaluate the biological plausibility of a disease-specific probiotic intervention.
METHODS: Two complementary cohorts were prospectively enrolled. In the clinical observational cohort (n = 45), fecal samples collected within 48 h of birth were analyzed by Nanopore 16S rRNA sequencing across three groups: infants without RDS (control group, n = 25), infants with RDS who did not receive SRT (RDS(S-) group, n = 7), and infants with RDS who received SRT (RDS(S+) group, n = 13). In the probiotic discovery cohort (n = 40), gut microbiota of infants without RDS (CON group, n = 17) and infants with RDS (RDS group, n = 23) were characterized by metagenomic sequencing and culturomics. Candidate probiotic strains were evaluated in a fermenter for intestinal microbiota model (FIMM) and a fecal microbiota transplantation (FMT) mouse model.
RESULTS: The RDS(S-) group exhibited depletion of beneficial taxa including Bifidobacterium and Lacticaseibacillus and enrichment of opportunistic pathogens including Enterococcus and Staphylococcus. Following SRT, gut microbial profiles partially shifted toward those of the control group. Limosilactobacillus fermentum SLAM_LAF05 and Bifidobacterium longum SLAM_BIL02 were identified as CON-enriched candidate probiotic strains through direct microbiome comparison and selected based on superior acid and bile tolerance and adhesion capacity. In the FIMM model, probiotic supplementation increased microbial diversity and suppressed opportunistic pathogens. In the FMT mouse model, probiotic supplementation was associated with upregulation of ZO-1, MUC2, and Reg3g, reduction of fecal calprotectin, and restoration of serum IgG levels.
CONCLUSIONS: This study provides an early translational characterization of RDS-associated gut dysbiosis and its partial resolution following SRT, and establishes proof-of-concept for a disease-specific probiotic approach. These findings offer a new perspective on the interplay between gut microbial dynamics and the early postnatal respiratory course, and provide a basis for future investigations into microbiota-targeted strategies in neonates with RDS.
Additional Links: PMID-42316154
Publisher:
PubMed:
Citation:
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@article {pmid42316154,
year = {2026},
author = {Seo, E and Kim, SH and Kwak, MJ and Hwang, JK and Mustafa, G and Chang, YS and Hoh, JK and Jeon, BH and Park, HK and Kim, Y},
title = {Gut dysbiosis associated with neonatal respiratory distress syndrome and biological plausibility of disease-specific probiotic intervention: a translational study.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08462-x},
pmid = {42316154},
issn = {1479-5876},
support = {202400000002957//College of Medicine, Hanyang University/ ; RS-2023-00255939//Korea Institute of Energy Technology Evaluation and Planning/ ; NSIT; RS-2025-16068814//National Research Foundation of Korea/ ; },
abstract = {BACKGROUND: Neonatal respiratory distress syndrome (RDS) is among the most prevalent morbidities in late preterm and term infants. Although the gut-lung axis has been implicated in neonatal respiratory disease, the relationship between RDS and early gut microbiome composition remains poorly characterized. This study aimed to characterize gut microbiome alterations associated with RDS and surfactant replacement therapy (SRT), and to evaluate the biological plausibility of a disease-specific probiotic intervention.
METHODS: Two complementary cohorts were prospectively enrolled. In the clinical observational cohort (n = 45), fecal samples collected within 48 h of birth were analyzed by Nanopore 16S rRNA sequencing across three groups: infants without RDS (control group, n = 25), infants with RDS who did not receive SRT (RDS(S-) group, n = 7), and infants with RDS who received SRT (RDS(S+) group, n = 13). In the probiotic discovery cohort (n = 40), gut microbiota of infants without RDS (CON group, n = 17) and infants with RDS (RDS group, n = 23) were characterized by metagenomic sequencing and culturomics. Candidate probiotic strains were evaluated in a fermenter for intestinal microbiota model (FIMM) and a fecal microbiota transplantation (FMT) mouse model.
