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ESP: PubMed Auto Bibliography 23 Apr 2026 at 01:54 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: 2026-04-21
Hypnotic and sleep-promoting effects of Limosilactobacillus reuteri LM1063 on pentobarbital-induced sleep and electroencephalogram analysis in mice.
Scientific reports, 16(1):.
UNLABELLED: Sleep disturbances are an increasing health concern, and limitations associated with long-term use of conventional hypnotics have prompted interest in alternative approaches that support sleep health. Growing evidence suggests that the gut–brain axis contributes to sleep regulation; however, the effects of probiotics on objective sleep parameters and their underlying mechanisms remain incompletely understood and may vary across probiotic strains. The present study investigated the sleep–modulating effects of a selected probiotic strain, Limosilactobacillus reuteri LM1063 (LM1063), using murine models. Sleep latency and duration were assessed using a pentobarbital-induced sleep test, and sleep architecture was evaluated by electroencephalogram (EEG) recordings, including rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. To explore potential mechanisms, neurochemical analyses focusing on key neurotransmitters, including gamma-aminobutyric acid (GABA) and serotonin, were conducted. Administration of LM1063 significantly shortened sleep latency and prolonged sleep duration in mice. EEG analysis revealed shifts in overall sleep architecture toward a sleep-favorable state without disruption of normal sleep organization. These sleep-related changes were accompanied by modulation of GABAergic and serotonergic neurochemical pathways. In conclusion, LM1063 exerts strain-specific sleep-modulating effects through neurochemical mechanisms associated with the gut–brain axis. By integrating behavioral sleep assessment, electrophysiological analysis, and neurochemical profiling, this study provides mechanistic insight supporting the potential translational application of microbiome-targeted approaches for promoting sleep health.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-42833-0.
Additional Links: PMID-41803210
PubMed:
Citation:
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@article {pmid41803210,
year = {2026},
author = {Kim, MG and Seo, E and Eor, JY and Kang, A and Kim, TR and Sohn, M and Kim, Y},
title = {Hypnotic and sleep-promoting effects of Limosilactobacillus reuteri LM1063 on pentobarbital-induced sleep and electroencephalogram analysis in mice.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41803210},
issn = {2045-2322},
support = {RS-2025-16068814//National Research Foundation of Korea/ ; },
abstract = {UNLABELLED: Sleep disturbances are an increasing health concern, and limitations associated with long-term use of conventional hypnotics have prompted interest in alternative approaches that support sleep health. Growing evidence suggests that the gut–brain axis contributes to sleep regulation; however, the effects of probiotics on objective sleep parameters and their underlying mechanisms remain incompletely understood and may vary across probiotic strains. The present study investigated the sleep–modulating effects of a selected probiotic strain, Limosilactobacillus reuteri LM1063 (LM1063), using murine models. Sleep latency and duration were assessed using a pentobarbital-induced sleep test, and sleep architecture was evaluated by electroencephalogram (EEG) recordings, including rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. To explore potential mechanisms, neurochemical analyses focusing on key neurotransmitters, including gamma-aminobutyric acid (GABA) and serotonin, were conducted. Administration of LM1063 significantly shortened sleep latency and prolonged sleep duration in mice. EEG analysis revealed shifts in overall sleep architecture toward a sleep-favorable state without disruption of normal sleep organization. These sleep-related changes were accompanied by modulation of GABAergic and serotonergic neurochemical pathways. In conclusion, LM1063 exerts strain-specific sleep-modulating effects through neurochemical mechanisms associated with the gut–brain axis. By integrating behavioral sleep assessment, electrophysiological analysis, and neurochemical profiling, this study provides mechanistic insight supporting the potential translational application of microbiome-targeted approaches for promoting sleep health.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-42833-0.},
}
RevDate: 2026-04-20
Porphyromonas gingivalis produces a functional HemH ferrochelatase important for its survival in a heme-limited environment.
Scientific reports, 16(1):.
UNLABELLED: Porphyromonas gingivalis, the keystone pathogen responsible for dysbiosis in the oral microbiome, the development of periodontal diseases, and the contribution to systemic comorbidities, is a heme auxotroph. It encodes only four enzymes in the heme biosynthesis pathway (HemD, HemN, HemG, and HemH). Comparative genomic analyses demonstrated that, while many Bacteroidota members have lost most of the canonical heme biosynthetic enzymes, Porphyromonas species uniquely retained a ferrochelatase (HemH) homolog. This study aimed to functionally characterize the P. gingivalis HemH protein to prove its hypothesized role in heme formation. HemH can bind heme and PPIX and insert iron or manganese ions into the PPIX ring. The deletion of the hemH gene triggers a heme-starvation response characterized by transcriptional activation of heme uptake systems and virulence-associated genes, coupled with repression of transport and surface proteins preferentially expressed in heme-rich conditions. Therefore, it is proposed that HemH may play a role in maintaining proper heme homeostasis. In a heme-limited environment, P. gingivalis may use intracellular iron and PPIX reserves to synthesize heme by HemH, thereby contributing to heme supply.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-41999-x.
Additional Links: PMID-41807505
PubMed:
Citation:
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@article {pmid41807505,
year = {2026},
author = {Śmiga, M and Roszkiewicz, E and Wojtal, N and Olczak, T},
title = {Porphyromonas gingivalis produces a functional HemH ferrochelatase important for its survival in a heme-limited environment.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41807505},
issn = {2045-2322},
support = {2023/51/D/NZ6/00324//Narodowe Centrum Nauki/ ; },
abstract = {UNLABELLED: Porphyromonas gingivalis, the keystone pathogen responsible for dysbiosis in the oral microbiome, the development of periodontal diseases, and the contribution to systemic comorbidities, is a heme auxotroph. It encodes only four enzymes in the heme biosynthesis pathway (HemD, HemN, HemG, and HemH). Comparative genomic analyses demonstrated that, while many Bacteroidota members have lost most of the canonical heme biosynthetic enzymes, Porphyromonas species uniquely retained a ferrochelatase (HemH) homolog. This study aimed to functionally characterize the P. gingivalis HemH protein to prove its hypothesized role in heme formation. HemH can bind heme and PPIX and insert iron or manganese ions into the PPIX ring. The deletion of the hemH gene triggers a heme-starvation response characterized by transcriptional activation of heme uptake systems and virulence-associated genes, coupled with repression of transport and surface proteins preferentially expressed in heme-rich conditions. Therefore, it is proposed that HemH may play a role in maintaining proper heme homeostasis. In a heme-limited environment, P. gingivalis may use intracellular iron and PPIX reserves to synthesize heme by HemH, thereby contributing to heme supply.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-41999-x.},
}
RevDate: 2026-04-21
Akkermansia muciniphila confers renal protection in chronic kidney disease: a multi-omics mechanistic investigation.
BMC microbiology, 26(1):.
BACKGROUND: Akkermansia muciniphila (A. muciniphila) improved serum metabolism and renal fibrosis in the mouse model of chronic kidney disease (CKD) via the gut-kidney axis, slowing renal function decline. However, the biological components and underlying metabolic pathways remain unclear. Using a CKD mouse model, we aimed to identify the biological constituents of A. muciniphila that drive its regulatory effects in renal injury. Integrated microbiome and metabolomics analyses further elucidated the metabolic mechanisms of renoprotection, providing a theoretical foundation for the development of evidence-based clinical interventions.
METHODS: A CKD mouse model was established using 5/6 nephrectomy, with sham-operated mice (n = 7) serving as controls. Twenty-eight CKD mice were randomly assigned to four groups and treated with PBS, A. muciniphila, pasteurised A. muciniphila, or A. muciniphila combined with vancomycin by gavage. Serum and kidney tissues were collected to assess renal function, and histopathology was performed to identify the key biological components of A. muciniphila. Faecal samples were subjected to integrated microbiome and metabolomic analyses to identify the metabolic pathways involved in renoprotection. Behavioural experiments were performed to observe the effect of A. muciniphila on the behaviour of CKD mice. Single-factor analysis of variance and post-hoc tests were used for intergroup comparisons.
RESULTS: Serum analysis showed that the levels of serum creatinine, urea nitrogen and cystatin C in mice treated with A. muciniphila combined with vancomycin were significantly decreased. Reverse-transcription polymerase chain reaction showed that the renal injury marker Kim-1 was significantly decreased after A. muciniphila intervention. The levels of the renal injury (Ngal) and fibrosis (Col1a1, TIMP-1 and Fibronectin) markers showed a downward trend. 16 S rRNA analysis revealed that, following A. muciniphila intervention, the health index of the intestinal flora in CKD mice was significantly increased; however, the abundances of Turicibacter, Dubosiella and norank_f_UCG-010 were decreased. Metabolomic analysis revealed a strong correlation between A. muciniphila and the tryptophan metabolic pathway. Behavioural experiments showed that the exercise activity and anxiety-like behaviour of CKD mice were significantly improved after intervention with A. muciniphila, and the effect of A. muciniphila combined with vancomycin was better than that of A. muciniphila or pasteurised A. muciniphila alone.
CONCLUSION: Our findings demonstrate that A. muciniphila combined with vancomycin intervention ameliorates kidney injury, body dysfunction, and anxiety-like behaviour, while delaying disease progression in CKD mice. These effects suggest that bioactive substances secreted by A. muciniphila play a key regulatory role and are closely related to tryptophan metabolism in the intestine. In addition, our results indicate that dysbiosis of the gut microbiota in CKD mice suppresses the regulatory potential of A. muciniphila. This study lays an experimental foundation for future biological mechanism research.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04868-1.
Additional Links: PMID-41820827
PubMed:
Citation:
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@article {pmid41820827,
year = {2026},
author = {Ban, Y and Zhang, H and Xu, Y and Chen, F and Wei, Q and Wen, X and Yin, L and Dong, Z and Zhou, Q and Ge, W},
title = {Akkermansia muciniphila confers renal protection in chronic kidney disease: a multi-omics mechanistic investigation.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {},
pmid = {41820827},
issn = {1471-2180},
support = {202303//Lianyungang Health Science and Technology Project-202303 in Lianyungang City/ ; JOUMIRF010//Research Fund Project, College of Marine Pharmaceutical Industry, Jiangsu Ocean University/ ; },
abstract = {BACKGROUND: Akkermansia muciniphila (A. muciniphila) improved serum metabolism and renal fibrosis in the mouse model of chronic kidney disease (CKD) via the gut-kidney axis, slowing renal function decline. However, the biological components and underlying metabolic pathways remain unclear. Using a CKD mouse model, we aimed to identify the biological constituents of A. muciniphila that drive its regulatory effects in renal injury. Integrated microbiome and metabolomics analyses further elucidated the metabolic mechanisms of renoprotection, providing a theoretical foundation for the development of evidence-based clinical interventions.
METHODS: A CKD mouse model was established using 5/6 nephrectomy, with sham-operated mice (n = 7) serving as controls. Twenty-eight CKD mice were randomly assigned to four groups and treated with PBS, A. muciniphila, pasteurised A. muciniphila, or A. muciniphila combined with vancomycin by gavage. Serum and kidney tissues were collected to assess renal function, and histopathology was performed to identify the key biological components of A. muciniphila. Faecal samples were subjected to integrated microbiome and metabolomic analyses to identify the metabolic pathways involved in renoprotection. Behavioural experiments were performed to observe the effect of A. muciniphila on the behaviour of CKD mice. Single-factor analysis of variance and post-hoc tests were used for intergroup comparisons.
RESULTS: Serum analysis showed that the levels of serum creatinine, urea nitrogen and cystatin C in mice treated with A. muciniphila combined with vancomycin were significantly decreased. Reverse-transcription polymerase chain reaction showed that the renal injury marker Kim-1 was significantly decreased after A. muciniphila intervention. The levels of the renal injury (Ngal) and fibrosis (Col1a1, TIMP-1 and Fibronectin) markers showed a downward trend. 16 S rRNA analysis revealed that, following A. muciniphila intervention, the health index of the intestinal flora in CKD mice was significantly increased; however, the abundances of Turicibacter, Dubosiella and norank_f_UCG-010 were decreased. Metabolomic analysis revealed a strong correlation between A. muciniphila and the tryptophan metabolic pathway. Behavioural experiments showed that the exercise activity and anxiety-like behaviour of CKD mice were significantly improved after intervention with A. muciniphila, and the effect of A. muciniphila combined with vancomycin was better than that of A. muciniphila or pasteurised A. muciniphila alone.
CONCLUSION: Our findings demonstrate that A. muciniphila combined with vancomycin intervention ameliorates kidney injury, body dysfunction, and anxiety-like behaviour, while delaying disease progression in CKD mice. These effects suggest that bioactive substances secreted by A. muciniphila play a key regulatory role and are closely related to tryptophan metabolism in the intestine. In addition, our results indicate that dysbiosis of the gut microbiota in CKD mice suppresses the regulatory potential of A. muciniphila. This study lays an experimental foundation for future biological mechanism research.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-026-04868-1.},
}
RevDate: 2026-04-21
A novel obesity index reveals obesity-associated microbiota changes after weight loss intervention in a Spanish population.
Nutrition journal, 25(1):.
BACKGROUND & OBJECTIVES: Gut microbiota specific taxa influencing a higher or lower risk for developing obesity and related metabolic parameters remain unclear. Here, we aimed to identify gut microbiome fingerprints associated with obesity using an integrated obesity index (OBIndex), and to evaluate how these profiles change after a hypocaloric nutritional intervention with two different diets.
SUBJECTS & METHODS: 295 Spanish adult volunteers participating in the Obekit study were classified into LOW or HIGH degree of obesity according to a novel obesity index (OBIndex), based on the combination of three parameters: body mass index (BMI), fat mass (%), and waist circumference (WC). Differential abundant taxa between the two groups were investigated, at baseline together with the changes in their abundance after a weight-loss intervention with two different hypocaloric diets (Moderately high protein (MHP) and low fat (LF)).
RESULTS: The classification of participants using the OBIndex effectively differentiated obesity status, overcoming the inherent limitations of BMI, WC, and fat mass when considered individually. MHP diet was associated with an improvement in obesity status in women, while LF diet showed better outcomes in men. In relation to these improvements, changes in gut microbiota were observed. We found that Mediterraneibacter levels decreased only in men who experienced a significant improvement in their obesity status. Additionally, Agathobacter levels in participants who improved their physiological condition were reduced to match those of individuals who already exhibited a healthier status at baseline. Alongside these findings, we identified two poorly studied genera, Pseudobutyricicoccus and Intestinimonas, which were associated with a healthier profile at baseline and increased in abundance following the nutritional intervention.
CONCLUSIONS: Our OBIndex helped to achieve a more accurate separation of our volunteers regarding their obesity status and, thus, identifying four obesity strong related bacteria. Particularly, Mediterraneibacter and Agathobacter were related to a worse obesity status whereas Pseudobutyricicoccus and Intestinimonas showed a negative association with obesity status suggesting a potential protective or anti-obesity role.
TRIAL REGISTRATION: The study protocol was approved by the ethical committee at the University of Navarra (Registration No. IR.MUI.RESEARCH.REC.1401.370) and registered online at clinicaltrials.gov (identifier NCT02737267).
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12937-026-01313-x.
Additional Links: PMID-41827016
PubMed:
Citation:
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@article {pmid41827016,
year = {2026},
author = {Alonso-Allende, J and Riezu-Boj, JI and Hualde, AR and Milagro, FI and Aranaz, P},
title = {A novel obesity index reveals obesity-associated microbiota changes after weight loss intervention in a Spanish population.},
journal = {Nutrition journal},
volume = {25},
number = {1},
pages = {},
pmid = {41827016},
issn = {1475-2891},
support = {CB12/03/30002//Centro de Investigación Biomédica en Red-Fisiopatología de la Obesidad y Nutrición/ ; 0011-1383-2022-000000//Gobierno de Navarra/ ; PID2022-141766OB-I00//Ministerio de Ciencia, Innovación y Universidades/ ; },
abstract = {BACKGROUND & OBJECTIVES: Gut microbiota specific taxa influencing a higher or lower risk for developing obesity and related metabolic parameters remain unclear. Here, we aimed to identify gut microbiome fingerprints associated with obesity using an integrated obesity index (OBIndex), and to evaluate how these profiles change after a hypocaloric nutritional intervention with two different diets.
SUBJECTS & METHODS: 295 Spanish adult volunteers participating in the Obekit study were classified into LOW or HIGH degree of obesity according to a novel obesity index (OBIndex), based on the combination of three parameters: body mass index (BMI), fat mass (%), and waist circumference (WC). Differential abundant taxa between the two groups were investigated, at baseline together with the changes in their abundance after a weight-loss intervention with two different hypocaloric diets (Moderately high protein (MHP) and low fat (LF)).
RESULTS: The classification of participants using the OBIndex effectively differentiated obesity status, overcoming the inherent limitations of BMI, WC, and fat mass when considered individually. MHP diet was associated with an improvement in obesity status in women, while LF diet showed better outcomes in men. In relation to these improvements, changes in gut microbiota were observed. We found that Mediterraneibacter levels decreased only in men who experienced a significant improvement in their obesity status. Additionally, Agathobacter levels in participants who improved their physiological condition were reduced to match those of individuals who already exhibited a healthier status at baseline. Alongside these findings, we identified two poorly studied genera, Pseudobutyricicoccus and Intestinimonas, which were associated with a healthier profile at baseline and increased in abundance following the nutritional intervention.
CONCLUSIONS: Our OBIndex helped to achieve a more accurate separation of our volunteers regarding their obesity status and, thus, identifying four obesity strong related bacteria. Particularly, Mediterraneibacter and Agathobacter were related to a worse obesity status whereas Pseudobutyricicoccus and Intestinimonas showed a negative association with obesity status suggesting a potential protective or anti-obesity role.
TRIAL REGISTRATION: The study protocol was approved by the ethical committee at the University of Navarra (Registration No. IR.MUI.RESEARCH.REC.1401.370) and registered online at clinicaltrials.gov (identifier NCT02737267).
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12937-026-01313-x.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Microbiome-derived metabolites alleviate chronic pain in a reserpine-induced model of fibromyalgia.
iScience, 29(4):115406.
Fibromyalgia is a chronic pain disorder driven by central sensitization and neuroinflammation, increasingly linked to gut-brain axis dysfunction. Here, we delineate a gut-to-CNS axis for pain modulation, demonstrating that an acetate-producing diet alleviates reserpine-induced-fibromyalgia in a rodent model. We show that diet rich in acetylated high-amylose maize starch shifts the gut microbiome to favor acetate-producing bacteria, increasing systemic acetate levels and reducing pain hypersensitivity. This is associated with reduced spinal microglia activation and anti-inflammatory cytokine gene expression, with elevated IL-10 mRNA in the DRG and IL-10, IL-2, and IL-6 in the spinal cord. Electrophysiologically, we observe reduced hyperexcitability in the dorsal horn and increased inhibitory activity. The mechanism driving this change involves reduced prostaglandin-E2 (PGE2)-mediated suppression of glycinergic inhibition, a direct consequence of maintaining microglia in quiescent state. These findings link dietary metabolites to reduced fibromyalgia-like pathology and identify targeted nutrition as a potential disease-modifying therapy for chronic pain.
Additional Links: PMID-42006347
PubMed:
Citation:
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@article {pmid42006347,
year = {2026},
author = {Chen, S and Shanmuganathan, D and Imlach, WL},
title = {Microbiome-derived metabolites alleviate chronic pain in a reserpine-induced model of fibromyalgia.},
journal = {iScience},
volume = {29},
number = {4},
pages = {115406},
pmid = {42006347},
issn = {2589-0042},
abstract = {Fibromyalgia is a chronic pain disorder driven by central sensitization and neuroinflammation, increasingly linked to gut-brain axis dysfunction. Here, we delineate a gut-to-CNS axis for pain modulation, demonstrating that an acetate-producing diet alleviates reserpine-induced-fibromyalgia in a rodent model. We show that diet rich in acetylated high-amylose maize starch shifts the gut microbiome to favor acetate-producing bacteria, increasing systemic acetate levels and reducing pain hypersensitivity. This is associated with reduced spinal microglia activation and anti-inflammatory cytokine gene expression, with elevated IL-10 mRNA in the DRG and IL-10, IL-2, and IL-6 in the spinal cord. Electrophysiologically, we observe reduced hyperexcitability in the dorsal horn and increased inhibitory activity. The mechanism driving this change involves reduced prostaglandin-E2 (PGE2)-mediated suppression of glycinergic inhibition, a direct consequence of maintaining microglia in quiescent state. These findings link dietary metabolites to reduced fibromyalgia-like pathology and identify targeted nutrition as a potential disease-modifying therapy for chronic pain.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Gut microbial signatures and stability are associated with a co-diagnosis of endometriosis and inflammatory bowel disease.
iScience, 29(4):115437.
Emerging evidence suggests that the gut microbiota plays a crucial role in endometriosis (Endo) and inflammatory bowel disease (IBD). This study aimed to explore gut microbial signatures in women with either or both conditions, compared to healthy controls. Fecal samples underwent 16S rRNA sequencing to profile the gut microbiome. Endo-IBD patients had the most profound alterations including reduced microbial richness and evenness as well as bacterial signature changes. Specific bacteria taxa, including Akkermansia and Alistipes, were notably depleted in Endo-IBD patients, suggesting a compromised gut barrier and heightened inflammatory potential. Conversely, Blautia was enriched in Endo-IBD patients. Longitudinal microbiome assessment indicated a persistent dysbiotic signature in Endo-IBD and IBD groups, with microbial instability correlating with disease severity. The findings highlight an intensified impact of having a diagnosis of both conditions and further highlights the potential for microbiome-based diagnostics and the design of personalized interventions to restore microbial balance.