RESULTS: The RDS(S-) group exhibited depletion of beneficial taxa including Bifidobacterium and Lacticaseibacillus and enrichment of opportunistic pathogens including Enterococcus and Staphylococcus. Following SRT, gut microbial profiles partially shifted toward those of the control group. Limosilactobacillus fermentum SLAM_LAF05 and Bifidobacterium longum SLAM_BIL02 were identified as CON-enriched candidate probiotic strains through direct microbiome comparison and selected based on superior acid and bile tolerance and adhesion capacity. In the FIMM model, probiotic supplementation increased microbial diversity and suppressed opportunistic pathogens. In the FMT mouse model, probiotic supplementation was associated with upregulation of ZO-1, MUC2, and Reg3g, reduction of fecal calprotectin, and restoration of serum IgG levels.
CONCLUSIONS: This study provides an early translational characterization of RDS-associated gut dysbiosis and its partial resolution following SRT, and establishes proof-of-concept for a disease-specific probiotic approach. These findings offer a new perspective on the interplay between gut microbial dynamics and the early postnatal respiratory course, and provide a basis for future investigations into microbiota-targeted strategies in neonates with RDS.},
}
RevDate: 2026-06-19
Human microbiome alterations in Epstein-Barr Virus infection: a systematic review.
Gut pathogens pii:10.1186/s13099-026-00854-0 [Epub ahead of print].
Epstein-Barr virus (EBV) is associated with several malignancies and immune-mediated conditions, but its relationship with human microbial communities remains incompletely understood. We systematically searched PubMed, Embase, and Scopus for human studies evaluating EBV-associated alterations in the microbiome. Because of substantial clinical and methodological heterogeneity, findings were synthesized narratively, and study quality was assessed using the ROBINS-I tool. Nine observational studies published between 2017 and 2025 were included, covering the oral cavity, nasopharynx, gut, gastric tissue, and subgingival plaque. EBV positivity or EBV-related clinical status was associated with niche-specific microbial shifts, including altered gut bacterial profiles, distinct microbial patterns in EBV-associated gastric cancer tissue, and enrichment of oral-associated pathobionts in nasopharyngeal carcinoma compartments. Alpha- and beta-diversity findings were inconsistent across studies. Overall, the evidence suggests context-dependent alterations in the microbiome in EBV-positive or EBV-related disease settings. However, these findings should be interpreted as EBV-associated rather than EBV-specific, particularly when EBV status overlaps with malignancy. The small observational evidence base, heterogeneous EBV-status definitions, methodological variability, and residual confounding limit causal inference. Larger longitudinal and standardized multi-omic studies are needed to clarify directionality, mechanisms, and clinical relevance.
Additional Links: PMID-42316315
Publisher:
PubMed:
Citation:
show bibtex listing
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@article {pmid42316315,
year = {2026},
author = {Zebardast, A and Javadi, K},
title = {Human microbiome alterations in Epstein-Barr Virus infection: a systematic review.},
journal = {Gut pathogens},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13099-026-00854-0},
pmid = {42316315},
issn = {1757-4749},
support = {724137379//Babol University of Medical Sciences/ ; },
abstract = {Epstein-Barr virus (EBV) is associated with several malignancies and immune-mediated conditions, but its relationship with human microbial communities remains incompletely understood. We systematically searched PubMed, Embase, and Scopus for human studies evaluating EBV-associated alterations in the microbiome. Because of substantial clinical and methodological heterogeneity, findings were synthesized narratively, and study quality was assessed using the ROBINS-I tool. Nine observational studies published between 2017 and 2025 were included, covering the oral cavity, nasopharynx, gut, gastric tissue, and subgingival plaque. EBV positivity or EBV-related clinical status was associated with niche-specific microbial shifts, including altered gut bacterial profiles, distinct microbial patterns in EBV-associated gastric cancer tissue, and enrichment of oral-associated pathobionts in nasopharyngeal carcinoma compartments. Alpha- and beta-diversity findings were inconsistent across studies. Overall, the evidence suggests context-dependent alterations in the microbiome in EBV-positive or EBV-related disease settings. However, these findings should be interpreted as EBV-associated rather than EBV-specific, particularly when EBV status overlaps with malignancy. The small observational evidence base, heterogeneous EBV-status definitions, methodological variability, and residual confounding limit causal inference. Larger longitudinal and standardized multi-omic studies are needed to clarify directionality, mechanisms, and clinical relevance.},
}
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