Additional Links: PMID-42006367
PubMed:
Citation:
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@article {pmid42006367,
year = {2026},
author = {Damm, GK and Zhang, F and Koentgen, S and Jayawardana, T and Houshyar, Y and Read, S and Condous, G and El-Assaad, F and Hold, GL},
title = {Gut microbial signatures and stability are associated with a co-diagnosis of endometriosis and inflammatory bowel disease.},
journal = {iScience},
volume = {29},
number = {4},
pages = {115437},
pmid = {42006367},
issn = {2589-0042},
abstract = {Emerging evidence suggests that the gut microbiota plays a crucial role in endometriosis (Endo) and inflammatory bowel disease (IBD). This study aimed to explore gut microbial signatures in women with either or both conditions, compared to healthy controls. Fecal samples underwent 16S rRNA sequencing to profile the gut microbiome. Endo-IBD patients had the most profound alterations including reduced microbial richness and evenness as well as bacterial signature changes. Specific bacteria taxa, including Akkermansia and Alistipes, were notably depleted in Endo-IBD patients, suggesting a compromised gut barrier and heightened inflammatory potential. Conversely, Blautia was enriched in Endo-IBD patients. Longitudinal microbiome assessment indicated a persistent dysbiotic signature in Endo-IBD and IBD groups, with microbial instability correlating with disease severity. The findings highlight an intensified impact of having a diagnosis of both conditions and further highlights the potential for microbiome-based diagnostics and the design of personalized interventions to restore microbial balance.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
The Uterine Microbiota in Mares With Endometritis: Impacts of Antibiotic Treatment.
Veterinary medicine international, 2026:5270993.
Despite growing interest in the role of the reproductive microbiota, the uterine microbiota of mares has been only scarcely investigated using sequencing approaches. The aims of this study were to describe the uterine microbiota of mares with endometritis and the effects of antibiotic treatment using both 16S rRNA sequencing and culture. Five mares with clinical signs of endometritis and a positive bacteriological culture were enrolled. During the follicular phase (T0), uterine samples were collected using a double-guarded cytobrush and swab for microbiome and bacteriological analysis, respectively. Following the antimicrobial susceptibility test, they were treated with intrauterine infusions of ceftiofur sodium, and samplings were repeated during the subsequent follicular phase (T1). According to bacterial culture, at T0, Streptococcus equi zooepidemicus was identified in 4 mares and Escherichia coli in one. At T1, 3 mares resulted negative, one was positive for Staphylococcus xylosus, and one continued to test positive for E. coli. According to NGS, the most represented genera at T0 were Streptococcus, Escherichia-Shigella, Corynebacterium, Arcanobacterium, Porphyromonas, and Staphylococcus. The first 3 genera dominated the microbiome of 4 mares with a relative abundance ranging from 44% to 99%. At T1, these genera's relative abundance dropped, and the most abundant were Acinetobacter, Staphylococcus, and Pseudomonas. Furthermore, after intrauterine infusion of ceftiofur, the microbiome was more diverse, according to Shannon and Simpson indexes (p < 0.05).
Additional Links: PMID-42006445
PubMed:
Citation:
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@article {pmid42006445,
year = {2026},
author = {Donato, GG and Nebbia, P and Stella, MC and Gionechetti, F and Ala, U and Cristofoli, D and Robino, P and Pallavicini, A and Nervo, T},
title = {The Uterine Microbiota in Mares With Endometritis: Impacts of Antibiotic Treatment.},
journal = {Veterinary medicine international},
volume = {2026},
number = {},
pages = {5270993},
pmid = {42006445},
issn = {2090-8113},
abstract = {Despite growing interest in the role of the reproductive microbiota, the uterine microbiota of mares has been only scarcely investigated using sequencing approaches. The aims of this study were to describe the uterine microbiota of mares with endometritis and the effects of antibiotic treatment using both 16S rRNA sequencing and culture. Five mares with clinical signs of endometritis and a positive bacteriological culture were enrolled. During the follicular phase (T0), uterine samples were collected using a double-guarded cytobrush and swab for microbiome and bacteriological analysis, respectively. Following the antimicrobial susceptibility test, they were treated with intrauterine infusions of ceftiofur sodium, and samplings were repeated during the subsequent follicular phase (T1). According to bacterial culture, at T0, Streptococcus equi zooepidemicus was identified in 4 mares and Escherichia coli in one. At T1, 3 mares resulted negative, one was positive for Staphylococcus xylosus, and one continued to test positive for E. coli. According to NGS, the most represented genera at T0 were Streptococcus, Escherichia-Shigella, Corynebacterium, Arcanobacterium, Porphyromonas, and Staphylococcus. The first 3 genera dominated the microbiome of 4 mares with a relative abundance ranging from 44% to 99%. At T1, these genera's relative abundance dropped, and the most abundant were Acinetobacter, Staphylococcus, and Pseudomonas. Furthermore, after intrauterine infusion of ceftiofur, the microbiome was more diverse, according to Shannon and Simpson indexes (p < 0.05).},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Plant-bacteria hybrid nanovesicles for targeted sonodynamic therapy: A microbiome-friendly precision strike against H. pylori infections.
Materials today. Bio, 38:103085.
Rising antibiotic resistance and adverse effects on commensal gut microbiota severely compromise conventional antibiotic therapies for Helicobacter pylori infection. Sonodynamic therapy (SDT), which employs low-intensity ultrasound to activate sonosensitizers for localized generation of cytotoxic reactive oxygen species (ROS), presents a promising non-antibiotic alternative with minimal resistance development risk. However, the efficacy of SDT is inherently constrained by the short diffusion radius and lifetime of ROS. Herein, we developed a homologous-targeting biomimetic sonosensitizer platform to overcome this limitation: hybrid membrane nanovesicles (TNVs-DMVs) engineered from turmeric plant-derived exosome-like nanovesicles (TNVs) and H. pylori-derived double membrane vesicles (DMVs). TNVs contain sonosensitizer curcumin and improve its solubility, yet SDT efficacy against H. pylori is limited. The DMVs endow TNVs-DMVs with intrinsic homologous targeting capability towards H. pylori, significantly enhancing the intracellular delivery of curcumin and subsequent ROS generation within bacterial cells. As a result, TNVs-DMVs achieved potent eradication of H. pylori in both acidic and neutral conditions without inducing detectable resistance. Moreover, TNVs-DMVs exhibited superior mucus penetration compared to TNVs alone, enabling effective elimination of H. pylori and its biofilms residing within the protective gastric mucus layer. In an H. pylori-infected mouse model, TNVs-DMVs mediated SDT demonstrated efficacy surpassing free TNVs and comparable to standard triple antibiotic therapy. Importantly, unlike triple therapy which depletes commensal flora, TNVs-DMVs treatment not only preserves intestinal microbiota homeostasis but also significantly increases populations of beneficial bacteria. This rationally designed TNVs-DMVs platform represents a transformative therapeutic modality, offering resistance-free eradication of H. pylori while maintaining microbiome health, distinct from conventional antibiotics.
Additional Links: PMID-42006709
PubMed:
Citation:
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@article {pmid42006709,
year = {2026},
author = {Yang, L and Ye, Q and Peng, X and Yu, J and Xiao, X and Wang, L and Yang, YY and Yuan, P and Tian, GB and Ding, X},
title = {Plant-bacteria hybrid nanovesicles for targeted sonodynamic therapy: A microbiome-friendly precision strike against H. pylori infections.},
journal = {Materials today. Bio},
volume = {38},
number = {},
pages = {103085},
pmid = {42006709},
issn = {2590-0064},
abstract = {Rising antibiotic resistance and adverse effects on commensal gut microbiota severely compromise conventional antibiotic therapies for Helicobacter pylori infection. Sonodynamic therapy (SDT), which employs low-intensity ultrasound to activate sonosensitizers for localized generation of cytotoxic reactive oxygen species (ROS), presents a promising non-antibiotic alternative with minimal resistance development risk. However, the efficacy of SDT is inherently constrained by the short diffusion radius and lifetime of ROS. Herein, we developed a homologous-targeting biomimetic sonosensitizer platform to overcome this limitation: hybrid membrane nanovesicles (TNVs-DMVs) engineered from turmeric plant-derived exosome-like nanovesicles (TNVs) and H. pylori-derived double membrane vesicles (DMVs). TNVs contain sonosensitizer curcumin and improve its solubility, yet SDT efficacy against H. pylori is limited. The DMVs endow TNVs-DMVs with intrinsic homologous targeting capability towards H. pylori, significantly enhancing the intracellular delivery of curcumin and subsequent ROS generation within bacterial cells. As a result, TNVs-DMVs achieved potent eradication of H. pylori in both acidic and neutral conditions without inducing detectable resistance. Moreover, TNVs-DMVs exhibited superior mucus penetration compared to TNVs alone, enabling effective elimination of H. pylori and its biofilms residing within the protective gastric mucus layer. In an H. pylori-infected mouse model, TNVs-DMVs mediated SDT demonstrated efficacy surpassing free TNVs and comparable to standard triple antibiotic therapy. Importantly, unlike triple therapy which depletes commensal flora, TNVs-DMVs treatment not only preserves intestinal microbiota homeostasis but also significantly increases populations of beneficial bacteria. This rationally designed TNVs-DMVs platform represents a transformative therapeutic modality, offering resistance-free eradication of H. pylori while maintaining microbiome health, distinct from conventional antibiotics.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Natural carrier-free self-assembled binary polyphenol nanoparticles remodel the gut microenvironment for inflammatory bowel disease prevention.
Materials today. Bio, 38:103063.
Developing biocompatible, multi-target therapeutics remains a critical challenge in the management of inflammatory bowel disease (IBD). Herein, we engineered a carrier-free nanoplatform (Cur-Ant NPs) via the facile self-assembly of two natural polyphenols: curcumin (Cur) and anthocyanin (Ant). Spectroscopic analysis and molecular dynamics simulations confirmed that the assembly is stabilized by robust π-π stacking and hydrogen bonding networks, yielding uniform, spherical nanostructures with integrated functionality. In a dextran sulfate sodium (DSS)-induced colitis model, orally administered Cur-Ant NPs demonstrated superior therapeutic efficacy compared to both free polyphenols and the clinical standard, sulfasalazine (SASP). The nanoparticles' potent anti-inflammatory activity was initially validated in a zebrafish model, where they effectively inhibited neutrophil infiltration and scavenged reactive oxygen species (ROS). These protective effects were further substantiated in a murine model, where multi-omics analysis revealed a tripartite mechanism of action: reinforcing the intestinal epithelial barrier, mitigating pro-inflammatory cytokine responses, and remodeling the dysbiotic gut microbiome. Our findings establish Cur-Ant NPs as a potent, safe candidate for IBD prevention and highlight a scalable, green engineering strategy for designing next-generation nanomedicines based on the supramolecular co-assembly of natural bioactive agents.
Additional Links: PMID-42006721
PubMed:
Citation:
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@article {pmid42006721,
year = {2026},
author = {Xie, Q and Xu, H and Yang, X and Chen, Y and Xu, ZZ},
title = {Natural carrier-free self-assembled binary polyphenol nanoparticles remodel the gut microenvironment for inflammatory bowel disease prevention.},
journal = {Materials today. Bio},
volume = {38},
number = {},
pages = {103063},
pmid = {42006721},
issn = {2590-0064},
abstract = {Developing biocompatible, multi-target therapeutics remains a critical challenge in the management of inflammatory bowel disease (IBD). Herein, we engineered a carrier-free nanoplatform (Cur-Ant NPs) via the facile self-assembly of two natural polyphenols: curcumin (Cur) and anthocyanin (Ant). Spectroscopic analysis and molecular dynamics simulations confirmed that the assembly is stabilized by robust π-π stacking and hydrogen bonding networks, yielding uniform, spherical nanostructures with integrated functionality. In a dextran sulfate sodium (DSS)-induced colitis model, orally administered Cur-Ant NPs demonstrated superior therapeutic efficacy compared to both free polyphenols and the clinical standard, sulfasalazine (SASP). The nanoparticles' potent anti-inflammatory activity was initially validated in a zebrafish model, where they effectively inhibited neutrophil infiltration and scavenged reactive oxygen species (ROS). These protective effects were further substantiated in a murine model, where multi-omics analysis revealed a tripartite mechanism of action: reinforcing the intestinal epithelial barrier, mitigating pro-inflammatory cytokine responses, and remodeling the dysbiotic gut microbiome. Our findings establish Cur-Ant NPs as a potent, safe candidate for IBD prevention and highlight a scalable, green engineering strategy for designing next-generation nanomedicines based on the supramolecular co-assembly of natural bioactive agents.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
The role of gut microbiota mediated ferroptosis in PCOS and the therapeutic potential of Chinese herbal medicine.
Frontiers in medicine, 13:1730795.
Polycystic ovary syndrome (PCOS) is a complex reproductive endocrine metabolic disorder whose pathogenesis remains incompletely understood. In recent years, the role of ferroptosis-a novel form of iron-dependent programmed cell death-in the pathogenesis of PCOS has gradually drawn attention. This review proposes an innovative perspective: gut microbiota dysbiosis may be a potential upstream trigger of ferroptosis in PCOS ovarian granulosa cells. Microbiome dysbiosis disrupts iron homeostasis and reduces the production of antioxidant metabolites such as short-chain fatty acids (SCFAs) and bile acids (BAs), thereby exacerbating systemic and local ovarian oxidative stress. This induces ferroptosis, leading to impaired follicular development and insulin resistance. Traditional Chinese Medicine (TCM) demonstrates significant potential in regulating gut microbiota and inhibiting ferroptosis. Based on this, this study explores the role of the gut microbiota-ferroptosis axis in PCOS, focusing on the scientific rationale and application prospects of treating PCOS by intervening in this axis using TCM monomers and compounds such as berberine and quercetin. With its multi-target regulatory effects and favorable safety profile, TCM may offer benefits as an adjunct or alternative to conventional therapies. This research aims to provide theoretical references for developing novel therapeutic strategies.
Additional Links: PMID-42006870
PubMed:
Citation:
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@article {pmid42006870,
year = {2026},
author = {Lv, Y and Li, D and Ding, N and Kuang, H},
title = {The role of gut microbiota mediated ferroptosis in PCOS and the therapeutic potential of Chinese herbal medicine.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1730795},
pmid = {42006870},
issn = {2296-858X},
abstract = {Polycystic ovary syndrome (PCOS) is a complex reproductive endocrine metabolic disorder whose pathogenesis remains incompletely understood. In recent years, the role of ferroptosis-a novel form of iron-dependent programmed cell death-in the pathogenesis of PCOS has gradually drawn attention. This review proposes an innovative perspective: gut microbiota dysbiosis may be a potential upstream trigger of ferroptosis in PCOS ovarian granulosa cells. Microbiome dysbiosis disrupts iron homeostasis and reduces the production of antioxidant metabolites such as short-chain fatty acids (SCFAs) and bile acids (BAs), thereby exacerbating systemic and local ovarian oxidative stress. This induces ferroptosis, leading to impaired follicular development and insulin resistance. Traditional Chinese Medicine (TCM) demonstrates significant potential in regulating gut microbiota and inhibiting ferroptosis. Based on this, this study explores the role of the gut microbiota-ferroptosis axis in PCOS, focusing on the scientific rationale and application prospects of treating PCOS by intervening in this axis using TCM monomers and compounds such as berberine and quercetin. With its multi-target regulatory effects and favorable safety profile, TCM may offer benefits as an adjunct or alternative to conventional therapies. This research aims to provide theoretical references for developing novel therapeutic strategies.},
}
RevDate: 2026-04-21
Cats on dry kibble diet have significantly different microbiome than those on canned wet food.
npj veterinary sciences, 1(1):1.
Domestic cats (Felis catus) are understudied regarding how commercial diets impact their gut microbiomes. Here, we reanalyzed the 16S rRNA gene (V4) amplicon sequencing Kittybiome dataset, using new tools and techniques. Results demonstrated significant microbial composition differences between cats eating commercial dry kibble diets and those eating canned wet food. Kibble-fed cats showed enriched Prevotella, Bifidobacterium, and Megamonas amplicon sequencing variants (ASVs), linked to carbohydrate metabolism and metabolic disease.
Additional Links: PMID-42006912
PubMed:
Citation:
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@article {pmid42006912,
year = {2026},
author = {Allaband, C and Ganz, HH and Rojas, CA and Knight, R},
title = {Cats on dry kibble diet have significantly different microbiome than those on canned wet food.},
journal = {npj veterinary sciences},
volume = {1},
number = {1},
pages = {1},
pmid = {42006912},
issn = {3059-328X},
abstract = {Domestic cats (Felis catus) are understudied regarding how commercial diets impact their gut microbiomes. Here, we reanalyzed the 16S rRNA gene (V4) amplicon sequencing Kittybiome dataset, using new tools and techniques. Results demonstrated significant microbial composition differences between cats eating commercial dry kibble diets and those eating canned wet food. Kibble-fed cats showed enriched Prevotella, Bifidobacterium, and Megamonas amplicon sequencing variants (ASVs), linked to carbohydrate metabolism and metabolic disease.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Olanzapine and peripheral metabolic dysregulation: organ-resolved mechanisms, risk, and MASLD-aligned care pathways.
Frontiers in pharmacology, 16:1729264.
This review examines how olanzapine drives metabolic injury beyond the brain and why an organ-resolved perspective is needed. We synthesize clinical signals of early weight gain, insulin resistance, dyslipidemia, and steatotic liver disease, and integrate translational evidence across liver, adipose tissue, skeletal muscle, pancreatic β-cells, and the gut-liver axis. Mechanistic strands include disordered hepatic lipid handling, suppression of brown-fat thermogenesis, β-cell endoplasmic-reticulum stress with impaired secretion, and skeletal-muscle insulin-signaling defects with altered epigenetic programs that blunt glucose disposal. We summarize modifiers of risk across life stage, treatment exposure, genetic variation, smoking status, and pregnancy, and distill a pragmatic pathway that prioritizes early reassessment, MASLD-aligned liver evaluation, targeted lifestyle treatment, metformin for early deterioration, and GLP-1 receptor agonists when required. We advance the view that weight-independent extra-cerebral mechanisms are central to olanzapine's metabolic liability and that psychiatric practice should adopt metabolic frameworks used in hepatology and endocrinology. We propose an agenda for organ-specific human phenotyping and exposure-aware designs that integrate therapeutic drug monitoring with microbiome, metabolomics, and bile-acid profiling, alongside comparative trials that test stepped algorithms within psychiatric care. This perspective outlines a path to preserve antipsychotic efficacy while reducing preventable systemic metabolic harm.
Additional Links: PMID-42007333
PubMed:
Citation:
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@article {pmid42007333,
year = {2025},
author = {Weng, S and Lin, J and Chai, D},
title = {Olanzapine and peripheral metabolic dysregulation: organ-resolved mechanisms, risk, and MASLD-aligned care pathways.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1729264},
pmid = {42007333},
issn = {1663-9812},
abstract = {This review examines how olanzapine drives metabolic injury beyond the brain and why an organ-resolved perspective is needed. We synthesize clinical signals of early weight gain, insulin resistance, dyslipidemia, and steatotic liver disease, and integrate translational evidence across liver, adipose tissue, skeletal muscle, pancreatic β-cells, and the gut-liver axis. Mechanistic strands include disordered hepatic lipid handling, suppression of brown-fat thermogenesis, β-cell endoplasmic-reticulum stress with impaired secretion, and skeletal-muscle insulin-signaling defects with altered epigenetic programs that blunt glucose disposal. We summarize modifiers of risk across life stage, treatment exposure, genetic variation, smoking status, and pregnancy, and distill a pragmatic pathway that prioritizes early reassessment, MASLD-aligned liver evaluation, targeted lifestyle treatment, metformin for early deterioration, and GLP-1 receptor agonists when required. We advance the view that weight-independent extra-cerebral mechanisms are central to olanzapine's metabolic liability and that psychiatric practice should adopt metabolic frameworks used in hepatology and endocrinology. We propose an agenda for organ-specific human phenotyping and exposure-aware designs that integrate therapeutic drug monitoring with microbiome, metabolomics, and bile-acid profiling, alongside comparative trials that test stepped algorithms within psychiatric care. This perspective outlines a path to preserve antipsychotic efficacy while reducing preventable systemic metabolic harm.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
An overview of the role of the gut microbiota in rheumatoid arthritis.
Microbiome research reports, 5(1):3.
Rheumatoid arthritis (RA) is a chronic autoimmune disease preceded by a prolonged preclinical phase marked by the emergence of autoantibodies and mucosal immune dysregulation. Evidence from human studies and animal models consistently demonstrates that gut microbiota dysbiosis contributes to this transition, particularly through impaired intestinal barrier function, activation of pro-inflammatory pathways, and molecular mimicry. Specific taxa - including Prevotella copri, Collinsella aerofaciens, and reductions in butyrate-producing bacteria - have been linked to heightened systemic inflammation, increased T helper 17 responses, and the generation of RA-associated autoantibodies. Current research also indicates that anti-rheumatic medications such as methotrexate, sulfasalazine, and minocycline produce measurable shifts in gut microbial composition, suggesting that microbiota-drug interactions may influence treatment response. Therapeutic approaches aimed at modifying gut ecology - including dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation - show early potential in restoring microbial balance, improving intestinal barrier integrity, and reducing inflammatory markers, although evidence in the preclinical RA stage remains limited. Additionally, emerging data highlight the importance of intestinal autophagy and microRNA networks in regulating epithelial integrity and systemic immune activation. Taken together, the literature supports a mechanistic link between gut dysbiosis and the onset of RA. It points to microbiota-targeted strategies as promising avenues for delaying or preventing disease progression. Future studies should prioritize longitudinal analyses and interventional trials focusing specifically on individuals at risk for RA.
Additional Links: PMID-42007373
PubMed:
Citation:
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@article {pmid42007373,
year = {2026},
author = {Poznyak, AV and Vatlin, AA and Pavshintsev, VV and Mitkin, NA and Maltseva, ON and Utkina, AS and Orekhov, AN},
title = {An overview of the role of the gut microbiota in rheumatoid arthritis.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {3},
pmid = {42007373},
issn = {2771-5965},
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disease preceded by a prolonged preclinical phase marked by the emergence of autoantibodies and mucosal immune dysregulation. Evidence from human studies and animal models consistently demonstrates that gut microbiota dysbiosis contributes to this transition, particularly through impaired intestinal barrier function, activation of pro-inflammatory pathways, and molecular mimicry. Specific taxa - including Prevotella copri, Collinsella aerofaciens, and reductions in butyrate-producing bacteria - have been linked to heightened systemic inflammation, increased T helper 17 responses, and the generation of RA-associated autoantibodies. Current research also indicates that anti-rheumatic medications such as methotrexate, sulfasalazine, and minocycline produce measurable shifts in gut microbial composition, suggesting that microbiota-drug interactions may influence treatment response. Therapeutic approaches aimed at modifying gut ecology - including dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation - show early potential in restoring microbial balance, improving intestinal barrier integrity, and reducing inflammatory markers, although evidence in the preclinical RA stage remains limited. Additionally, emerging data highlight the importance of intestinal autophagy and microRNA networks in regulating epithelial integrity and systemic immune activation. Taken together, the literature supports a mechanistic link between gut dysbiosis and the onset of RA. It points to microbiota-targeted strategies as promising avenues for delaying or preventing disease progression. Future studies should prioritize longitudinal analyses and interventional trials focusing specifically on individuals at risk for RA.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
A responder-informed gut microbial consortium enhances anti-PD-1 efficacy in a mouse cancer model.
Microbiome research reports, 5(1):2.
Aim: Immune checkpoint inhibitors (ICIs), particularly anti-programmed cell death protein 1 (PD-1) therapy, have improved cancer treatment outcomes, yet durable benefit is achieved in only a subset of patients. Growing evidence implicates the gut microbiome as a modulator of ICI responsiveness, but defined and experimentally validated microbial strategies remain limited. This study aimed to identify responder-associated gut microbes and to evaluate a defined bacterial consortium for enhancing PD-1 blockade efficacy. Methods: Publicly available shotgun metagenomic datasets from anti-PD-1-treated cancer patients were re-analyzed to compare gut microbiome profiles between responders and non-responders. Bacterial taxa reproducibly enriched in responders were selected based on consistency across analytical criteria and cultivability and assembled into a four-strain consortium (UJ-04). The immune-adjuvant potential of UJ-04, alone or combined with anti-PD-1 therapy, was evaluated in a B16-F10 melanoma mouse model, with tumor growth and immune responses assessed by flow cytometry. Results: Metagenomic re-analysis identified four commensal bacterial taxa consistently enriched in responder patients, forming the defined UJ-04 consortium. While UJ-04 alone showed minimal antitumor activity, combination treatment with anti-PD-1 significantly enhanced tumor growth inhibition compared with anti-PD-1 monotherapy. This effect was accompanied by increased intratumoral CD8[+] T cells and natural killer cells, with concordant immune trends in peripheral compartments. Conclusion: A responder-informed, defined microbial consortium functionally translates clinical microbiome associations into in vivo validation and enhances PD-1 blockade efficacy by modulating host antitumor immunity. These findings support defined bacterial consortia as microbiome-based immunomodulatory adjuncts for immunotherapy.
Additional Links: PMID-42007374
PubMed:
Citation:
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@article {pmid42007374,
year = {2026},
author = {Jeong, UJ and Ali, M and Park, YJ and You, JS and Yoon, SS},
title = {A responder-informed gut microbial consortium enhances anti-PD-1 efficacy in a mouse cancer model.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {2},
pmid = {42007374},
issn = {2771-5965},
abstract = {Aim: Immune checkpoint inhibitors (ICIs), particularly anti-programmed cell death protein 1 (PD-1) therapy, have improved cancer treatment outcomes, yet durable benefit is achieved in only a subset of patients. Growing evidence implicates the gut microbiome as a modulator of ICI responsiveness, but defined and experimentally validated microbial strategies remain limited. This study aimed to identify responder-associated gut microbes and to evaluate a defined bacterial consortium for enhancing PD-1 blockade efficacy. Methods: Publicly available shotgun metagenomic datasets from anti-PD-1-treated cancer patients were re-analyzed to compare gut microbiome profiles between responders and non-responders. Bacterial taxa reproducibly enriched in responders were selected based on consistency across analytical criteria and cultivability and assembled into a four-strain consortium (UJ-04). The immune-adjuvant potential of UJ-04, alone or combined with anti-PD-1 therapy, was evaluated in a B16-F10 melanoma mouse model, with tumor growth and immune responses assessed by flow cytometry. Results: Metagenomic re-analysis identified four commensal bacterial taxa consistently enriched in responder patients, forming the defined UJ-04 consortium. While UJ-04 alone showed minimal antitumor activity, combination treatment with anti-PD-1 significantly enhanced tumor growth inhibition compared with anti-PD-1 monotherapy. This effect was accompanied by increased intratumoral CD8[+] T cells and natural killer cells, with concordant immune trends in peripheral compartments. Conclusion: A responder-informed, defined microbial consortium functionally translates clinical microbiome associations into in vivo validation and enhances PD-1 blockade efficacy by modulating host antitumor immunity. These findings support defined bacterial consortia as microbiome-based immunomodulatory adjuncts for immunotherapy.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Predicting Dietary Impact on Multiple Sclerosis-Related Symptoms With the Gut Microbiome: A Pilot Study Using Unsupervised Machine Learning.
Brain and behavior, 16(4):e71394.
BACKGROUND: Multiple sclerosis (MS) is a neurodegenerative disease where dietary intervention has emerged as a potential adjunct treatment. Recently, the modified Paleolithic elimination (MPE) diet, also known as the Wahls diet, and the low-saturated fat (LSF) diet, also known as the Swank diet, were linked to reduced fatigue and improved quality of life (QoL) in the WAVES study (NCT02914964). However, how diet impacts these outcomes remains unclear. As diet impacts gut microbiota, we investigated whether the baseline gut microbiota can predict response to diet in people with MS (pwMS).
METHODS: We performed fecal 16s rRNA sequencing to profile the microbiome changes associated with pwMS receiving the MPE (n = 11) and LSF diet (n = 12). Next, we utilized topic modeling, a machine learning technique, to determine whether baseline microbiome features predicted diet response in the combined MPE + LSF dietary cohort (n = 23).
RESULTS: Specific genera significantly differed over time on both diets. On the MPE diet, Hungateiclostridiaceae, Ruminiclostridium, and Shuttleworthia decreased, while Coriobacteriaceae Collinsella decreased on LSF. Predictive machine-learning analysis associated a baseline microbiome enriched with Akkermansia, Bacteroides, and Barnesiella with fatigue response in the combined MPE + LSF cohort. For a non-response in Mental QoL improvement in the combined MPE + LSF cohort, our analysis associated an enrichment of Faecalibacterium and Alistipes at the start of the diet.
DISCUSSION: Utilizing topic modeling, this pilot study identified baseline microbiota communities linked to improvements in fatigue and Mental QoL in pwMS on dietary intervention. These findings highlight the microbiota's role in dietary response and the potential for personalized nutrition. Given the small cohort and exploratory design, the results are hypothesis-generating and require validation in larger mechanistic studies.
Additional Links: PMID-42007545
PubMed:
Citation:
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@article {pmid42007545,
year = {2026},
author = {Meza, LA and Fitzjerrells, RL and Shemirani, F and Titcomb, TJ and Rubenstein, LM and Eyck, PT and Snetselaar, LG and Shahi, SK and Wahls, TL and Mangalam, AK},
title = {Predicting Dietary Impact on Multiple Sclerosis-Related Symptoms With the Gut Microbiome: A Pilot Study Using Unsupervised Machine Learning.},
journal = {Brain and behavior},
volume = {16},
number = {4},
pages = {e71394},
pmid = {42007545},
issn = {2162-3279},
support = {1RO1AI137075//NIAID/NIH/ ; 1I01CX002212//US Department of Veteran Affairs/ ; 1F31DE033564-01//NIDCR/NIH/ ; NIEHS/NIH P30 ES005605//University of Iowa Environmental Health Sciences Research Center/ ; UM1TR004403//National Center for Advancing Translational Sciences of the NIH/ ; 1506-04312//National Multiple Sclerosis Society/ ; //P. Heppelmann and M. Wacek Fund/ ; //the Carver Trust Pilot Grant/ ; //Center for Biocatalysis and Bioprocessing/ ; //University of Iowa institutional funds/ ; //Carter Chapman Shreve Family Foundation/ ; //Carter Chapman Shreve Fellowship Fund/ ; //Helen Harris Fund/ ; //University of Iowa College of Public Health Preventive Intervention Center/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Pilot Projects ; Male ; *Multiple Sclerosis/diet therapy/microbiology ; Female ; Adult ; Middle Aged ; *Unsupervised Machine Learning ; Feces/microbiology ; Quality of Life ; *Diet, Paleolithic ; *Diet ; RNA, Ribosomal, 16S ; },
abstract = {BACKGROUND: Multiple sclerosis (MS) is a neurodegenerative disease where dietary intervention has emerged as a potential adjunct treatment. Recently, the modified Paleolithic elimination (MPE) diet, also known as the Wahls diet, and the low-saturated fat (LSF) diet, also known as the Swank diet, were linked to reduced fatigue and improved quality of life (QoL) in the WAVES study (NCT02914964). However, how diet impacts these outcomes remains unclear. As diet impacts gut microbiota, we investigated whether the baseline gut microbiota can predict response to diet in people with MS (pwMS).
METHODS: We performed fecal 16s rRNA sequencing to profile the microbiome changes associated with pwMS receiving the MPE (n = 11) and LSF diet (n = 12). Next, we utilized topic modeling, a machine learning technique, to determine whether baseline microbiome features predicted diet response in the combined MPE + LSF dietary cohort (n = 23).
RESULTS: Specific genera significantly differed over time on both diets. On the MPE diet, Hungateiclostridiaceae, Ruminiclostridium, and Shuttleworthia decreased, while Coriobacteriaceae Collinsella decreased on LSF. Predictive machine-learning analysis associated a baseline microbiome enriched with Akkermansia, Bacteroides, and Barnesiella with fatigue response in the combined MPE + LSF cohort. For a non-response in Mental QoL improvement in the combined MPE + LSF cohort, our analysis associated an enrichment of Faecalibacterium and Alistipes at the start of the diet.
DISCUSSION: Utilizing topic modeling, this pilot study identified baseline microbiota communities linked to improvements in fatigue and Mental QoL in pwMS on dietary intervention. These findings highlight the microbiota's role in dietary response and the potential for personalized nutrition. Given the small cohort and exploratory design, the results are hypothesis-generating and require validation in larger mechanistic studies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
Pilot Projects
Male
*Multiple Sclerosis/diet therapy/microbiology
Female
Adult
Middle Aged
*Unsupervised Machine Learning
Feces/microbiology
Quality of Life
*Diet, Paleolithic
*Diet
RNA, Ribosomal, 16S
RevDate: 2026-04-21
Pseudoalteromonas is a symbiont of marine invertebrates that exhibits broad patterns of phylosymbiosis.
The ISME journal pii:8659212 [Epub ahead of print].
Despite growing insights into the composition of marine invertebrate microbiomes, our understanding of their ecological and evolutionary patterns remains poor, owing to limited sampling depth and low-resolution datasets. Previous studies have provided conflicting results that both confirm and deny the existence of phylosymbiosis between marine invertebrates and marine bacteria. Here, we investigated potential animal-microbe symbioses in Pseudoalteromonas, a bacterial genus consistently identified as a core microbiome taxon in diverse invertebrates. Using a pangenomic analysis of 236 free-living and invertebrate-associated bacterial strains (including two new nematode-associated isolates generated in this study), we confirm that Pseudoalteromonas is a symbiont with substantial evidence of phylosymbiosis across at least three marine invertebrate phyla (e.g., Nematoda, Mollusca, and Cnidaria). Patterns of symbiosis were consistent irrespective of geography (including in Antarctica), with FISH images from nematodes indicating that bacterial symbionts form biofilms in the mouth and esophagus and are sometimes present in female nematode ovaries exhibiting stunted development. The evolutionary history of Pseudoalteromonas is marked by substantial host-switching and lifestyle transitions, and host-associated genomes suggest that these bacteria are facultative symbionts involved in nutritional symbioses. In marine environments, we hypothesize that horizontally acquired symbionts may have co-evolved with invertebrates, using host mucus as a physical niche and food source, while providing their animal hosts with Vitamin B, amino acids, and bioavailable carbon compounds in return.
Additional Links: PMID-42007585
Publisher:
PubMed:
Citation:
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@article {pmid42007585,
year = {2026},
author = {De Santiago, A and Barnes, S and Pereira, TJ and Marcellino-Barros, M and Durden, L and Han, MK and Thrash, JC and Bik, HM},
title = {Pseudoalteromonas is a symbiont of marine invertebrates that exhibits broad patterns of phylosymbiosis.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wrag091},
pmid = {42007585},
issn = {1751-7370},
abstract = {Despite growing insights into the composition of marine invertebrate microbiomes, our understanding of their ecological and evolutionary patterns remains poor, owing to limited sampling depth and low-resolution datasets. Previous studies have provided conflicting results that both confirm and deny the existence of phylosymbiosis between marine invertebrates and marine bacteria. Here, we investigated potential animal-microbe symbioses in Pseudoalteromonas, a bacterial genus consistently identified as a core microbiome taxon in diverse invertebrates. Using a pangenomic analysis of 236 free-living and invertebrate-associated bacterial strains (including two new nematode-associated isolates generated in this study), we confirm that Pseudoalteromonas is a symbiont with substantial evidence of phylosymbiosis across at least three marine invertebrate phyla (e.g., Nematoda, Mollusca, and Cnidaria). Patterns of symbiosis were consistent irrespective of geography (including in Antarctica), with FISH images from nematodes indicating that bacterial symbionts form biofilms in the mouth and esophagus and are sometimes present in female nematode ovaries exhibiting stunted development. The evolutionary history of Pseudoalteromonas is marked by substantial host-switching and lifestyle transitions, and host-associated genomes suggest that these bacteria are facultative symbionts involved in nutritional symbioses. In marine environments, we hypothesize that horizontally acquired symbionts may have co-evolved with invertebrates, using host mucus as a physical niche and food source, while providing their animal hosts with Vitamin B, amino acids, and bioavailable carbon compounds in return.},
}
RevDate: 2026-04-21
A Synthetic Community from Campeiostachys nutans Rhizosphere in the Qinghai-Tibet Plateau Endow Alfalfa with the Ability to Resist Drought and Cold.
Journal of agricultural and food chemistry [Epub ahead of print].
Campeiostachys nutans, widely distributed in the Qinghai-Tibet Plateau, possesses notable stress tolerance, yet the exploration of its functional rhizosphere microbes remains limited. In this study, we characterized bacterial variations across rhizosphere surrounding soil, rhizosphere, and endosphere compartments from five grassland types, isolated core strains, and established a synthetic community (SynCom). Results revealed that under PEG-induced drought, SynCom significantly altered alfalfa responses by scavenging reactive oxygen species (ROS), modulating immune gene expression, and synthesizing glutamate metabolites. Additionally, SynCom inoculation conferred cold resistance to alfalfa by enhancing photosynthetic activity, boosting antioxidant enzymes, and producing osmotic adjustment compounds like trehalose. This investigation underscores the capacity of core rhizosphere taxa to enhance stress tolerance, offering novel perspectives for developing microbial inoculants to improve crop productivity under drought and cold stress.
Additional Links: PMID-42007648
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PubMed:
Citation:
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@article {pmid42007648,
year = {2026},
author = {Xu, S and Cao, Z and Ma, K and Song, J and Miao, Y and Li, Q and Song, D and Fu, J and Yang, P},
title = {A Synthetic Community from Campeiostachys nutans Rhizosphere in the Qinghai-Tibet Plateau Endow Alfalfa with the Ability to Resist Drought and Cold.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c14225},
pmid = {42007648},
issn = {1520-5118},
abstract = {Campeiostachys nutans, widely distributed in the Qinghai-Tibet Plateau, possesses notable stress tolerance, yet the exploration of its functional rhizosphere microbes remains limited. In this study, we characterized bacterial variations across rhizosphere surrounding soil, rhizosphere, and endosphere compartments from five grassland types, isolated core strains, and established a synthetic community (SynCom). Results revealed that under PEG-induced drought, SynCom significantly altered alfalfa responses by scavenging reactive oxygen species (ROS), modulating immune gene expression, and synthesizing glutamate metabolites. Additionally, SynCom inoculation conferred cold resistance to alfalfa by enhancing photosynthetic activity, boosting antioxidant enzymes, and producing osmotic adjustment compounds like trehalose. This investigation underscores the capacity of core rhizosphere taxa to enhance stress tolerance, offering novel perspectives for developing microbial inoculants to improve crop productivity under drought and cold stress.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Mapping the Research Landscape and Evolutionary Trends of the Oral Microbiome in Periodontitis.
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica, 134(4):e70209.
The conceptual transition from the "Red Complex" paradigm to the "Ecological Plaque Hypothesis" has fundamentally reshaped the understanding of periodontitis, but a quantitative mapping of this intellectual evolution and its emerging research frontiers remains limited. This study systematically characterized the global research landscape and evolutionary trends of the oral microbiome in periodontitis from 2000 to 2025. English-language articles published between 2000 and 17 November 2025 were retrieved from the Web of Science Core Collection and Scopus databases. After deduplication, bibliometric analyses were performed on 2827 unique publications to evaluate spatiotemporal distributions, collaboration patterns, thematic evolution, and citation bursts. The results revealed exponential growth in publications, particularly after 2020, with the United States and China leading global contributions. Thematic evolution analyses demonstrated a clear shift from single-pathogen-focused research, exemplified by Porphyromonas gingivalis, toward ecological frameworks emphasizing dysbiosis and microbial community structure. Recent citation bursts highlighted growing attention to broader microbial taxa, inflammatory mediators, clinically relevant periodontal indicators, microbiome-based therapeutic strategies, and methodological standardization. Overall, research on the oral microbiome in periodontitis has evolved toward a host-microbiome systems biology framework, with future studies likely to emphasize functional multi-omics integration, AI-assisted diagnostics, and precision interventions targeting oral-systemic health links.
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@article {pmid42007708,
year = {2026},
author = {Wang, X and Ma, Y and Yang, Y and Dong, Q},
title = {Mapping the Research Landscape and Evolutionary Trends of the Oral Microbiome in Periodontitis.},
journal = {APMIS : acta pathologica, microbiologica, et immunologica Scandinavica},
volume = {134},
number = {4},
pages = {e70209},
doi = {10.1111/apm.70209},
pmid = {42007708},
issn = {1600-0463},
mesh = {Humans ; *Periodontitis/microbiology ; *Microbiota ; *Mouth/microbiology ; Dysbiosis/microbiology ; Bibliometrics ; },
abstract = {The conceptual transition from the "Red Complex" paradigm to the "Ecological Plaque Hypothesis" has fundamentally reshaped the understanding of periodontitis, but a quantitative mapping of this intellectual evolution and its emerging research frontiers remains limited. This study systematically characterized the global research landscape and evolutionary trends of the oral microbiome in periodontitis from 2000 to 2025. English-language articles published between 2000 and 17 November 2025 were retrieved from the Web of Science Core Collection and Scopus databases. After deduplication, bibliometric analyses were performed on 2827 unique publications to evaluate spatiotemporal distributions, collaboration patterns, thematic evolution, and citation bursts. The results revealed exponential growth in publications, particularly after 2020, with the United States and China leading global contributions. Thematic evolution analyses demonstrated a clear shift from single-pathogen-focused research, exemplified by Porphyromonas gingivalis, toward ecological frameworks emphasizing dysbiosis and microbial community structure. Recent citation bursts highlighted growing attention to broader microbial taxa, inflammatory mediators, clinically relevant periodontal indicators, microbiome-based therapeutic strategies, and methodological standardization. Overall, research on the oral microbiome in periodontitis has evolved toward a host-microbiome systems biology framework, with future studies likely to emphasize functional multi-omics integration, AI-assisted diagnostics, and precision interventions targeting oral-systemic health links.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Periodontitis/microbiology
*Microbiota
*Mouth/microbiology
Dysbiosis/microbiology
Bibliometrics
RevDate: 2026-04-20
A synthetic microbial community for soybean biofertilization designed via chlorophyll-based iterative selection.
Applied and environmental microbiology [Epub ahead of print].
Improving the effectiveness of microbial inoculants for soybean is essential to enhance biological nitrogen fixation and reduce fertilizer dependence; however, inoculated Bradyrhizobium strains frequently display inconsistent field performance. Inoculation is usually carried out with single-strain formulations, overlooking the possible influence of the native soil microbiota on nodulation success. This limitation may be addressed by formulating inoculants with consortia that include selected members of the soil microbiota. To this end, a synthetic microbial community (SynCom) was developed through a host-mediated microbiome engineering approach guided by leaf chlorophyll content as a rapid, non-destructive plant trait. The experiment was initiated by inoculating soybean plants with a consortium of 9 Bradyrhizobium spp. and 14 non-rhizobial soil isolates. Across eight consecutive selection rounds under gnotobiotic conditions, rhizosphere communities associated with superior plant performance were pooled and propagated. Recurrent selection induced significant shifts in community composition, consistently favoring Bradyrhizobium diazoefficiens as the dominant nodulating member and enriching taxa from Pseudomonadales, Burkholderiales, and Sphingomonadales. Sequencing-based profiling and network analysis suggested the emergence of a cohesive and functionally enriched community, with increased potential for nitrogen transformations and organic matter turnover. When evaluated in non-sterile soil, the SynCom derived from the sixth selection round increased nodule number and biomass relative to an uninoculated control and a commercial inoculant strain. These results suggest that plant-guided selection can steer rhizosphere community assembly toward beneficial configurations and support the development of improved soybean bioinoculants.IMPORTANCESoybean [Glycine max (L.) Merr.] is a major global crop characterized by high seed protein content, which demands elevated nitrogen assimilation. To meet this demand, the crop can utilize atmospheric nitrogen through the process of biological nitrogen fixation in symbiosis with Bradyrhizobium bacteria, thus mitigating soil nitrogen depletion. Although Bradyrhizobium-based inoculants are applied at sowing, their interplay with other members of the rhizosphere microbiota remains poorly understood. It is well documented that plants and rhizosphere microbiota interact to shape plant growth and soil productivity. Therefore, this work evaluated the inoculation of soybean with a synthetic microbial consortium as a strategy to develop new-generation inoculants. These bioinputs are designed to harness plant-soil-microbe interactions to improve soybean productivity while preserving soil properties.
Additional Links: PMID-42007760
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PubMed:
Citation:
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@article {pmid42007760,
year = {2026},
author = {Brignoli, D and Colla, D and Frickel-Critto, E and Castells, CB and Pérez-Giménez, J and Lodeiro, AR},
title = {A synthetic microbial community for soybean biofertilization designed via chlorophyll-based iterative selection.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0254825},
doi = {10.1128/aem.02548-25},
pmid = {42007760},
issn = {1098-5336},
abstract = {Improving the effectiveness of microbial inoculants for soybean is essential to enhance biological nitrogen fixation and reduce fertilizer dependence; however, inoculated Bradyrhizobium strains frequently display inconsistent field performance. Inoculation is usually carried out with single-strain formulations, overlooking the possible influence of the native soil microbiota on nodulation success. This limitation may be addressed by formulating inoculants with consortia that include selected members of the soil microbiota. To this end, a synthetic microbial community (SynCom) was developed through a host-mediated microbiome engineering approach guided by leaf chlorophyll content as a rapid, non-destructive plant trait. The experiment was initiated by inoculating soybean plants with a consortium of 9 Bradyrhizobium spp. and 14 non-rhizobial soil isolates. Across eight consecutive selection rounds under gnotobiotic conditions, rhizosphere communities associated with superior plant performance were pooled and propagated. Recurrent selection induced significant shifts in community composition, consistently favoring Bradyrhizobium diazoefficiens as the dominant nodulating member and enriching taxa from Pseudomonadales, Burkholderiales, and Sphingomonadales. Sequencing-based profiling and network analysis suggested the emergence of a cohesive and functionally enriched community, with increased potential for nitrogen transformations and organic matter turnover. When evaluated in non-sterile soil, the SynCom derived from the sixth selection round increased nodule number and biomass relative to an uninoculated control and a commercial inoculant strain. These results suggest that plant-guided selection can steer rhizosphere community assembly toward beneficial configurations and support the development of improved soybean bioinoculants.IMPORTANCESoybean [Glycine max (L.) Merr.] is a major global crop characterized by high seed protein content, which demands elevated nitrogen assimilation. To meet this demand, the crop can utilize atmospheric nitrogen through the process of biological nitrogen fixation in symbiosis with Bradyrhizobium bacteria, thus mitigating soil nitrogen depletion. Although Bradyrhizobium-based inoculants are applied at sowing, their interplay with other members of the rhizosphere microbiota remains poorly understood. It is well documented that plants and rhizosphere microbiota interact to shape plant growth and soil productivity. Therefore, this work evaluated the inoculation of soybean with a synthetic microbial consortium as a strategy to develop new-generation inoculants. These bioinputs are designed to harness plant-soil-microbe interactions to improve soybean productivity while preserving soil properties.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Distinct early-life gut microbiota patterns across SGA, AGA, and LGA infants.
European journal of pediatrics, 185(5):.
UNLABELLED: Birthweight-for-gestational-age influences neonatal physiology and health, yet its role in shaping early gut microbiome development remains insufficiently defined. Small-for-gestational-age (SGA), appropriate-for-gestational-age (AGA), and large-for-gestational-age (LGA) infants may exhibit distinct microbial maturation patterns that could influence later metabolic and developmental outcomes. We conducted a prospective cohort study and enrolled 50 late-preterm and term infants and classified them into SGA (n=18), AGA (n=20), and LGA (n=12). Serial fecal samples were collected at four postnatal time windows (0-14 and 15-80 days). 16S rRNA gene sequencing using Oxford Nanopore MinION characterized microbial composition, diversity, and community networks. Bioinformatic analyses included alpha- and beta-diversity metrics, co-occurrence network analysis, and functional pathway inference using PICRUSt2 mapped to the MetaCyc database. Clinical variables, including feeding pattern and antibiotic exposure, were assessed. Gut microbiome development differed according to birthweight categories. Microbial diversity increased with postnatal age, with SGA infants showing distinct community structures over time. Firmicutes predominated across all groups, while specific taxa exhibited group-specific patterns, including enrichment of Streptococcus spp. in LGA infants and Klebsiella spp. in SGA infants. Co-occurrence network analysis revealed a stable gut microbiota in LGA infants.
CONCLUSION: Birthweight-for-gestational-age status was associated with distinct trajectories of early gut microbial maturation. SGA infants exhibited delayed microbial stabilization and fragmented interaction networks, whereas LGA infants demonstrated relatively early establishment of stable, Streptococcus-enriched communities. These growth-specific microbial patterns may reflect differences in early metabolic programming and highlight the potential importance of tailored microbiome-targeted strategies to optimize neonatal development.
WHAT IS KNOWN: • Abnormal fetal growth is associated with increased neonatal morbidity and long-term metabolic risk. • Early-life gut microbiota play an important role in immune and metabolic development.
WHAT IS NEW: • This longitudinal study demonstrates growth-specific trajectories of early gut microbial maturation among SGA, AGA, and LGA infants born at ≥35-week gestation. • SGA infants exhibit delayed microbial stabilization and fragmented microbial interaction networks, whereas LGA infants show relatively earlier establishment of stable microbial communities.
Additional Links: PMID-42008183
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Citation:
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@article {pmid42008183,
year = {2026},
author = {Hwang, JK and Lim, SM and Kwak, MJ and Kim, SH and Kang, Y and Mustafa, G and Tanpure, RS and Jeon, BH and Hoh, JK and Park, HK},
title = {Distinct early-life gut microbiota patterns across SGA, AGA, and LGA infants.},
journal = {European journal of pediatrics},
volume = {185},
number = {5},
pages = {},
pmid = {42008183},
issn = {1432-1076},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Infant, Newborn ; Prospective Studies ; Female ; Male ; *Infant, Small for Gestational Age/growth & development ; Infant ; *Birth Weight ; Feces/microbiology ; Gestational Age ; RNA, Ribosomal, 16S ; Infant, Large for Gestational Age ; },
abstract = {UNLABELLED: Birthweight-for-gestational-age influences neonatal physiology and health, yet its role in shaping early gut microbiome development remains insufficiently defined. Small-for-gestational-age (SGA), appropriate-for-gestational-age (AGA), and large-for-gestational-age (LGA) infants may exhibit distinct microbial maturation patterns that could influence later metabolic and developmental outcomes. We conducted a prospective cohort study and enrolled 50 late-preterm and term infants and classified them into SGA (n=18), AGA (n=20), and LGA (n=12). Serial fecal samples were collected at four postnatal time windows (0-14 and 15-80 days). 16S rRNA gene sequencing using Oxford Nanopore MinION characterized microbial composition, diversity, and community networks. Bioinformatic analyses included alpha- and beta-diversity metrics, co-occurrence network analysis, and functional pathway inference using PICRUSt2 mapped to the MetaCyc database. Clinical variables, including feeding pattern and antibiotic exposure, were assessed. Gut microbiome development differed according to birthweight categories. Microbial diversity increased with postnatal age, with SGA infants showing distinct community structures over time. Firmicutes predominated across all groups, while specific taxa exhibited group-specific patterns, including enrichment of Streptococcus spp. in LGA infants and Klebsiella spp. in SGA infants. Co-occurrence network analysis revealed a stable gut microbiota in LGA infants.
CONCLUSION: Birthweight-for-gestational-age status was associated with distinct trajectories of early gut microbial maturation. SGA infants exhibited delayed microbial stabilization and fragmented interaction networks, whereas LGA infants demonstrated relatively early establishment of stable, Streptococcus-enriched communities. These growth-specific microbial patterns may reflect differences in early metabolic programming and highlight the potential importance of tailored microbiome-targeted strategies to optimize neonatal development.
WHAT IS KNOWN: • Abnormal fetal growth is associated with increased neonatal morbidity and long-term metabolic risk. • Early-life gut microbiota play an important role in immune and metabolic development.
WHAT IS NEW: • This longitudinal study demonstrates growth-specific trajectories of early gut microbial maturation among SGA, AGA, and LGA infants born at ≥35-week gestation. • SGA infants exhibit delayed microbial stabilization and fragmented microbial interaction networks, whereas LGA infants show relatively earlier establishment of stable microbial communities.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
Infant, Newborn
Prospective Studies
Female
Male
*Infant, Small for Gestational Age/growth & development
Infant
*Birth Weight
Feces/microbiology
Gestational Age
RNA, Ribosomal, 16S
Infant, Large for Gestational Age
RevDate: 2026-04-21
Sympathetic denervation alters pulmonary microbiota diversity and composition in mice.
International microbiology : the official journal of the Spanish Society for Microbiology [Epub ahead of print].
Additional Links: PMID-42008215
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Citation:
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@article {pmid42008215,
year = {2026},
author = {Zhang, J and Yang, X and Xie, L and Liu, Q and Zhang, X},
title = {Sympathetic denervation alters pulmonary microbiota diversity and composition in mice.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42008215},
issn = {1618-1905},
support = {SBGJ202103001//Health Commission of Henan Province/ ; },
}
RevDate: 2026-04-21
Fecal Microbiota Transplant and Multidrug-Resistant Organism Decolonization in Gastrointestinal Disease: A Randomized Clinical Trial.
JAMA internal medicine [Epub ahead of print].
IMPORTANCE: Gut colonization by multidrug-resistant organisms (MDROs) is a risk factor for infection with these pathogens. There are no approved therapeutic interventions to combat it.
OBJECTIVE: To assess the efficacy of fecal microbiota transplant (FMT) in causing MDRO decolonization and decreasing antimicrobial resistance (AMR) genes and its impact on gut microbiome, virome, and mycobiome composition in patients with gastrointestinal (GI) diseases.
This randomized, double-blind, sham-controlled clinical trial was conducted in a gastroenterology ward and intensive care unit at a tertiary care center in India. Participants were patients with GI diseases with persistent MDRO colonization. Patient recruitment occurred from July 2022 to June 2024, with follow-up completed in July 2024. Data were analyzed from October 1, 2024, to April 25, 2025.
INTERVENTION: FMT via colonoscopy or sham intervention (sigmoidoscopy with saline injection).
MAIN OUTCOMES AND MEASURES: Co-primary outcomes were MDRO decolonization rate and decrease in antimicrobial resistance genes (AMR) at 4 weeks after the intervention. Secondary outcomes included changes in stool microbiome (16S ribosomal RNA amplicon sequencing), virome (viruslike particles shotgun sequencing), and mycobiome (ITS2 sequencing); incidence of MDRO infections; and adverse events within 4 weeks.
RESULTS: Of 114 randomized patients (mean [SD] age, 40.6 [12.5] years; 80 [70.2%] male; 52 patients [45.6%] with pancreatitis; 43 patients [37.7%] with cirrhosis; 19 patients [16.7%] with other GI disorders), 58 received FMT and 56 received the sham intervention. Most patients were colonized with carbapenem-resistant Enterobacteriaceae or extended-spectrum β-lactamase-producing Enterobacteriaceae at baseline (55 patients [94.8%] in the FMT group and 56 patients [100%] in the sham group). Five patients (2 in the FMT group, 3 in the sham group) were lost to follow-up. Intention-to-treat analysis showed no significant differences in MDRO decolonization (18 patients [31.0%] in the FMT group vs 17 patients [30.4%] in the sham group; absolute difference, 0.6% [95% CI, -16.2% to 17.6%]; P = .94) or AMR genes (median [IQR], 2.5 [1.2 to 3.0] genes in the FMT group vs 2.0 [1.0 to 3.0] genes in the sham group; P = .68), with comparable adverse events. Among 71 patients who underwent 16S ribosomal RNA gene sequencing at 4 to 6 weeks after the intervention, enrichment of bacteria capable of producing short-chain fatty acids was observed in the FMT group. These microbial alterations were not observed in the sham group. However, viral diversity remained unchanged after FMT. Mycobiome analysis revealed that FMT induced only modest, transient alterations in the gut mycobiome.
CONCLUSIONS AND RELEVANCE: This randomized clinical trial found that while a single session of FMT did not significantly enhance MDRO decolonization or decrease AMR genes in patients with GI diseases, it modulated gut microbiome diversity and composition.
TRIAL REGISTRATION: Clinical Trials Registry-India Registration No. 2022/07/043847.
Additional Links: PMID-42008253
PubMed:
Citation:
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@article {pmid42008253,
year = {2026},
author = {Narang, H and Talukdar, D and Kumar, B and Mathur, P and Ningombam, A and Singh, M and Bajaj, A and Markandey, M and Kalaivani, M and Verma, M and Kaur, M and Bakshi, S and Jana, P and Jamdhade, M and Bhardwaj, N and Puraswani, M and Ashita, and Ahmed, N and Goyal, MK and Mubbunu, M and Thomas, DM and Mundhra, S and Prasad, S and Garg, R and Gupta, A and Shalimar, and Gunjan, D and Mahapatra, SJ and Agarwal, S and Saraya, A and Garg, P and Makharia, G and Kedia, S and Das, B and Ahuja, V},
title = {Fecal Microbiota Transplant and Multidrug-Resistant Organism Decolonization in Gastrointestinal Disease: A Randomized Clinical Trial.},
journal = {JAMA internal medicine},
volume = {},
number = {},
pages = {},
pmid = {42008253},
issn = {2168-6114},
abstract = {IMPORTANCE: Gut colonization by multidrug-resistant organisms (MDROs) is a risk factor for infection with these pathogens. There are no approved therapeutic interventions to combat it.
OBJECTIVE: To assess the efficacy of fecal microbiota transplant (FMT) in causing MDRO decolonization and decreasing antimicrobial resistance (AMR) genes and its impact on gut microbiome, virome, and mycobiome composition in patients with gastrointestinal (GI) diseases.
This randomized, double-blind, sham-controlled clinical trial was conducted in a gastroenterology ward and intensive care unit at a tertiary care center in India. Participants were patients with GI diseases with persistent MDRO colonization. Patient recruitment occurred from July 2022 to June 2024, with follow-up completed in July 2024. Data were analyzed from October 1, 2024, to April 25, 2025.
INTERVENTION: FMT via colonoscopy or sham intervention (sigmoidoscopy with saline injection).
MAIN OUTCOMES AND MEASURES: Co-primary outcomes were MDRO decolonization rate and decrease in antimicrobial resistance genes (AMR) at 4 weeks after the intervention. Secondary outcomes included changes in stool microbiome (16S ribosomal RNA amplicon sequencing), virome (viruslike particles shotgun sequencing), and mycobiome (ITS2 sequencing); incidence of MDRO infections; and adverse events within 4 weeks.
RESULTS: Of 114 randomized patients (mean [SD] age, 40.6 [12.5] years; 80 [70.2%] male; 52 patients [45.6%] with pancreatitis; 43 patients [37.7%] with cirrhosis; 19 patients [16.7%] with other GI disorders), 58 received FMT and 56 received the sham intervention. Most patients were colonized with carbapenem-resistant Enterobacteriaceae or extended-spectrum β-lactamase-producing Enterobacteriaceae at baseline (55 patients [94.8%] in the FMT group and 56 patients [100%] in the sham group). Five patients (2 in the FMT group, 3 in the sham group) were lost to follow-up. Intention-to-treat analysis showed no significant differences in MDRO decolonization (18 patients [31.0%] in the FMT group vs 17 patients [30.4%] in the sham group; absolute difference, 0.6% [95% CI, -16.2% to 17.6%]; P = .94) or AMR genes (median [IQR], 2.5 [1.2 to 3.0] genes in the FMT group vs 2.0 [1.0 to 3.0] genes in the sham group; P = .68), with comparable adverse events. Among 71 patients who underwent 16S ribosomal RNA gene sequencing at 4 to 6 weeks after the intervention, enrichment of bacteria capable of producing short-chain fatty acids was observed in the FMT group. These microbial alterations were not observed in the sham group. However, viral diversity remained unchanged after FMT. Mycobiome analysis revealed that FMT induced only modest, transient alterations in the gut mycobiome.
CONCLUSIONS AND RELEVANCE: This randomized clinical trial found that while a single session of FMT did not significantly enhance MDRO decolonization or decrease AMR genes in patients with GI diseases, it modulated gut microbiome diversity and composition.
TRIAL REGISTRATION: Clinical Trials Registry-India Registration No. 2022/07/043847.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Gut site and sex-specific enrichment of bacterial taxa and predicted metabolic pathways in wild American black bear (Ursus americanus).
PloS one, 21(4):e0345317.
American black bears' (Ursus americanus) omnivorous feeding strategy, simple gut morphology, and rapid transit time prevent regulation of the gut microbiome (GMB). We analyzed stable isotopes and 16S rRNA sequences from 48 wild bears to assess the impacts of diet, age, gut site, and sex on GMB composition and PICRUSt2-predicted functional pathways. While alpha and beta diversity did not differ, we identified bacterial taxa and predicted pathways enriched based on gut site and sex. Enterococcus, Incertae, Papillibacter, and Shuttleworthia were enriched in jejunum samples (linear discriminant analysis effect size ≥ 3.5, p = 0.0374); and 6 genera drove colonic Bray-Curtis distances (SIMPER): Weisella (p = 0.0099), Anaeroplasma (p = 0.0495), Megamonas (p = 0.0099), Cellulosilyticum (p = 0.0495), Escherichia-Shigella (p = 0.0396) and Ochrobactrum (p = 0.0297). EdgeR identified isoflavonoid biosynthesis (p-adj = 0.001) and isoterpenoid biosynthesis (p-adj = 0.006) enriched in the colon, and SNARE interaction in vesicular transport (p-adj = 0.000) and secondary bile acid synthesis (p-adj = 0.005) enriched in females. Our findings provide nuanced insights to specific taxa and putative metabolic pathways that reflect sex and gut site differences in black bears, with important implications for understanding bear physiology and informing wildlife management.
Additional Links: PMID-42008544
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Citation:
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@article {pmid42008544,
year = {2026},
author = {McKenney, EA and De Jesus, E and Hatfield, T and Hayes, D and Holder, K and Ivarsson, C and Morais, N and Payne, H and Simpson, K and Staal, AM and Thompson, H and Hildreth, R and Olfenbuttel, C and Lafferty, DJR},
title = {Gut site and sex-specific enrichment of bacterial taxa and predicted metabolic pathways in wild American black bear (Ursus americanus).},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0345317},
pmid = {42008544},
issn = {1932-6203},
mesh = {Animals ; *Ursidae/microbiology/metabolism ; *Gastrointestinal Microbiome ; Female ; Male ; *Bacteria/genetics/classification ; RNA, Ribosomal, 16S/genetics ; *Metabolic Networks and Pathways ; Sex Factors ; Animals, Wild/microbiology ; },
abstract = {American black bears' (Ursus americanus) omnivorous feeding strategy, simple gut morphology, and rapid transit time prevent regulation of the gut microbiome (GMB). We analyzed stable isotopes and 16S rRNA sequences from 48 wild bears to assess the impacts of diet, age, gut site, and sex on GMB composition and PICRUSt2-predicted functional pathways. While alpha and beta diversity did not differ, we identified bacterial taxa and predicted pathways enriched based on gut site and sex. Enterococcus, Incertae, Papillibacter, and Shuttleworthia were enriched in jejunum samples (linear discriminant analysis effect size ≥ 3.5, p = 0.0374); and 6 genera drove colonic Bray-Curtis distances (SIMPER): Weisella (p = 0.0099), Anaeroplasma (p = 0.0495), Megamonas (p = 0.0099), Cellulosilyticum (p = 0.0495), Escherichia-Shigella (p = 0.0396) and Ochrobactrum (p = 0.0297). EdgeR identified isoflavonoid biosynthesis (p-adj = 0.001) and isoterpenoid biosynthesis (p-adj = 0.006) enriched in the colon, and SNARE interaction in vesicular transport (p-adj = 0.000) and secondary bile acid synthesis (p-adj = 0.005) enriched in females. Our findings provide nuanced insights to specific taxa and putative metabolic pathways that reflect sex and gut site differences in black bears, with important implications for understanding bear physiology and informing wildlife management.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Ursidae/microbiology/metabolism
*Gastrointestinal Microbiome
Female
Male
*Bacteria/genetics/classification
RNA, Ribosomal, 16S/genetics
*Metabolic Networks and Pathways
Sex Factors
Animals, Wild/microbiology
RevDate: 2026-04-20
Domestic travel as a driver for the dissemination of mcr-1 in healthy travelers in China: a prospective, genomic epidemiological and gut microbiome study.
Antimicrobial agents and chemotherapy [Epub ahead of print].
The global spread of plasmid-mediated colistin resistance gene mcr-1 poses a significant threat to public health. Although international travel is a known driver of antimicrobial resistance, the role of domestic travel in high-prevalence settings remains unclear. We conducted a prospective cohort study of 81 healthy volunteers traveling in China (June-September 2022). Fecal samples collected before and after travel were screened for mcr-1-positive Escherichia coli (MCRPEC). Antimicrobial resistance genes (ARGs), virulence factors (VFs), plasmid replicons, and gut microbial dynamics were investigated using whole-genome sequencing and 16S rRNA sequencing. Risk factors were analyzed using logistic regression analysis. Of the 81 participants who were negative for mcr-1 at baseline, 12 (14.8%) acquired mcr-1 after travel. Acquisition was associated with residence near poultry farms (odds ratio [OR] = 5.9, P = 0.04) and diarrhea during travel (OR = 11.22, P = 0.027). MCRPEC exhibited marked genetic diversity comprising 10 sequence types and the carriage of additional 23 ARGs and nine adherence-associated VFs. mcr-1 was located on IncI2, IncX4, IncHI2, or IncP plasmids, with 91.7% (n = 11) transferable in conjugation assays. Gut microbiome analysis showed increased α-diversity, but a stable community structure, indicating colonization without major disruption. Our study demonstrated that domestic travel in China substantially contributes to the dissemination of mcr-1. Poultry exposure and gastrointestinal disturbances are key risk factors. Genetic diversity, plasmid transferability, and co-carriage of resistance and virulence determinants highlight the risk of onward spread. Antimicrobial resistance surveillance should extend beyond international travel and incorporate domestic mobility within a "One Health" framework.
Additional Links: PMID-42008653
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@article {pmid42008653,
year = {2026},
author = {Wu, M and Chen, Y and Su, M and Wu, H and Luo, L and Ao, X and Zhao, C and Shui, J and Wen, S and Lin, J and Pu, J and Zeng, J and Jiang, Y and Ng, H and Zhang, Z and Hu, M and Huang, B and Xu, L and Chen, C and Shen, C},
title = {Domestic travel as a driver for the dissemination of mcr-1 in healthy travelers in China: a prospective, genomic epidemiological and gut microbiome study.},
journal = {Antimicrobial agents and chemotherapy},
volume = {},
number = {},
pages = {e0174625},
doi = {10.1128/aac.01746-25},
pmid = {42008653},
issn = {1098-6596},
abstract = {The global spread of plasmid-mediated colistin resistance gene mcr-1 poses a significant threat to public health. Although international travel is a known driver of antimicrobial resistance, the role of domestic travel in high-prevalence settings remains unclear. We conducted a prospective cohort study of 81 healthy volunteers traveling in China (June-September 2022). Fecal samples collected before and after travel were screened for mcr-1-positive Escherichia coli (MCRPEC). Antimicrobial resistance genes (ARGs), virulence factors (VFs), plasmid replicons, and gut microbial dynamics were investigated using whole-genome sequencing and 16S rRNA sequencing. Risk factors were analyzed using logistic regression analysis. Of the 81 participants who were negative for mcr-1 at baseline, 12 (14.8%) acquired mcr-1 after travel. Acquisition was associated with residence near poultry farms (odds ratio [OR] = 5.9, P = 0.04) and diarrhea during travel (OR = 11.22, P = 0.027). MCRPEC exhibited marked genetic diversity comprising 10 sequence types and the carriage of additional 23 ARGs and nine adherence-associated VFs. mcr-1 was located on IncI2, IncX4, IncHI2, or IncP plasmids, with 91.7% (n = 11) transferable in conjugation assays. Gut microbiome analysis showed increased α-diversity, but a stable community structure, indicating colonization without major disruption. Our study demonstrated that domestic travel in China substantially contributes to the dissemination of mcr-1. Poultry exposure and gastrointestinal disturbances are key risk factors. Genetic diversity, plasmid transferability, and co-carriage of resistance and virulence determinants highlight the risk of onward spread. Antimicrobial resistance surveillance should extend beyond international travel and incorporate domestic mobility within a "One Health" framework.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Connecting habitats, boosting disease resistance: Spatial connectivity enhances amphibian microbiome defenses against fungal pathogen.
Proceedings of the National Academy of Sciences of the United States of America, 123(17):e2520745123.
Disruption of habitat connectivity alters host movement patterns and pathogen exposure in wildlife. Changes in exposure dynamics have led to increased research interest in host-associated microbial communities (i.e., microbiomes), particularly in how repeated encounters with pathogens may drive microbial filtering processes that favor the assembly of pathogen-inhibiting microbiomes, a concept known as the adaptive microbiome principle. Understanding how habitat connectivity and pathogen exposure shape adaptive microbiomes remains a key frontier in disease ecology. For widely distributed waterborne pathogens such as the amphibian chytrid fungus Batrachochytrium dendrobatidis (Bd), sustained host exposure in contiguous terrestrial-aquatic habitats may promote selection of microbiomes with enhanced antifungal properties. In contrast, under conditions of high habitat split, where key habitats such as forests and water bodies are spatially disconnected, limited exposure to Bd during the pre-tbreeding and overwintering seasons may hinder the selection of Bd-inhibitory microbiomes that are critical for host protection during the subsequent breeding season, when pathogen exposure in water bodies is at its peak. Our results demonstrate that habitat split may limit recruitment of putative Bd-inhibitory skin bacteria, while Bd loads increase with habitat split for certain amphibian species. Results from Joint Species Distribution Models also indicate that habitat split is a key driver of reduced skin bacterial diversity, even after accounting for biotic and abiotic metrics. Our study provides evidence that spatial connectivity among natural habitats is essential for maintaining multiple levels of biodiversity, from host species to their associated functional microbiomes, highlighting a critical link between environmental disturbance, microbial defenses, and disease dynamics.
Additional Links: PMID-42008677
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@article {pmid42008677,
year = {2026},
author = {Medina, D and Martins, RA and Prist, PR and Buttimer, S and Neely, WJ and Schuck, LK and Greenspan, SE and Lyra, ML and Kearns, PJ and Woodhams, DC and Bletz, MC and São-Pedro, VA and Haddad, CFB and Becker, CG},
title = {Connecting habitats, boosting disease resistance: Spatial connectivity enhances amphibian microbiome defenses against fungal pathogen.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {17},
pages = {e2520745123},
doi = {10.1073/pnas.2520745123},
pmid = {42008677},
issn = {1091-6490},
support = {IOS-1947681 DEB-2227340 DEB-2413542 BII-2120084//NSF (NSF)/ ; 2021/10639-5//Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)/ ; IOS-1845634 and BII 2120084//NSF (NSF)/ ; },
mesh = {Animals ; *Batrachochytrium/pathogenicity ; *Microbiota ; *Ecosystem ; *Amphibians/microbiology ; *Disease Resistance ; *Mycoses/microbiology/veterinary ; Host-Pathogen Interactions ; Chytridiomycota ; },
abstract = {Disruption of habitat connectivity alters host movement patterns and pathogen exposure in wildlife. Changes in exposure dynamics have led to increased research interest in host-associated microbial communities (i.e., microbiomes), particularly in how repeated encounters with pathogens may drive microbial filtering processes that favor the assembly of pathogen-inhibiting microbiomes, a concept known as the adaptive microbiome principle. Understanding how habitat connectivity and pathogen exposure shape adaptive microbiomes remains a key frontier in disease ecology. For widely distributed waterborne pathogens such as the amphibian chytrid fungus Batrachochytrium dendrobatidis (Bd), sustained host exposure in contiguous terrestrial-aquatic habitats may promote selection of microbiomes with enhanced antifungal properties. In contrast, under conditions of high habitat split, where key habitats such as forests and water bodies are spatially disconnected, limited exposure to Bd during the pre-tbreeding and overwintering seasons may hinder the selection of Bd-inhibitory microbiomes that are critical for host protection during the subsequent breeding season, when pathogen exposure in water bodies is at its peak. Our results demonstrate that habitat split may limit recruitment of putative Bd-inhibitory skin bacteria, while Bd loads increase with habitat split for certain amphibian species. Results from Joint Species Distribution Models also indicate that habitat split is a key driver of reduced skin bacterial diversity, even after accounting for biotic and abiotic metrics. Our study provides evidence that spatial connectivity among natural habitats is essential for maintaining multiple levels of biodiversity, from host species to their associated functional microbiomes, highlighting a critical link between environmental disturbance, microbial defenses, and disease dynamics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Batrachochytrium/pathogenicity
*Microbiota
*Ecosystem
*Amphibians/microbiology
*Disease Resistance
*Mycoses/microbiology/veterinary
Host-Pathogen Interactions
Chytridiomycota
RevDate: 2026-04-20
CmpDate: 2026-04-21
Cancer epigenetics: unraveling etiology and mechanisms to advance prevention.
Journal of the National Cancer Institute. Monographs, 2026(72):44-58.
The increased understanding of epigenetics has significantly advanced our understanding of cancer development, especially regarding environmental, occupational, and lifestyle exposures. Unlike genetic mutations, epigenetic changes may be reversible, making them critical mediators and promising targets for cancer prevention and control. This review synthesizes two decades of transformative research by the International Agency for Research on Cancer (IARC), which positioned the epigenome as a central focus in cancer epidemiology and mechanistic research among the 10 Key Characteristics (KCs) of carcinogens by the IARC Monographs program. From foundational in vitro and animal studies to large-scale population-based research, IARC researchers contributed to unraveling epigenetic mechanisms of carcinogenesis and identifying epigenetic biomarkers of exposures and cancer risk. We highlight progress in epigenetic biomarker development, mechanistic epigenomics, toxico-epigenomics, and the interplay between diet, microbiome, and epigenome. As IARC marks its 60th anniversary, this review underscores the growing role of epigenetics in guiding global cancer prevention efforts and public health strategies.
Additional Links: PMID-42008732
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PubMed:
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@article {pmid42008732,
year = {2026},
author = {Herceg, Z and Ghantous, A and Gheit, T and Rahman Talukdar, F and Matar, C and Chung, F and Korenjak, M and Zavadil, J and Ribeiro Pinto, LF and Fry, RC and Khoueiry, R},
title = {Cancer epigenetics: unraveling etiology and mechanisms to advance prevention.},
journal = {Journal of the National Cancer Institute. Monographs},
volume = {2026},
number = {72},
pages = {44-58},
doi = {10.1093/jncimonographs/lgaf044},
pmid = {42008732},
issn = {1745-6614},
mesh = {Humans ; *Neoplasms/prevention & control/genetics/etiology/epidemiology ; *Epigenesis, Genetic ; *Epigenomics/methods ; Animals ; Biomarkers, Tumor/genetics ; },
abstract = {The increased understanding of epigenetics has significantly advanced our understanding of cancer development, especially regarding environmental, occupational, and lifestyle exposures. Unlike genetic mutations, epigenetic changes may be reversible, making them critical mediators and promising targets for cancer prevention and control. This review synthesizes two decades of transformative research by the International Agency for Research on Cancer (IARC), which positioned the epigenome as a central focus in cancer epidemiology and mechanistic research among the 10 Key Characteristics (KCs) of carcinogens by the IARC Monographs program. From foundational in vitro and animal studies to large-scale population-based research, IARC researchers contributed to unraveling epigenetic mechanisms of carcinogenesis and identifying epigenetic biomarkers of exposures and cancer risk. We highlight progress in epigenetic biomarker development, mechanistic epigenomics, toxico-epigenomics, and the interplay between diet, microbiome, and epigenome. As IARC marks its 60th anniversary, this review underscores the growing role of epigenetics in guiding global cancer prevention efforts and public health strategies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Neoplasms/prevention & control/genetics/etiology/epidemiology
*Epigenesis, Genetic
*Epigenomics/methods
Animals
Biomarkers, Tumor/genetics
RevDate: 2026-04-21
CmpDate: 2026-04-21
Intrahepatic cholestasis of pregnancy in Chile: Analysis of epidemiological change and a microbiological hypothesis.
Medwave, 26(3):e3161.
Intrahepatic cholestasis of pregnancy is a gestational pathology with an unusual epidemiological and pathophysiological behavior that remains partially unexplained. Its current global incidence ranges from 0.1% to 2%. However, in Chile, the incidence reached up to 15% in the 1970s, with a marked decrease over subsequent decades, being nowadays about 1 to 2%. The reasons for this historical change are not fully understood. A literature-based analysis was conducted, focusing on clinical, microbiological, and epidemiological studies on intrahepatic cholestasis and other hepatobiliary diseases. The aim of this was to explore existing evidence and to propose a microbiological hypothesis that could help explain the epidemiological transition observed in Chile. Notably, the temporal reduction in incidence paralleled a nationwide decline in biliary disease and typhoid fever. We hypothesize that the eradication or significant reduction of certain pathogens, such as Typhi, may have contributed to the normalization of intrahepatic cholestasis of pregnancy rates in Chile.
Additional Links: PMID-42008798
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@article {pmid42008798,
year = {2026},
author = {Contreras Vidal, C and Carvajal Cabrera, J},
title = {Intrahepatic cholestasis of pregnancy in Chile: Analysis of epidemiological change and a microbiological hypothesis.},
journal = {Medwave},
volume = {26},
number = {3},
pages = {e3161},
doi = {10.5867/medwave.2026.03.3161},
pmid = {42008798},
issn = {0717-6384},
mesh = {Humans ; Pregnancy ; Chile/epidemiology ; *Cholestasis, Intrahepatic/epidemiology/microbiology ; Female ; *Pregnancy Complications/epidemiology/microbiology ; Incidence ; Typhoid Fever/epidemiology ; Pregnancy Complications, Infectious/epidemiology/microbiology ; },
abstract = {Intrahepatic cholestasis of pregnancy is a gestational pathology with an unusual epidemiological and pathophysiological behavior that remains partially unexplained. Its current global incidence ranges from 0.1% to 2%. However, in Chile, the incidence reached up to 15% in the 1970s, with a marked decrease over subsequent decades, being nowadays about 1 to 2%. The reasons for this historical change are not fully understood. A literature-based analysis was conducted, focusing on clinical, microbiological, and epidemiological studies on intrahepatic cholestasis and other hepatobiliary diseases. The aim of this was to explore existing evidence and to propose a microbiological hypothesis that could help explain the epidemiological transition observed in Chile. Notably, the temporal reduction in incidence paralleled a nationwide decline in biliary disease and typhoid fever. We hypothesize that the eradication or significant reduction of certain pathogens, such as Typhi, may have contributed to the normalization of intrahepatic cholestasis of pregnancy rates in Chile.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Pregnancy
Chile/epidemiology
*Cholestasis, Intrahepatic/epidemiology/microbiology
Female
*Pregnancy Complications/epidemiology/microbiology
Incidence
Typhoid Fever/epidemiology
Pregnancy Complications, Infectious/epidemiology/microbiology
RevDate: 2026-04-20
Advancing precision medicine in pancreatic cancer using novel biomarkers and clinical targets.
Molecular aspects of medicine, 109:101476 pii:S0098-2997(26)00032-4 [Epub ahead of print].
Precision-guided therapy is imperative in the battle against pancreatic ductal adenocarcinoma (PDAC), one of the most lethal solid malignancies with limited improvements in survival despite advances in molecular profiling and systemic therapy. While oncogenic drivers such as KRAS, TP53, CDKN2A, and SMAD4 are nearly ubiquitous, their translation into effective targeted therapies has been constrained by profound tumor heterogeneity, a therapy-resistant tumor microenvironment (TME), and a paucity of predictive biomarkers. In parallel, clinical outcomes are increasingly shaped by extrinsic modifiers, including metabolic disease, chronic inflammation, and microbiome dysregulation, which remain under-integrated into current treatment paradigms. Recent progress in precision oncology has enabled regulatory approval of biomarker-defined therapies for select PDAC subsets, including immune checkpoint inhibitors for mismatch repair-deficient tumors, PARP inhibitors for BRCA1/2-mutant disease, and combination cytotoxic regimens such as NALIRIFOX in the metastatic setting. However, these advances benefit only a minority of patients, underscoring the urgent need for improved patient stratification and rational combination strategies. Emerging clinical and translational studies highlight the promise of integrating multi-omic profiling, liquid biopsies, functional precision models (organoids and patient-derived xenografts), and artificial intelligence-driven analytics to uncover actionable vulnerabilities, monitor response, and guide adaptive trial design. In this review, we critically evaluate the clinical relevance of molecular, metabolic, and microenvironmental determinants of PDAC progression and therapeutic resistance. We focus on translational bottlenecks that have limited clinical success to date and highlight biomarker-driven strategies, ongoing clinical trials, and emerging technologies poised to shift treatment from uniform algorithms toward biologically informed, patient-specific therapeutic approaches in pancreatic cancer.
Additional Links: PMID-42008879
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PubMed:
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@article {pmid42008879,
year = {2026},
author = {Murthy, D and Seyhan, AA and den Hollander, P and Lu, S and Kuburich, NA and Gould, C and Karam, AA and Sun, K and Schupp, PG and Safran, H and Kurzrock, R and El-Deiry, W and Mani, SA},
title = {Advancing precision medicine in pancreatic cancer using novel biomarkers and clinical targets.},
journal = {Molecular aspects of medicine},
volume = {109},
number = {},
pages = {101476},
doi = {10.1016/j.mam.2026.101476},
pmid = {42008879},
issn = {1872-9452},
abstract = {Precision-guided therapy is imperative in the battle against pancreatic ductal adenocarcinoma (PDAC), one of the most lethal solid malignancies with limited improvements in survival despite advances in molecular profiling and systemic therapy. While oncogenic drivers such as KRAS, TP53, CDKN2A, and SMAD4 are nearly ubiquitous, their translation into effective targeted therapies has been constrained by profound tumor heterogeneity, a therapy-resistant tumor microenvironment (TME), and a paucity of predictive biomarkers. In parallel, clinical outcomes are increasingly shaped by extrinsic modifiers, including metabolic disease, chronic inflammation, and microbiome dysregulation, which remain under-integrated into current treatment paradigms. Recent progress in precision oncology has enabled regulatory approval of biomarker-defined therapies for select PDAC subsets, including immune checkpoint inhibitors for mismatch repair-deficient tumors, PARP inhibitors for BRCA1/2-mutant disease, and combination cytotoxic regimens such as NALIRIFOX in the metastatic setting. However, these advances benefit only a minority of patients, underscoring the urgent need for improved patient stratification and rational combination strategies. Emerging clinical and translational studies highlight the promise of integrating multi-omic profiling, liquid biopsies, functional precision models (organoids and patient-derived xenografts), and artificial intelligence-driven analytics to uncover actionable vulnerabilities, monitor response, and guide adaptive trial design. In this review, we critically evaluate the clinical relevance of molecular, metabolic, and microenvironmental determinants of PDAC progression and therapeutic resistance. We focus on translational bottlenecks that have limited clinical success to date and highlight biomarker-driven strategies, ongoing clinical trials, and emerging technologies poised to shift treatment from uniform algorithms toward biologically informed, patient-specific therapeutic approaches in pancreatic cancer.},
}
RevDate: 2026-04-20
Chronic Inflammation in Virus-suppressed People Living with Human Immunodeficiency Virus Infection: A Microbiology-oriented Perspective on Gut Barrier Failure, Microbial Translocation, and Immune Activation.
Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy pii:S1341-321X(26)00070-X [Epub ahead of print].
Potent antiretroviral therapy (ART) has transformed human immunodeficiency virus (HIV) infection into a chronic manageable condition; however, many people living with HIV (PLWH) exhibit persistent immune activation and inflammation despite long-term virological suppression. Residual inflammation is strongly associated with an increased risk of cardiovascular disease, chronic kidney disease, metabolic dysfunction-associated steatotic liver disease, cancer, and neurocognitive impairment. This review summarizes the current evidence on the microbiology-oriented mechanisms that sustain this state. We first outline a multifactorial network in which incomplete repair of intestinal mucosal damage, dysbiosis, reduced short-chain fatty acid production, and disturbed bile acid metabolism generate a patchy "leaky gut." Continuous translocation of bacterial lipopolysaccharide, fungal β-D-glucan, and other microbial products activates monocyte-macrophage and portal-liver inflammatory circuits. These inputs interact with intermittent HIV antigen expression from latent reservoirs, inflammatory cell death, chronic coinfections, lymphoid tissue fibrosis, mitochondrial dysfunction, and traditional lifestyle-related risk factors. Together, they establish a self-reinforcing gut-liver-immune axis that maintains low-grade inflammation and a procoagulant milieu under viral suppression. We then link these mechanisms to organ-specific complications and review the intervention data, focusing on early ART initiation, statin therapy, and cotrimoxazole prophylaxis as a proof-of-concept that modifying inflammatory and mucosal pressures can improve outcomes. Finally, we highlight research priorities and argue that the effective prevention of long-term complications in virally suppressed PLWH requires combination strategies targeting multiple nodes of this network, with particular attention to gut barrier repair and microbiome modulation.
Additional Links: PMID-42009106
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Citation:
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@article {pmid42009106,
year = {2026},
author = {Yoshino, Y and Kimura, Y and Ito, F},
title = {Chronic Inflammation in Virus-suppressed People Living with Human Immunodeficiency Virus Infection: A Microbiology-oriented Perspective on Gut Barrier Failure, Microbial Translocation, and Immune Activation.},
journal = {Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy},
volume = {},
number = {},
pages = {102972},
doi = {10.1016/j.jiac.2026.102972},
pmid = {42009106},
issn = {1437-7780},
abstract = {Potent antiretroviral therapy (ART) has transformed human immunodeficiency virus (HIV) infection into a chronic manageable condition; however, many people living with HIV (PLWH) exhibit persistent immune activation and inflammation despite long-term virological suppression. Residual inflammation is strongly associated with an increased risk of cardiovascular disease, chronic kidney disease, metabolic dysfunction-associated steatotic liver disease, cancer, and neurocognitive impairment. This review summarizes the current evidence on the microbiology-oriented mechanisms that sustain this state. We first outline a multifactorial network in which incomplete repair of intestinal mucosal damage, dysbiosis, reduced short-chain fatty acid production, and disturbed bile acid metabolism generate a patchy "leaky gut." Continuous translocation of bacterial lipopolysaccharide, fungal β-D-glucan, and other microbial products activates monocyte-macrophage and portal-liver inflammatory circuits. These inputs interact with intermittent HIV antigen expression from latent reservoirs, inflammatory cell death, chronic coinfections, lymphoid tissue fibrosis, mitochondrial dysfunction, and traditional lifestyle-related risk factors. Together, they establish a self-reinforcing gut-liver-immune axis that maintains low-grade inflammation and a procoagulant milieu under viral suppression. We then link these mechanisms to organ-specific complications and review the intervention data, focusing on early ART initiation, statin therapy, and cotrimoxazole prophylaxis as a proof-of-concept that modifying inflammatory and mucosal pressures can improve outcomes. Finally, we highlight research priorities and argue that the effective prevention of long-term complications in virally suppressed PLWH requires combination strategies targeting multiple nodes of this network, with particular attention to gut barrier repair and microbiome modulation.},
}
RevDate: 2026-04-20
Emerging biomarkers for early detection of colorectal cancer.
Clinica chimica acta; international journal of clinical chemistry pii:S0009-8981(26)00195-6 [Epub ahead of print].
The worldwide impact of colorectal cancer (CRC) as a primary cause of cancer-related morbidity and mortality demonstrates the urgent need for better early detection methods and personalized treatment approaches. While colonoscopy and fecal tests have contributed to reduced mortality rates from CRC, they encounter important limitations stemming from their invasive procedures and insufficient sensitivity plus patient adherence issues. Consequently, the latest progress in molecular biology and omics technologies has enabled researchers to identify new biomarkers which present effective solutions for early detection and risk assessment while monitoring treatment efficacy. Therefore, this review explores new developments in CRC biomarker research through the lens of emerging liquid biopsy methods like circulating tumor DNA (ctDNA) and microRNAs (miRNAs) as well as genomic, epigenomic, gut microbiome, metabolomic, and proteomic markers. The usage of biomarker-based methods demonstrates transformative potential for CRC treatment by boosting survival rates and lessening global impact through precision medicine development in oncology.
Additional Links: PMID-42009160
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PubMed:
Citation:
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@article {pmid42009160,
year = {2026},
author = {Qannita, RA and Zenati, RA and Abuhelwa, AY and Alqudah, MAY and Aleidi, SM and El-Huneidi, W and Abu-Gharbieh, E and AlShareef, ZM and Alzoubi, KH and Bustanji, Y and Semreen, MH},
title = {Emerging biomarkers for early detection of colorectal cancer.},
journal = {Clinica chimica acta; international journal of clinical chemistry},
volume = {},
number = {},
pages = {121013},
doi = {10.1016/j.cca.2026.121013},
pmid = {42009160},
issn = {1873-3492},
abstract = {The worldwide impact of colorectal cancer (CRC) as a primary cause of cancer-related morbidity and mortality demonstrates the urgent need for better early detection methods and personalized treatment approaches. While colonoscopy and fecal tests have contributed to reduced mortality rates from CRC, they encounter important limitations stemming from their invasive procedures and insufficient sensitivity plus patient adherence issues. Consequently, the latest progress in molecular biology and omics technologies has enabled researchers to identify new biomarkers which present effective solutions for early detection and risk assessment while monitoring treatment efficacy. Therefore, this review explores new developments in CRC biomarker research through the lens of emerging liquid biopsy methods like circulating tumor DNA (ctDNA) and microRNAs (miRNAs) as well as genomic, epigenomic, gut microbiome, metabolomic, and proteomic markers. The usage of biomarker-based methods demonstrates transformative potential for CRC treatment by boosting survival rates and lessening global impact through precision medicine development in oncology.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Community Turnover and Connectivity at Two Study Sites in the North and Wadden Seas: Dynamics From Hours to Seasons.
Environmental microbiology, 28(4):e70310.
Microbial communities underpin ecosystem processes and biogeochemical cycles in marine ecosystems, yet their spatial and temporal dynamics at hourly scales remain poorly understood. We surveyed two stations from the North Sea (NS) and Wadden Sea (WS), generating six high-frequency time-series datasets across depths and seasons, complemented by sediment cores. Across seasons, the sites in the NS and the WS harbored distinct microbial communities shaped by contrasts in salinity, temperature, and potentially the quantity and lability of organic matter. Connectivity between communities was limited but favoured by known seasonal hydrographic exchanges. Despite taxonomic contrasts between sites, functional turnover remained low, with communities harbouring similar metabolic potential but being adapted to local conditions, suggesting potential functional redundancy. At hourly scales, community turnover was weaker and largely driven by vertical and horizontal mixing between water masses, occasional resuspension from sediments, or a summer bloom from a copiotroph. These shifts were transient and did not disrupt the coupling between taxonomic and functional composition. However, their immediate effects on ecosystem processes, such as organic matter remineralisation and nutrient recycling remain unclear. Continued high-resolution microbiome monitoring, paired with biogeochemical flux measurements, is needed to better predict climate-driven changes in coastal ecosystem functioning.
Additional Links: PMID-42009250
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@article {pmid42009250,
year = {2026},
author = {Ramond, P and de Groot, T and Niemann, H and Engelmann, JC},
title = {Community Turnover and Connectivity at Two Study Sites in the North and Wadden Seas: Dynamics From Hours to Seasons.},
journal = {Environmental microbiology},
volume = {28},
number = {4},
pages = {e70310},
doi = {10.1111/1462-2920.70310},
pmid = {42009250},
issn = {1462-2920},
support = {ERC-CoG-772923/ERC_/European Research Council/International ; //Wise NWO/ ; },
mesh = {Seasons ; *Microbiota ; *Seawater/microbiology ; *Geologic Sediments/microbiology ; North Sea ; Ecosystem ; *Bacteria/classification/genetics/isolation & purification ; Temperature ; Salinity ; Oceans and Seas ; },
abstract = {Microbial communities underpin ecosystem processes and biogeochemical cycles in marine ecosystems, yet their spatial and temporal dynamics at hourly scales remain poorly understood. We surveyed two stations from the North Sea (NS) and Wadden Sea (WS), generating six high-frequency time-series datasets across depths and seasons, complemented by sediment cores. Across seasons, the sites in the NS and the WS harbored distinct microbial communities shaped by contrasts in salinity, temperature, and potentially the quantity and lability of organic matter. Connectivity between communities was limited but favoured by known seasonal hydrographic exchanges. Despite taxonomic contrasts between sites, functional turnover remained low, with communities harbouring similar metabolic potential but being adapted to local conditions, suggesting potential functional redundancy. At hourly scales, community turnover was weaker and largely driven by vertical and horizontal mixing between water masses, occasional resuspension from sediments, or a summer bloom from a copiotroph. These shifts were transient and did not disrupt the coupling between taxonomic and functional composition. However, their immediate effects on ecosystem processes, such as organic matter remineralisation and nutrient recycling remain unclear. Continued high-resolution microbiome monitoring, paired with biogeochemical flux measurements, is needed to better predict climate-driven changes in coastal ecosystem functioning.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Seasons
*Microbiota
*Seawater/microbiology
*Geologic Sediments/microbiology
North Sea
Ecosystem
*Bacteria/classification/genetics/isolation & purification
Temperature
Salinity
Oceans and Seas
RevDate: 2026-04-21
CmpDate: 2026-04-21
Post-Heatwave Coral Health Coincides With Host-Specific Symbiodiniaceae-Bacteria Consortia.
Environmental microbiology, 28(4):e70306.
Coral reefs are facing unprecedented damage due to climate-driven marine heatwaves (MHWs). While coral response to elevated temperatures is inextricably linked to coral-associated microalgae (Symbiodiniaceae) and bacteria, the role of algal-bacterial interactions in affecting coral resilience to thermal stress remains obscure. Here we show coral health indicated by distinct compositions of Symbiodiniaceae-bacteria consortia in two coral species, the massive Porites lutea and the laminar Duncanopsammia peltata, upon exposure to an unusual MHW. P. lutea exhibited thermal resilience by maintaining an obligate partnership with the heat-tolerant Cladocopium C15 under both healthy and bleached states, alongside conservative bacterial community changes between the two states driven primarily by deterministic processes; whereas D. peltata associated with the heat-sensitive Cladocopium C1 in bleached state but the heat-tolerant Durusdinium D1/D4 in healthy state, with stochastically driven, more liberal bacterial community changes between the two states. This distinction between P. lutea and D. peltata in their Symbiodiniaceae-bacteria consortia reflects a specialist/generalist strategy in partner selection given the status of coral health, underscoring an evolutionary trade-off between high-fidelity symbioses for persistence under chronic stress and rapid microbiome turnover for transient bleaching resilience. Broadly, the host-specific, coordinated Symbiodiniaceae-bacteria community differentiation following MHWs, may inform future coral conservation and restoration practises in an era of escalating climate change.
Additional Links: PMID-42009295
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PubMed:
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@article {pmid42009295,
year = {2026},
author = {Zhang, H and Zheng, X and Wang, Q and Zhou, X and Cai, L and Zhan, L and Huang, D and Shi, T},
title = {Post-Heatwave Coral Health Coincides With Host-Specific Symbiodiniaceae-Bacteria Consortia.},
journal = {Environmental microbiology},
volume = {28},
number = {4},
pages = {e70306},
doi = {10.1111/1462-2920.70306},
pmid = {42009295},
issn = {1462-2920},
support = {2022YFC3102003//National Key Research and Development Program of China/ ; 2020YFA0607602//National Key Research and Development Program of China/ ; 2020017//Scientific Research Foundation of the Third Institute of Oceanography, Ministry of Natural Resources of China/ ; 2019017//Scientific Research Foundation of the Third Institute of Oceanography, Ministry of Natural Resources of China/ ; 42376110//National Natural Science Foundation of China/ ; 41876119//National Natural Science Foundation of China/ ; //global Ocean Negative Carbon Emission (ONCE) program/ ; 2023J06043//Science Fund for Distinguished Young Scholars of Fujian Province/ ; },
mesh = {Animals ; *Anthozoa/microbiology/physiology ; Symbiosis ; Coral Reefs ; *Hot Temperature ; *Bacteria/classification/genetics/isolation & purification ; *Dinoflagellida/physiology ; *Microbial Consortia ; Microbiota ; },
abstract = {Coral reefs are facing unprecedented damage due to climate-driven marine heatwaves (MHWs). While coral response to elevated temperatures is inextricably linked to coral-associated microalgae (Symbiodiniaceae) and bacteria, the role of algal-bacterial interactions in affecting coral resilience to thermal stress remains obscure. Here we show coral health indicated by distinct compositions of Symbiodiniaceae-bacteria consortia in two coral species, the massive Porites lutea and the laminar Duncanopsammia peltata, upon exposure to an unusual MHW. P. lutea exhibited thermal resilience by maintaining an obligate partnership with the heat-tolerant Cladocopium C15 under both healthy and bleached states, alongside conservative bacterial community changes between the two states driven primarily by deterministic processes; whereas D. peltata associated with the heat-sensitive Cladocopium C1 in bleached state but the heat-tolerant Durusdinium D1/D4 in healthy state, with stochastically driven, more liberal bacterial community changes between the two states. This distinction between P. lutea and D. peltata in their Symbiodiniaceae-bacteria consortia reflects a specialist/generalist strategy in partner selection given the status of coral health, underscoring an evolutionary trade-off between high-fidelity symbioses for persistence under chronic stress and rapid microbiome turnover for transient bleaching resilience. Broadly, the host-specific, coordinated Symbiodiniaceae-bacteria community differentiation following MHWs, may inform future coral conservation and restoration practises in an era of escalating climate change.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Anthozoa/microbiology/physiology
Symbiosis
Coral Reefs
*Hot Temperature
*Bacteria/classification/genetics/isolation & purification
*Dinoflagellida/physiology
*Microbial Consortia
Microbiota
RevDate: 2026-04-21
CmpDate: 2026-04-21
Protocol for a pilot feasibility randomised controlled trial of fecal microbiota transplantation for adolescent anorexia nervosa.
BMJ open, 16(4):e109115 pii:bmjopen-2025-109115.
INTRODUCTION: Despite its serious impact, anorexia nervosa (AN) remains one of the least understood mental illnesses, with significant gaps in effective treatment options. No medications have been deemed effective and only 50% of individuals respond to conventional psychotherapies. Gastrointestinal (GI) bacteria have been found to be altered in individuals with AN. While, Fecal microbiota transplantation (FMT) has shown potential for alleviating anxiety and depression, its effects remain understudied for individuals with AN. This study aims to determine whether oral capsular FMT is acceptable to adolescents with AN and results in clinical improvement in weight and/or psychological symptoms.
METHODS: This study will randomise 20 adolescents with AN, ages 12-17 years, to receive either FMT or placebo capsules. These 20 youth, as well as an additional 10 youth who decline trial enrolment, will participate in qualitative interviews. We will track recruitment rates and collect psychological and biological measures (blood, stool, urine and saliva) at multiple timepoints to assess how gut microbiota and their metabolites may influence the symptoms of AN. Interviews with participants and caregivers will explore their experiences and views on FMT as a treatment approach.
ETHICS AND DISSEMINATION: This study has received ethics approval by the Hamilton Integrated Research Ethics Board (#17493) and investigational drug approval by Health Canada (Dossier ID: c292423). Informed consent will be obtained by research staff from all participants. Findings will be disseminated through academic conferences, clinical forums and partnerships with advocacy organisations to reach clinicians, researchers and individuals with lived experience.
TRIAL REGISTRATION NUMBER: NCT06593366.
Additional Links: PMID-42009386
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@article {pmid42009386,
year = {2026},
author = {Couturier, J and Kenner, E and Nicula, M and Chowdhury, F and Surette, M and Pai, N},
title = {Protocol for a pilot feasibility randomised controlled trial of fecal microbiota transplantation for adolescent anorexia nervosa.},
journal = {BMJ open},
volume = {16},
number = {4},
pages = {e109115},
doi = {10.1136/bmjopen-2025-109115},
pmid = {42009386},
issn = {2044-6055},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; Adolescent ; *Anorexia Nervosa/therapy/psychology ; Pilot Projects ; Feasibility Studies ; Child ; Female ; Male ; Randomized Controlled Trials as Topic ; Gastrointestinal Microbiome ; },
abstract = {INTRODUCTION: Despite its serious impact, anorexia nervosa (AN) remains one of the least understood mental illnesses, with significant gaps in effective treatment options. No medications have been deemed effective and only 50% of individuals respond to conventional psychotherapies. Gastrointestinal (GI) bacteria have been found to be altered in individuals with AN. While, Fecal microbiota transplantation (FMT) has shown potential for alleviating anxiety and depression, its effects remain understudied for individuals with AN. This study aims to determine whether oral capsular FMT is acceptable to adolescents with AN and results in clinical improvement in weight and/or psychological symptoms.
METHODS: This study will randomise 20 adolescents with AN, ages 12-17 years, to receive either FMT or placebo capsules. These 20 youth, as well as an additional 10 youth who decline trial enrolment, will participate in qualitative interviews. We will track recruitment rates and collect psychological and biological measures (blood, stool, urine and saliva) at multiple timepoints to assess how gut microbiota and their metabolites may influence the symptoms of AN. Interviews with participants and caregivers will explore their experiences and views on FMT as a treatment approach.
ETHICS AND DISSEMINATION: This study has received ethics approval by the Hamilton Integrated Research Ethics Board (#17493) and investigational drug approval by Health Canada (Dossier ID: c292423). Informed consent will be obtained by research staff from all participants. Findings will be disseminated through academic conferences, clinical forums and partnerships with advocacy organisations to reach clinicians, researchers and individuals with lived experience.
TRIAL REGISTRATION NUMBER: NCT06593366.},
}
MeSH Terms:
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Humans
*Fecal Microbiota Transplantation/methods
Adolescent
*Anorexia Nervosa/therapy/psychology
Pilot Projects
Feasibility Studies
Child
Female
Male
Randomized Controlled Trials as Topic
Gastrointestinal Microbiome
RevDate: 2026-04-20
Microbiome modulating remedies for chronic diseases: a review of current interventions and future directions.
Inflammopharmacology [Epub ahead of print].
Additional Links: PMID-42009997
PubMed:
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@article {pmid42009997,
year = {2026},
author = {Swain, MP and Mehta, CH and Padya, BS and Sharma, S and Velagacherla, V and Mitra, A and Mohanty, S and Mukherjee, T},
title = {Microbiome modulating remedies for chronic diseases: a review of current interventions and future directions.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {42009997},
issn = {1568-5608},
}
RevDate: 2026-04-20
Microbiome signature of Parkinson's disease in healthy and genetically at-risk individuals.
Nature medicine [Epub ahead of print].
Parkinson's disease (PD) is a major cause of disability. GBA1 variants are the most common genetic risk factor for PD and increase the risk up to 30-fold. Why only approximately 20% of GBA1 variant carriers develop PD remains unknown. Here, by combining clinical and fecal metagenomics data from 271 patients with PD, from 43 carriers of GBA1 variants not manifesting PD symptoms (GBA-NMC) and from 150 healthy controls, and using an innovative microbiome analysis, combining differential abundance of species and coherence of differential abundance variation between the groups as assessed by Cliff's delta (δ), we show that the composition of a large component of the gut microbiome (approximately 25%) in GBA-NMC is intermediate between healthy controls and patients with PD. This component is strongly correlated with disease progression in patients and prodromal symptoms suggestive of future development of PD in both GBA-NMC and healthy individuals. We found microbiome alterations similar to those described here in three independent cohorts from the United States, Korea and Turkey, totaling 638 patients with PD and 319 healthy controls, and we conclude that gut microbiome alterations can identify both genetically and non-genetically at-risk individuals in the general population who may be progressing toward PD, thus serving as an early marker of disease development in the premanifest phase.
Additional Links: PMID-42010118
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Citation:
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@article {pmid42010118,
year = {2026},
author = {Menozzi, E and Ren, Y and Geiger, M and Macnaughtan, J and Avenali, M and Toffoli, M and Gilles, M and Calabrese, R and Mitrotti, P and Gallo, L and Famechon, A and Del Pozo, SL and Mezabrovschi, R and Koletsi, S and Loefflad, N and Yalkic, S and Limbachiya, N and Clasen, F and Yildirim, S and Shoaie, S and Blottière, H and Morabito, C and David, A and Quinquis, B and Pons, N and Le Chatelier, E and Valzania, F and Cavallieri, F and Fioravanti, V and Toschi, G and Blandini, F and Almeida, M and Ehrlich, SD and Meslier, V and Schapira, AHV},
title = {Microbiome signature of Parkinson's disease in healthy and genetically at-risk individuals.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42010118},
issn = {1546-170X},
support = {MR/T046007/1//EU Joint Programme - Neurodegenerative Disease Research (Programi i Përbashkët i BE-së për Kërkimet mbi Sëmundjet Neuro-degjeneruese)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; ASAP-000420//Michael J. Fox Foundation for Parkinson's Research (Michael J. Fox Foundation)/ ; },
abstract = {Parkinson's disease (PD) is a major cause of disability. GBA1 variants are the most common genetic risk factor for PD and increase the risk up to 30-fold. Why only approximately 20% of GBA1 variant carriers develop PD remains unknown. Here, by combining clinical and fecal metagenomics data from 271 patients with PD, from 43 carriers of GBA1 variants not manifesting PD symptoms (GBA-NMC) and from 150 healthy controls, and using an innovative microbiome analysis, combining differential abundance of species and coherence of differential abundance variation between the groups as assessed by Cliff's delta (δ), we show that the composition of a large component of the gut microbiome (approximately 25%) in GBA-NMC is intermediate between healthy controls and patients with PD. This component is strongly correlated with disease progression in patients and prodromal symptoms suggestive of future development of PD in both GBA-NMC and healthy individuals. We found microbiome alterations similar to those described here in three independent cohorts from the United States, Korea and Turkey, totaling 638 patients with PD and 319 healthy controls, and we conclude that gut microbiome alterations can identify both genetically and non-genetically at-risk individuals in the general population who may be progressing toward PD, thus serving as an early marker of disease development in the premanifest phase.},
}
RevDate: 2026-04-20
Considerations for the design of impactful citizen-science projects in microbiome research.
Nature protocols [Epub ahead of print].
Citizen science offers a transformative approach to microbiome research. It allows the collection of rich, context-specific data from diverse sources, such as varying human populations and environments. Here, we describe guidelines that cover the design and implementation of community-engaged citizen-science projects focused on microbiome research. We outline essential research steps, beginning with defining the objectives and forming a transdisciplinary team, and continuing with community interaction, standardized self-sampling protocols, strategies for data processing, analysis and communication of results to community members and policymakers, as well as the implementation of robust data management practices that uphold participant privacy and data sovereignty. The guidelines highlight culturally-sensitive outreach strategies and capacity building in research teams and communities, emphasizing ethical considerations and tailored recruitment strategies. Community engagement may help reduce sampling bias but does not automatically ensure participant diversity: intentional inclusion strategies are essential. They cover culturally sensitive outreach, ethical considerations and tailored recruitment approaches that support inclusive participation and meaningful collaboration. These recommendations draw inspiration from a range of health and environment-related citizen-science projects in Belgium, Peru and Cameroon, and collaborative projects across the world. Specific examples highlight the importance of adapting methodologies to diverse cultural contexts and logistical constraints. While wet-laboratory sample processing and downstream analyses are detailed elsewhere, this Perspective focuses on the unique considerations and best practices needed for designing impactful cocreative citizen-science projects that combine scientific discovery with community, environmental health and well-being. It can serve as a blueprint for future citizen-science initiatives that aim to expand access to microbiome research, foster global collaboration and promote long-term research equity and environmental sustainability.
Additional Links: PMID-42010351
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Citation:
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@article {pmid42010351,
year = {2026},
author = {Ahannach, S and Condori-Catachura, S and Dillen, J and Dricot, C and Gehrmann, T and Wittouck, S and Kenfack, JM and Van Beeck, W and De Boeck, I and Eilers, T and Ticlla, M and Santullo Latorre, A and Smets, W and Temmermans, J and Arconada Nuin, E and , and Van Puyvelde, S and Spacova, I and Verhoeven, V and Lebeer, S},
title = {Considerations for the design of impactful citizen-science projects in microbiome research.},
journal = {Nature protocols},
volume = {},
number = {},
pages = {},
pmid = {42010351},
issn = {1750-2799},
abstract = {Citizen science offers a transformative approach to microbiome research. It allows the collection of rich, context-specific data from diverse sources, such as varying human populations and environments. Here, we describe guidelines that cover the design and implementation of community-engaged citizen-science projects focused on microbiome research. We outline essential research steps, beginning with defining the objectives and forming a transdisciplinary team, and continuing with community interaction, standardized self-sampling protocols, strategies for data processing, analysis and communication of results to community members and policymakers, as well as the implementation of robust data management practices that uphold participant privacy and data sovereignty. The guidelines highlight culturally-sensitive outreach strategies and capacity building in research teams and communities, emphasizing ethical considerations and tailored recruitment strategies. Community engagement may help reduce sampling bias but does not automatically ensure participant diversity: intentional inclusion strategies are essential. They cover culturally sensitive outreach, ethical considerations and tailored recruitment approaches that support inclusive participation and meaningful collaboration. These recommendations draw inspiration from a range of health and environment-related citizen-science projects in Belgium, Peru and Cameroon, and collaborative projects across the world. Specific examples highlight the importance of adapting methodologies to diverse cultural contexts and logistical constraints. While wet-laboratory sample processing and downstream analyses are detailed elsewhere, this Perspective focuses on the unique considerations and best practices needed for designing impactful cocreative citizen-science projects that combine scientific discovery with community, environmental health and well-being. It can serve as a blueprint for future citizen-science initiatives that aim to expand access to microbiome research, foster global collaboration and promote long-term research equity and environmental sustainability.},
}
RevDate: 2026-04-20
Altered microbial cargo in fecal microbiome-derived outer membrane vesicles as novel biomarkers for vascular dementia.
BMC microbiology pii:10.1186/s12866-026-05040-5 [Epub ahead of print].
Additional Links: PMID-42010400
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PubMed:
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@article {pmid42010400,
year = {2026},
author = {Li, X and Wei, W and Wei, S and Xu, W and Mo, L and Wang, J and Zhu, H and Liu, Z and Jin, F},
title = {Altered microbial cargo in fecal microbiome-derived outer membrane vesicles as novel biomarkers for vascular dementia.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05040-5},
pmid = {42010400},
issn = {1471-2180},
support = {2022A21//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2022A10//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2022A14//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2022A22//the Doctoral Research Startup Project of Central People's Hospital of Zhanjiang/ ; 2021X091662//Weifang Municipal Health Commission Scientific Research Project/ ; 2022A1515010749//the Natural Science Foundation of Guangdong Province/ ; 2024B01238//Zhanjiang City Science and Technology Plan Project/ ; },
}
RevDate: 2026-04-21
Metagenomics reveals gut microbial differences and ecological adaptation in plateau zokor (Eospalax baileyi) populations.
BMC microbiology pii:10.1186/s12866-026-05069-6 [Epub ahead of print].
Additional Links: PMID-42010457
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PubMed:
Citation:
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@article {pmid42010457,
year = {2026},
author = {Guo, J and Liang, C and Cairang, L and Si, L and Yan, J and Liu, D},
title = {Metagenomics reveals gut microbial differences and ecological adaptation in plateau zokor (Eospalax baileyi) populations.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-05069-6},
pmid = {42010457},
issn = {1471-2180},
support = {LHZX-2023-02//Sanjiangyuan National Park Joint Grant from the Chinese Academy of Sciences and the People's Government of Qinghai Province/ ; },
}
RevDate: 2026-04-21
Trimethylamine-producing microbe Bacillus megaterium KCTC 3007 promotes antitumor immunity in endometrial cancer via type I interferon response pathways.
Microbiome pii:10.1186/s40168-026-02373-1 [Epub ahead of print].
BACKGROUND: Endometrial cancer (ECa) is one of the most common gynecologic malignancies, with limited therapeutic responses in metastatic or recurrent cases. The bacterial microbiota has emerged as a key modulator of carcinogenesis and antitumor immunity. However, the role of endometrial microbiota in ECa pathogenesis and prognosis remains poorly understood.
METHODS: We performed comprehensive multi-omics analysis integrating metatranscriptomics, transcriptomics, and targeted metabolomics from 60 ECa and 18 benign patients. RNA sequencing enabled simultaneous profiling of active tissue-resident microbiota and host gene expression. Serum metabolomics was conducted on all patients. Identified microbial-metabolite associations were validated through in vitro co-culture experiments using peripheral blood mononuclear cells (PBMCs), cancer cell lines, RNA sequencing, and live cell imaging.
RESULTS: ECa patients exhibited significantly altered microbial diversity and composition compared to benign controls. Through integrated multi-omics analysis, we identified Bacillus megaterium (BM) KCTC 3007 as a beneficial microbe associated with prolonged recurrence-free survival. In an exploratory analysis of ECa subtypes, Cupriavidus taiwanensis and Marinomonas primoryensis showed potential links to poor prognosis, although these observations warrant caution due to the limited size of certain subgroups. Tissue BM abundance positively correlated with serum trimethylamine N-oxide (TMAO) levels, particularly in postmenopausal women. In vitro experiments demonstrated that BM KCTC 3007 enhanced antitumor immunity by promoting interleukin and type I interferon expression, expanding CD8 + T cell populations, and increasing immune cell-tumor cell interactions. RNA sequencing revealed activation of interferon alpha response and immune cell proliferation pathways, with IFNAR1 identified as a key upstream regulator. TMAO treatment recapitulated these immune-activating effects, enhancing CD8 + T cell responses and preferentially inducing pyroptotic cancer cell death.
CONCLUSIONS: We provide the first evidence that tissue-resident BM KCTC 3007 promotes antitumor immunity in ECa through TMAO production and subsequent type I interferon-mediated immune activation. This integrated multi-omics approach establishes a complete microbe-metabolite-host mechanistic pathway and highlights the therapeutic potential of TMAO-producing probiotic strains for ECa treatment. Video Abstract.
Additional Links: PMID-42010642
Publisher:
PubMed:
Citation:
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@article {pmid42010642,
year = {2026},
author = {Min, K and Kim, SI and Lee, M and Kim, Y and Jeong, C and Kim, S and Kim, SJ and Kim, H and Cho, B and Joo, Y and Park, H and Lee, M},
title = {Trimethylamine-producing microbe Bacillus megaterium KCTC 3007 promotes antitumor immunity in endometrial cancer via type I interferon response pathways.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02373-1},
pmid = {42010642},
issn = {2049-2618},
support = {grant of the MD-PhD/Medical Scientist Training Program//Korea Health Industry Development Institute/Republic of Korea ; KGCR-2022-01//Korean Gynecologic Cancer Research/ ; 2022R1A2C2008976 and RS-2023-00228315//Ministry of Science and ICT, Korean Government/ ; },
abstract = {BACKGROUND: Endometrial cancer (ECa) is one of the most common gynecologic malignancies, with limited therapeutic responses in metastatic or recurrent cases. The bacterial microbiota has emerged as a key modulator of carcinogenesis and antitumor immunity. However, the role of endometrial microbiota in ECa pathogenesis and prognosis remains poorly understood.
METHODS: We performed comprehensive multi-omics analysis integrating metatranscriptomics, transcriptomics, and targeted metabolomics from 60 ECa and 18 benign patients. RNA sequencing enabled simultaneous profiling of active tissue-resident microbiota and host gene expression. Serum metabolomics was conducted on all patients. Identified microbial-metabolite associations were validated through in vitro co-culture experiments using peripheral blood mononuclear cells (PBMCs), cancer cell lines, RNA sequencing, and live cell imaging.
RESULTS: ECa patients exhibited significantly altered microbial diversity and composition compared to benign controls. Through integrated multi-omics analysis, we identified Bacillus megaterium (BM) KCTC 3007 as a beneficial microbe associated with prolonged recurrence-free survival. In an exploratory analysis of ECa subtypes, Cupriavidus taiwanensis and Marinomonas primoryensis showed potential links to poor prognosis, although these observations warrant caution due to the limited size of certain subgroups. Tissue BM abundance positively correlated with serum trimethylamine N-oxide (TMAO) levels, particularly in postmenopausal women. In vitro experiments demonstrated that BM KCTC 3007 enhanced antitumor immunity by promoting interleukin and type I interferon expression, expanding CD8 + T cell populations, and increasing immune cell-tumor cell interactions. RNA sequencing revealed activation of interferon alpha response and immune cell proliferation pathways, with IFNAR1 identified as a key upstream regulator. TMAO treatment recapitulated these immune-activating effects, enhancing CD8 + T cell responses and preferentially inducing pyroptotic cancer cell death.
CONCLUSIONS: We provide the first evidence that tissue-resident BM KCTC 3007 promotes antitumor immunity in ECa through TMAO production and subsequent type I interferon-mediated immune activation. This integrated multi-omics approach establishes a complete microbe-metabolite-host mechanistic pathway and highlights the therapeutic potential of TMAO-producing probiotic strains for ECa treatment. Video Abstract.},
}
RevDate: 2026-04-21
A novel enterotype enriched with respiratory super-dominant pathobionts is associated with immunosuppression in pulmonary tuberculosis patients.
Journal of translational medicine pii:10.1186/s12967-026-08165-3 [Epub ahead of print].
BACKGROUND: Perturbations of the gut microbiota in pulmonary tuberculosis (PTB) patients, often antibiotic-induced, are frequently observed; however, the defining features of this dysbiosis and its relationship with clinical phenotypes remain insufficiently characterized.
METHODS: In this cross-sectional study, we collected fecal samples from 66 PTB patients and performed 16S rRNA gene (V3-V4) sequencing. Species-level taxonomic profiling was conducted using the Human Gut Microbiome Analysis Database (HGMAD). Enterotypes were constructed, and their associations with PTB were investigated. The predictive capacity of enterotype-specific microbial signatures (enterosignatures) for clinical phenotypes was assessed.
RESULTS: Taxonomic analysis revealed significantly reduced prevalence of high-abundance bacteria group in PTB patients (43.84%) compared to healthy controls (HC, 98.01%), indicating increased microbiota heterogeneity. Known pathogenic species, predominantly common respiratory opportunistic pathogens (e.g., Haemophilus parainfluenzae, Acinetobacter baumannii, Veillonella parvula), were more prevalent in the PTB cohort (21.37% vs. 11.49% in HC). Enterotype analysis revealed a distinct cluster, designated ETE (Enterobacterales-dominated enterotype), which was predominantly observed in PTB patients and differed from the conventional Prevotella-dominated enterotype (ETP) and Bacteroides-dominated enterotype (ETB), identified in HC. ETE was significantly enriched in taxa including Acinetobacter baumannii, Enterococcus, Veillonella, Pseudomonas, and Streptococcus, exhibited lower alpha diversity, and functional inference using PICRUSt2 suggested relative lower immune-related pathways. Clinically, ETE was associated with lower cellular immunity and a trend toward higher C-reactive protein (CRP) levels. A model based on ten super-dominant respiratory pathobionts enterosignatures effectively predicted key clinical phenotypes, with area under the curves (AUCs) of 0.83 for CD4[+] T-cell count, 0.74 for CD8[+] T-cell count, 0.74 for CD4[+]/CD8[+] ratio, 0.93 for CRP, 0.78 for CA125, and 0.70 for Mtb positivity. SHapley Additive exPlanation (SHAP) analysis identified Enterobacterales and Veillonella as key negative predictors for T-cell counts, while Streptococcus and Enterobacteriaceae were positive predictors for CRP. In the CA125 model, Veillonella acted as a positive predictor and Enterobacterales as a negative predictor.
CONCLUSION: This cross-sectional study identifies a distinct, PTB-associated enterotype (ETE) characterized by enrichment of respiratory pathobionts and associated with altered immune parameters in PTB patients. Enterosignatures derive from ETE represent exploratory biomarkers with promising predictive capacity for clinical outcomes, though their generalizability warrants validation in independent, prospective cohorts.
Additional Links: PMID-42010662
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Citation:
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@article {pmid42010662,
year = {2026},
author = {Yuan, T and Chen, J and Zheng, H and Pu, J and Li, L and Lu, S and Sun, Y and Lin, W and Yang, J and Xu, J},
title = {A novel enterotype enriched with respiratory super-dominant pathobionts is associated with immunosuppression in pulmonary tuberculosis patients.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08165-3},
pmid = {42010662},
issn = {1479-5876},
abstract = {BACKGROUND: Perturbations of the gut microbiota in pulmonary tuberculosis (PTB) patients, often antibiotic-induced, are frequently observed; however, the defining features of this dysbiosis and its relationship with clinical phenotypes remain insufficiently characterized.
METHODS: In this cross-sectional study, we collected fecal samples from 66 PTB patients and performed 16S rRNA gene (V3-V4) sequencing. Species-level taxonomic profiling was conducted using the Human Gut Microbiome Analysis Database (HGMAD). Enterotypes were constructed, and their associations with PTB were investigated. The predictive capacity of enterotype-specific microbial signatures (enterosignatures) for clinical phenotypes was assessed.
RESULTS: Taxonomic analysis revealed significantly reduced prevalence of high-abundance bacteria group in PTB patients (43.84%) compared to healthy controls (HC, 98.01%), indicating increased microbiota heterogeneity. Known pathogenic species, predominantly common respiratory opportunistic pathogens (e.g., Haemophilus parainfluenzae, Acinetobacter baumannii, Veillonella parvula), were more prevalent in the PTB cohort (21.37% vs. 11.49% in HC). Enterotype analysis revealed a distinct cluster, designated ETE (Enterobacterales-dominated enterotype), which was predominantly observed in PTB patients and differed from the conventional Prevotella-dominated enterotype (ETP) and Bacteroides-dominated enterotype (ETB), identified in HC. ETE was significantly enriched in taxa including Acinetobacter baumannii, Enterococcus, Veillonella, Pseudomonas, and Streptococcus, exhibited lower alpha diversity, and functional inference using PICRUSt2 suggested relative lower immune-related pathways. Clinically, ETE was associated with lower cellular immunity and a trend toward higher C-reactive protein (CRP) levels. A model based on ten super-dominant respiratory pathobionts enterosignatures effectively predicted key clinical phenotypes, with area under the curves (AUCs) of 0.83 for CD4[+] T-cell count, 0.74 for CD8[+] T-cell count, 0.74 for CD4[+]/CD8[+] ratio, 0.93 for CRP, 0.78 for CA125, and 0.70 for Mtb positivity. SHapley Additive exPlanation (SHAP) analysis identified Enterobacterales and Veillonella as key negative predictors for T-cell counts, while Streptococcus and Enterobacteriaceae were positive predictors for CRP. In the CA125 model, Veillonella acted as a positive predictor and Enterobacterales as a negative predictor.
CONCLUSION: This cross-sectional study identifies a distinct, PTB-associated enterotype (ETE) characterized by enrichment of respiratory pathobionts and associated with altered immune parameters in PTB patients. Enterosignatures derive from ETE represent exploratory biomarkers with promising predictive capacity for clinical outcomes, though their generalizability warrants validation in independent, prospective cohorts.},
}
RevDate: 2026-04-21
Metabolome-driven rhizosphere microbiome assembly determining the health of medicinal herb (Angelica sinensis) against root rot.
Microbiome pii:10.1186/s40168-026-02393-x [Epub ahead of print].
BACKGROUND: The rhizosphere-associated microbiota plays a crucial role in plant responses to disease stress. Plant secondary metabolites are recognized as crucial mediators in the assembly of rhizosphere microbial communities, particularly by enhancing the colonization of beneficial microorganisms. Despite this recognized importance, a deeper understanding of how such metabolome-driven microbiome assembly specifically determines plant resistance against soil-borne diseases is still lacking.
RESULTS: Here, we focused on the widely planted medicinal plant Angelica sinensis and demonstrated that root rot-diseased rhizosphere soils (DRS) exhibited a higher relative abundance of Fusarium and a lower relative abundance of Streptomyces compared to healthy rhizosphere soils (HRS). Shotgun metagenomic sequencing revealed that metabolism-associated genes, particularly those related to steroid degradation, are significantly enriched in HRS samples. Subsequent genome and functional gene analysis of Streptomyces revealed that the steroid degradation-related genes are associated with rhizosphere colonization in hosts. Rhizosphere Streptomyces S15 directly antagonized Fusarium and enhanced the root resistance of A. sinensis. Comparative metabolomics showed that A. sinensis plants from HRS secreted more lipid and lipid-like molecules than those from DRS, especially sterol lipids and long-chain fatty acids, which promoted the growth of Streptomyces S15 isolates. Transcriptome analysis validated that the lipid hormones are essential for sporulation, biofilm formation, and streptomycin biosynthesis of S15 strain. Finally, exogenous application of synbiotics (lipid prebiotics and S15) to A. sinensis resulted in the enrichment of S15-homologous Streptomyces amplicon sequence variant (ASV), further establishing beneficial bacterial communities in Fusarium-stressed rhizospheres.
CONCLUSIONS: Our study proposes that A. sinensis recruits steroid-metabolizing Streptomyces species by exuding key lipid compounds (i.e., methyl jasmonate and brassinolide) to combat Fusarium root rot. This study provides novel insights into using functional synbiotics as a promising strategy for manipulating plant-microbiome interactions to promote sustainable agriculture. Video Abstract.
Additional Links: PMID-42010711
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PubMed:
Citation:
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@article {pmid42010711,
year = {2026},
author = {You, C and Zhang, W and Guan, Y and Liang, Q and Nong, C and Yang, T and Li, M and Banerjee, S and Zhou, X and Wang, X and Xu, Y and Shen, Q and Wei, Z},
title = {Metabolome-driven rhizosphere microbiome assembly determining the health of medicinal herb (Angelica sinensis) against root rot.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02393-x},
pmid = {42010711},
issn = {2049-2618},
support = {2022YFC3501501//National Key Research and Development Program of China/ ; KJYQ2025034, KJYQ2024039//Fundamental Research Funds for the Central Universities/ ; BK20240194//the Natural Science Foundation of Jiangsu Province/ ; },
abstract = {BACKGROUND: The rhizosphere-associated microbiota plays a crucial role in plant responses to disease stress. Plant secondary metabolites are recognized as crucial mediators in the assembly of rhizosphere microbial communities, particularly by enhancing the colonization of beneficial microorganisms. Despite this recognized importance, a deeper understanding of how such metabolome-driven microbiome assembly specifically determines plant resistance against soil-borne diseases is still lacking.
RESULTS: Here, we focused on the widely planted medicinal plant Angelica sinensis and demonstrated that root rot-diseased rhizosphere soils (DRS) exhibited a higher relative abundance of Fusarium and a lower relative abundance of Streptomyces compared to healthy rhizosphere soils (HRS). Shotgun metagenomic sequencing revealed that metabolism-associated genes, particularly those related to steroid degradation, are significantly enriched in HRS samples. Subsequent genome and functional gene analysis of Streptomyces revealed that the steroid degradation-related genes are associated with rhizosphere colonization in hosts. Rhizosphere Streptomyces S15 directly antagonized Fusarium and enhanced the root resistance of A. sinensis. Comparative metabolomics showed that A. sinensis plants from HRS secreted more lipid and lipid-like molecules than those from DRS, especially sterol lipids and long-chain fatty acids, which promoted the growth of Streptomyces S15 isolates. Transcriptome analysis validated that the lipid hormones are essential for sporulation, biofilm formation, and streptomycin biosynthesis of S15 strain. Finally, exogenous application of synbiotics (lipid prebiotics and S15) to A. sinensis resulted in the enrichment of S15-homologous Streptomyces amplicon sequence variant (ASV), further establishing beneficial bacterial communities in Fusarium-stressed rhizospheres.
CONCLUSIONS: Our study proposes that A. sinensis recruits steroid-metabolizing Streptomyces species by exuding key lipid compounds (i.e., methyl jasmonate and brassinolide) to combat Fusarium root rot. This study provides novel insights into using functional synbiotics as a promising strategy for manipulating plant-microbiome interactions to promote sustainable agriculture. Video Abstract.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Exercise intensity as a modulator of gut microbiota and host metabolic health in obesity.
Gut microbes, 18(1):2661415.
The gut microbiome is shaped by complex interactions among host, environmental, and lifestyle factors, with exercise emerging as a reported modulator. Growing evidence suggests that exercise intensity, ranging from low to high, can differentially influence gut microbial composition, diversity, and functional outputs relevant to metabolic health. This narrative review synthesizes current findings examining intensity-dependent microbial adaptations in the context of obesity. Across animal models (n = 17) and limited human studies (n = 5), moderate-intensity training (MIT) and high-intensity interval training (HIIT) produce the most consistent microbiota shifts, while low-intensity training (LIT) exerts minimal effects. Reported taxa associated with beneficial outcomes consistent across animal and human investigations include Akkermansia (G), and Christensenellaceae (F). Mechanistically, intensity-dependent alterations in microbial communities may influence obesity-related pathways through modulation of short-chain fatty acid (SCFA) and bile acid metabolism, gut barrier integrity, endotoxemia, and inflammatory signaling. HIIT and MIT are linked to improved expression of tight junction proteins (ZO-1, Claudin, Occludin), reducing circulating lipopolysaccharide (LPS), and increasing SCFA-producing taxa; thus, supporting a role for the gut microbiome in mediating exercise-induced metabolic benefits. However, inconsistent findings between species, interindividual variability, and considerable heterogeneity in exercise intervention duration across both animal (4-16 weeks) and human (3-12 weeks) studies, as well as limited longitudinal human studies, underscore the need for deeper mechanistic investigations. Future research should employ metagenomic and metatranscriptomic profiling, integrate sex- and diet-stratified longitudinal designs, and clarify causal links between exercise-responsive taxa, microbial metabolites, and host physiology. Collectively, these data highlight exercise intensity as a key determinant of gut microbiome dynamics and reinforce the need for integrative, translational approaches to define its therapeutic potential for obesity and metabolic disorders.
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@article {pmid42010766,
year = {2026},
author = {Combs, D and Landeros, K and Garza, K and Azari, H and Abdelrahman, M and Albracht-Schulte, K},
title = {Exercise intensity as a modulator of gut microbiota and host metabolic health in obesity.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2661415},
doi = {10.1080/19490976.2026.2661415},
pmid = {42010766},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome/physiology ; Humans ; *Obesity/microbiology/metabolism ; Animals ; *Exercise/physiology ; Bacteria/classification/genetics/metabolism/isolation & purification ; Physical Conditioning, Animal ; Fatty Acids, Volatile/metabolism ; },
abstract = {The gut microbiome is shaped by complex interactions among host, environmental, and lifestyle factors, with exercise emerging as a reported modulator. Growing evidence suggests that exercise intensity, ranging from low to high, can differentially influence gut microbial composition, diversity, and functional outputs relevant to metabolic health. This narrative review synthesizes current findings examining intensity-dependent microbial adaptations in the context of obesity. Across animal models (n = 17) and limited human studies (n = 5), moderate-intensity training (MIT) and high-intensity interval training (HIIT) produce the most consistent microbiota shifts, while low-intensity training (LIT) exerts minimal effects. Reported taxa associated with beneficial outcomes consistent across animal and human investigations include Akkermansia (G), and Christensenellaceae (F). Mechanistically, intensity-dependent alterations in microbial communities may influence obesity-related pathways through modulation of short-chain fatty acid (SCFA) and bile acid metabolism, gut barrier integrity, endotoxemia, and inflammatory signaling. HIIT and MIT are linked to improved expression of tight junction proteins (ZO-1, Claudin, Occludin), reducing circulating lipopolysaccharide (LPS), and increasing SCFA-producing taxa; thus, supporting a role for the gut microbiome in mediating exercise-induced metabolic benefits. However, inconsistent findings between species, interindividual variability, and considerable heterogeneity in exercise intervention duration across both animal (4-16 weeks) and human (3-12 weeks) studies, as well as limited longitudinal human studies, underscore the need for deeper mechanistic investigations. Future research should employ metagenomic and metatranscriptomic profiling, integrate sex- and diet-stratified longitudinal designs, and clarify causal links between exercise-responsive taxa, microbial metabolites, and host physiology. Collectively, these data highlight exercise intensity as a key determinant of gut microbiome dynamics and reinforce the need for integrative, translational approaches to define its therapeutic potential for obesity and metabolic disorders.},
}
MeSH Terms:
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*Gastrointestinal Microbiome/physiology
Humans
*Obesity/microbiology/metabolism
Animals
*Exercise/physiology
Bacteria/classification/genetics/metabolism/isolation & purification
Physical Conditioning, Animal
Fatty Acids, Volatile/metabolism
RevDate: 2026-04-21
Tumor-resident bacteria in gastrointestinal cancers: from regulatory mechanisms to clinical implications.
Cancer biology & medicine pii:j.issn.2095-3941.2025.0686 [Epub ahead of print].
The human microbiome is increasingly recognized as a key contributor to the tumor microenvironment (TME). Advances in sequencing technologies have revealed the pivotal role of intratumoral microbiota in the development of gastrointestinal cancers. This review summarizes current knowledge on the characteristics and functional mechanisms of tumor-resident bacteria in colorectal, gastric, and hepatocellular carcinoma. We describe how these microbes affect carcinogenesis and disease progression through multiple pathways, including interactions between the microbiota and the host gut barrier, tumor cells, anti-tumor immunity, and other non-cellular components of the TME. In addition, the translational potential of intratumoral microbiota as diagnostic and prognostic biomarkers, as well as the influence on therapeutic responses, is discussed. A growing understanding of tumor-microbe interactions not only deepens insight into cancer biology but also opens new directions for innovative diagnostic and therapeutic strategies, highlighting the potential of targeting the intratumoral microbiome to improve patient outcomes in gastrointestinal oncology.
Additional Links: PMID-42010947
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@article {pmid42010947,
year = {2026},
author = {Zhang, Y and Tan, B and Zhou, Q and Xu, L and Zhou, L},
title = {Tumor-resident bacteria in gastrointestinal cancers: from regulatory mechanisms to clinical implications.},
journal = {Cancer biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.20892/j.issn.2095-3941.2025.0686},
pmid = {42010947},
issn = {2095-3941},
support = {2023ZD0501600//Non-communicable Chronic Diseases-National Science and Technology Major Project/ ; 82373080//National Nature Science Foundation of China/ ; 82403116//National Nature Science Foundation of China/ ; 2023ZT10Y094//Guangdong Pearl River Talent Program/ ; 2023QN10Y587//Guangdong Pearl River Talent Program/ ; 2022-KJXM-ZCQ-11//"the Science and Technology Empowering Inner Mongolia" Major Special Project of Inner Mongolia Autonomous Region/ ; },
abstract = {The human microbiome is increasingly recognized as a key contributor to the tumor microenvironment (TME). Advances in sequencing technologies have revealed the pivotal role of intratumoral microbiota in the development of gastrointestinal cancers. This review summarizes current knowledge on the characteristics and functional mechanisms of tumor-resident bacteria in colorectal, gastric, and hepatocellular carcinoma. We describe how these microbes affect carcinogenesis and disease progression through multiple pathways, including interactions between the microbiota and the host gut barrier, tumor cells, anti-tumor immunity, and other non-cellular components of the TME. In addition, the translational potential of intratumoral microbiota as diagnostic and prognostic biomarkers, as well as the influence on therapeutic responses, is discussed. A growing understanding of tumor-microbe interactions not only deepens insight into cancer biology but also opens new directions for innovative diagnostic and therapeutic strategies, highlighting the potential of targeting the intratumoral microbiome to improve patient outcomes in gastrointestinal oncology.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Impact of gut microbiome, plasma metabolites, peripheral immune cells, and circulating inflammatory protein on chronic spontaneous urticaria: Bidirectional 2-sample Mendelian randomization study and mediation analysis.
The journal of allergy and clinical immunology. Global, 5(3):100686.
BACKGROUND: Growing evidence links gut microbiota to chronic spontaneous urticaria (CSU), yet causality and underlying mediators remain unclear.
OBJECTIVE: We investigated causal relationships and potential mediators-specifically plasma metabolites, immune cells, and inflammatory proteins-through which gut microbes influence CSU risk.
METHODS: We applied 2-sample Mendelian randomization (MR) to genome-wide association study (GWAS) data on 430 gut microbial taxa, 1,400 plasma metabolites, 731 immune cell traits, and 91 inflammatory proteins. Analyses used inverse variance weighted, MR-Egger, weighted median, and weighted mode estimators, complemented by sensitivity, mediation, multivariable MR, and Bayesian colocalization tests for shared causal variants.
RESULTS: Eight gut taxa, 79 metabolites, 25 immune cell phenotypes, and 3 inflammatory proteins showed suggestive associated with CSU (all false discovery rate > .05). Galactonate mediated the effect of Paraprevotella on CSU, while N-acetyl leucine mediated the protective effect of Bacteroides; only the latter remained significant in multivariable MR. Immune cells and inflammatory proteins showed no significant mediation. Bayesian colocalization provided no evidence of shared causal variants between CSU and any of the 4 trait categories.
CONCLUSION: Gut microbiota may suggestively influence CSU risk via specific metabolite pathways, particularly N-acetyl leucine, though colocalization did not support shared genetic causality and no association survived multiple testing correction at false discovery rate < .05. These findings offer hypothesis-generating insights and candidate targets for further functional validation.
Additional Links: PMID-42011428
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@article {pmid42011428,
year = {2026},
author = {Deng, L and Yao, Y and Wang, Q and Lu, Z and Li, E and Hu, Y and Chen, J and Wang, G and Yu, T and Ji, J and Jiao, Q},
title = {Impact of gut microbiome, plasma metabolites, peripheral immune cells, and circulating inflammatory protein on chronic spontaneous urticaria: Bidirectional 2-sample Mendelian randomization study and mediation analysis.},
journal = {The journal of allergy and clinical immunology. Global},
volume = {5},
number = {3},
pages = {100686},
pmid = {42011428},
issn = {2772-8293},
abstract = {BACKGROUND: Growing evidence links gut microbiota to chronic spontaneous urticaria (CSU), yet causality and underlying mediators remain unclear.
OBJECTIVE: We investigated causal relationships and potential mediators-specifically plasma metabolites, immune cells, and inflammatory proteins-through which gut microbes influence CSU risk.
METHODS: We applied 2-sample Mendelian randomization (MR) to genome-wide association study (GWAS) data on 430 gut microbial taxa, 1,400 plasma metabolites, 731 immune cell traits, and 91 inflammatory proteins. Analyses used inverse variance weighted, MR-Egger, weighted median, and weighted mode estimators, complemented by sensitivity, mediation, multivariable MR, and Bayesian colocalization tests for shared causal variants.
RESULTS: Eight gut taxa, 79 metabolites, 25 immune cell phenotypes, and 3 inflammatory proteins showed suggestive associated with CSU (all false discovery rate > .05). Galactonate mediated the effect of Paraprevotella on CSU, while N-acetyl leucine mediated the protective effect of Bacteroides; only the latter remained significant in multivariable MR. Immune cells and inflammatory proteins showed no significant mediation. Bayesian colocalization provided no evidence of shared causal variants between CSU and any of the 4 trait categories.
CONCLUSION: Gut microbiota may suggestively influence CSU risk via specific metabolite pathways, particularly N-acetyl leucine, though colocalization did not support shared genetic causality and no association survived multiple testing correction at false discovery rate < .05. These findings offer hypothesis-generating insights and candidate targets for further functional validation.},
}
RevDate: 2026-04-21
Secoisolariciresinol diglucoside resolves systemic and skin inflammation in psoriatic mice by ameliorating the gut microbiome and modulating immune responses.
Food & function [Epub ahead of print].
Psoriasis is a chronic inflammatory skin disease that often imposes enormous psychological impact on the patient, potentially leading to psychiatric comorbidities or even suicidality. The currently available treatments do not always provide satisfactory results. Our previous work demonstrates that secoisolariciresinol diglucoside (SDG) has potent anti-inflammatory effects. In this study, we aimed to assess the effect of SDG on resolving the psoriatic inflammation using an imiquimod (IMQ)-induced mouse model and elucidate the underlying mechanisms. SDG and its metabolite enterolactone (ENL) exhibited potent curative effects on the skin pathology. In association with the resolution of the psoriatic inflammation, the lignans (SDG and ENL) significantly ameliorated gut dysbiosis. In the meantime, the Treg cells and the anti-inflammatory CD163 macrophages were greatly expanded in number, while the F4/80 and iNOS macrophages, the pro-inflammatory γδ T and Th17 cells, and a broad range of inflammatory cytokines along with STAT1 were drastically decreased. These results demonstrate that SDG treatment can effectively resolve the systemic and skin inflammation in psoriasis by ameliorating the gut microbiome and modulating immune responses. Collectively, this study provides useful information for the development of curative therapeutic strategies with natural products to treat psoriasis.
Additional Links: PMID-42011833
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@article {pmid42011833,
year = {2026},
author = {Yuan, BJ and Wang, YH and Lai, JR and Liu, L and Zhang, JW and Tian, HD and Johnston, RN and Liu, GR and Liu, SL},
title = {Secoisolariciresinol diglucoside resolves systemic and skin inflammation in psoriatic mice by ameliorating the gut microbiome and modulating immune responses.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo04965b},
pmid = {42011833},
issn = {2042-650X},
abstract = {Psoriasis is a chronic inflammatory skin disease that often imposes enormous psychological impact on the patient, potentially leading to psychiatric comorbidities or even suicidality. The currently available treatments do not always provide satisfactory results. Our previous work demonstrates that secoisolariciresinol diglucoside (SDG) has potent anti-inflammatory effects. In this study, we aimed to assess the effect of SDG on resolving the psoriatic inflammation using an imiquimod (IMQ)-induced mouse model and elucidate the underlying mechanisms. SDG and its metabolite enterolactone (ENL) exhibited potent curative effects on the skin pathology. In association with the resolution of the psoriatic inflammation, the lignans (SDG and ENL) significantly ameliorated gut dysbiosis. In the meantime, the Treg cells and the anti-inflammatory CD163 macrophages were greatly expanded in number, while the F4/80 and iNOS macrophages, the pro-inflammatory γδ T and Th17 cells, and a broad range of inflammatory cytokines along with STAT1 were drastically decreased. These results demonstrate that SDG treatment can effectively resolve the systemic and skin inflammation in psoriasis by ameliorating the gut microbiome and modulating immune responses. Collectively, this study provides useful information for the development of curative therapeutic strategies with natural products to treat psoriasis.},
}
RevDate: 2026-04-21
Pre-existing Gut Microbiome Dysbiosis Exacerbates Neuroinflammation and Vasospasm After Subarachnoid Hemorrhage in Mice.
Neurosurgery pii:00006123-990000000-02127 [Epub ahead of print].
BACKGROUND AND OBJECTIVES: Delayed cerebral ischemia remains a major determinant of poor outcomes after aneurysmal subarachnoid hemorrhage (SAH), yet effective preventive strategies are limited. The gut-brain axis has emerged as an important modulator of post-SAH neuroinflammation and vascular dysfunction. We hypothesized that pre-existing gut microbiome dysbiosis (GMD) exacerbates neuroinflammation and vasospasm after SAH.
METHODS: Male C57BL/6J mice underwent broad-spectrum antibiotic-induced gut microbiome depletion or control treatment, followed by endovascular perforation SAH or control surgery. Neurological function, body weight, and mortality were assessed longitudinally. Cerebral vasospasm was quantified by anterior cerebral artery morphometry. Endothelial activation and neuroinflammation were evaluated using intercellular adhesion molecule 1 and ionized calcium-binding adapter molecule 1 immunofluorescence. Immune cell populations in the brain and spleen were analyzed by flow cytometry, and serum cytokines were measured by multiplex assays. Gut microbiome composition was assessed using 16S rRNA sequencing in microbiota-intact mice.
RESULTS: SAH alone caused minimal early changes in gut microbial diversity or composition, indicating that early post-SAH outcomes were not driven by SAH-induced dysbiosis. By contrast, pre-existing GMD did not affect initial SAH severity but significantly worsened post-SAH outcomes, including weight loss, neurological deficits, and cerebral vasospasm. Vasospasm severity correlated robustly with endothelial intercellular adhesion molecule 1 expression and cortical ionized calcium-binding adapter molecule 1-positive microglia/macrophages. GMD amplified central and peripheral inflammatory responses, characterized by increased CD86-positive macrophages and neutrophils in the brain and splenic macrophage expansion. Systemically, GMD altered cytokine profiles, with elevated CCL5 and reduced granulocyte colony-stimulating factor, and CCL5 levels correlated with both neuroinflammation and vasospasm severity.
CONCLUSION: Pre-existing GMD exacerbates neurovascular inflammation, vasospasm, and neurological impairment after SAH through dysregulated central and systemic immune responses. These findings identify the gut-brain axis as a critical modulator of delayed cerebral ischemia-like pathology and suggest microbiome-targeted strategies as potential therapeutic approaches for SAH.
Additional Links: PMID-42012190
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@article {pmid42012190,
year = {2026},
author = {Matsukawa, H and Fujita, M and Kuramoto, Y and Kuwahara, S and Tsuji, S and Takeda, Y and Son, A and Kato, T and Shirakawa, M and Yoshimura, S},
title = {Pre-existing Gut Microbiome Dysbiosis Exacerbates Neuroinflammation and Vasospasm After Subarachnoid Hemorrhage in Mice.},
journal = {Neurosurgery},
volume = {},
number = {},
pages = {},
doi = {10.1227/neu.0000000000004035},
pmid = {42012190},
issn = {1524-4040},
support = {22H04349//Japan Society for the Promotion of Science (JSPS) KAKENHI Grant/ ; 22K16699//Japan Society for the Promotion of Science (JSPS) KAKENHI Grant/ ; 25K12352//Japan Society for the Promotion of Science (JSPS) KAKENHI Grant/ ; },
abstract = {BACKGROUND AND OBJECTIVES: Delayed cerebral ischemia remains a major determinant of poor outcomes after aneurysmal subarachnoid hemorrhage (SAH), yet effective preventive strategies are limited. The gut-brain axis has emerged as an important modulator of post-SAH neuroinflammation and vascular dysfunction. We hypothesized that pre-existing gut microbiome dysbiosis (GMD) exacerbates neuroinflammation and vasospasm after SAH.
METHODS: Male C57BL/6J mice underwent broad-spectrum antibiotic-induced gut microbiome depletion or control treatment, followed by endovascular perforation SAH or control surgery. Neurological function, body weight, and mortality were assessed longitudinally. Cerebral vasospasm was quantified by anterior cerebral artery morphometry. Endothelial activation and neuroinflammation were evaluated using intercellular adhesion molecule 1 and ionized calcium-binding adapter molecule 1 immunofluorescence. Immune cell populations in the brain and spleen were analyzed by flow cytometry, and serum cytokines were measured by multiplex assays. Gut microbiome composition was assessed using 16S rRNA sequencing in microbiota-intact mice.
RESULTS: SAH alone caused minimal early changes in gut microbial diversity or composition, indicating that early post-SAH outcomes were not driven by SAH-induced dysbiosis. By contrast, pre-existing GMD did not affect initial SAH severity but significantly worsened post-SAH outcomes, including weight loss, neurological deficits, and cerebral vasospasm. Vasospasm severity correlated robustly with endothelial intercellular adhesion molecule 1 expression and cortical ionized calcium-binding adapter molecule 1-positive microglia/macrophages. GMD amplified central and peripheral inflammatory responses, characterized by increased CD86-positive macrophages and neutrophils in the brain and splenic macrophage expansion. Systemically, GMD altered cytokine profiles, with elevated CCL5 and reduced granulocyte colony-stimulating factor, and CCL5 levels correlated with both neuroinflammation and vasospasm severity.
CONCLUSION: Pre-existing GMD exacerbates neurovascular inflammation, vasospasm, and neurological impairment after SAH through dysregulated central and systemic immune responses. These findings identify the gut-brain axis as a critical modulator of delayed cerebral ischemia-like pathology and suggest microbiome-targeted strategies as potential therapeutic approaches for SAH.},
}
RevDate: 2026-04-21
Formulation-dependent kinetics of Lacticaseibacillus paracasei Zhang in mice.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: The relationship between gut microbiota and human health has become one of the focal point in medical research. Probiotics, which modulate the gut microbiome, hold considerable promise for both prophylaxis and therapeutic intervention. This requires deeper insights into the kinetic changes and molecular mechanisms upon probiotic entry into the body. In this study, we utilized advanced molecular imaging to delineate the in vivo kinetic dynamics of two Lacticaseibacillus paracasei Zhang (L. paracasei Zhang, LPZ) formulations: a liquid culture and a lyophilized powder. Our results provide new insights into the gastrointestinal transit and growth kinetics of the different probiotics formulations. Strikingly, the liquid LPZ achieved its peak growth phase within a relatively short period of 6 to 8 h post-ingestion, culminating in a 270- to 680-fold increase in residues at the 24th hour post-ingestion when compared to the lyophilized powder LPZ. Furthermore, during peak in vivo replication, LPZ enhanced gut microbial diversity and enriched beneficial commensal communities. Functionally, LPZ ingestion attenuated virulence factors while upregulating carbohydrate-active enzymes. Notably, LPZ significantly reduced xanthine levels, a metabolite associated with hyperuricemia, thereby providing a mechanistic basis for the observed relief from gout symptoms. This supports the mechanism of prior clinical findings and paves the way for future clinical trials and therapeutic use of LPZ and related probiotics.
IMPORTANCE: The innovation of this study lies in visualizing the kinetic changes of two Lacticaseibacillus paracasei Zhang (L. paracasei Zhang, LPZ) formulations (a liquid culture and lyophilized powder) within the gastrointestinal tract. It was found that liquid LPZ proliferates in vivo with a higher retention rate. Furthermore, we also found that when liquid LPZ reaches its peak proliferation phase in vivo, it not only effectively promotes the proliferation of other beneficial bacteria and the production of their metabolites but also generates more carbohydrate-active enzymes while reducing virulence factors, thereby amplifying the functions of LPZ. Meanwhile, we observed that liquid LPZ significantly reduces the production of xanthine in vivo, indicating its potential to lower uric acid. In light of the aforementioned findings, we herein propose the concept of "probiotikinetics." These results provide new insights into the intake of LPZ, along with important evidence for its application in healthy populations.
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@article {pmid42012194,
year = {2026},
author = {Han, N and Bai, F and Wen, Q and Bi, Y and Yang, R and Han, Y},
title = {Formulation-dependent kinetics of Lacticaseibacillus paracasei Zhang in mice.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0363725},
doi = {10.1128/spectrum.03637-25},
pmid = {42012194},
issn = {2165-0497},
abstract = {UNLABELLED: The relationship between gut microbiota and human health has become one of the focal point in medical research. Probiotics, which modulate the gut microbiome, hold considerable promise for both prophylaxis and therapeutic intervention. This requires deeper insights into the kinetic changes and molecular mechanisms upon probiotic entry into the body. In this study, we utilized advanced molecular imaging to delineate the in vivo kinetic dynamics of two Lacticaseibacillus paracasei Zhang (L. paracasei Zhang, LPZ) formulations: a liquid culture and a lyophilized powder. Our results provide new insights into the gastrointestinal transit and growth kinetics of the different probiotics formulations. Strikingly, the liquid LPZ achieved its peak growth phase within a relatively short period of 6 to 8 h post-ingestion, culminating in a 270- to 680-fold increase in residues at the 24th hour post-ingestion when compared to the lyophilized powder LPZ. Furthermore, during peak in vivo replication, LPZ enhanced gut microbial diversity and enriched beneficial commensal communities. Functionally, LPZ ingestion attenuated virulence factors while upregulating carbohydrate-active enzymes. Notably, LPZ significantly reduced xanthine levels, a metabolite associated with hyperuricemia, thereby providing a mechanistic basis for the observed relief from gout symptoms. This supports the mechanism of prior clinical findings and paves the way for future clinical trials and therapeutic use of LPZ and related probiotics.
IMPORTANCE: The innovation of this study lies in visualizing the kinetic changes of two Lacticaseibacillus paracasei Zhang (L. paracasei Zhang, LPZ) formulations (a liquid culture and lyophilized powder) within the gastrointestinal tract. It was found that liquid LPZ proliferates in vivo with a higher retention rate. Furthermore, we also found that when liquid LPZ reaches its peak proliferation phase in vivo, it not only effectively promotes the proliferation of other beneficial bacteria and the production of their metabolites but also generates more carbohydrate-active enzymes while reducing virulence factors, thereby amplifying the functions of LPZ. Meanwhile, we observed that liquid LPZ significantly reduces the production of xanthine in vivo, indicating its potential to lower uric acid. In light of the aforementioned findings, we herein propose the concept of "probiotikinetics." These results provide new insights into the intake of LPZ, along with important evidence for its application in healthy populations.},
}
RevDate: 2026-04-21
Alcohol consumption and colorectal carcinogenesis: an exploration of the gut microbial pathway as a potential mediator.
European journal of nutrition, 65(4):.
Additional Links: PMID-42012708
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@article {pmid42012708,
year = {2026},
author = {Kværner, AS and Birkeland, E and Avershina, E and Botteri, E and Bucher-Johannessen, C and Knudsen, MD and Hjartåker, A and Page, CM and Hov, JR and Song, M and Randel, KR and Hoff, G and Rounge, TB and Berstad, P},
title = {Alcohol consumption and colorectal carcinogenesis: an exploration of the gut microbial pathway as a potential mediator.},
journal = {European journal of nutrition},
volume = {65},
number = {4},
pages = {},
pmid = {42012708},
issn = {1436-6215},
}
RevDate: 2026-04-21
Human Gut Microbiome Can Degrade the Sweetener Acesulfame K with Potential Damaging Effects in the Intestinal Barrier Function.
Journal of agricultural and food chemistry [Epub ahead of print].
Acesulfame K (Ace-K) is a commonly consumed sweetener, although knowledge about the Ace-K-gut microbiota interaction remains limited. This study evaluates dose-dependent effects of Ace-K on metataxonomics, metagenomics, and metabolic activity of children gut microbiota developed in a dynamic gut simulator. An Ace-K-dose dependent increase in Anaerostipes, Coprococcus, Subdoligranulum, Blautia, Sutterella wadsworthensis, Alistipes, and Bacteroides thetaiotaomicron was observed. Butyrate showed a dose-response increase that correlated with Ace-K consumption, suggesting its microbial metabolism. Increasing bacterial taxa showed sulfatase and amidase activities potentially capable of degrading Ace-K, releasing sulfamate and acetoacetate, which species such as Anaerostipes hadrus and Intestinimonas can metabolize to produce butyrate via the butanoyl-CoA pathway. Furthermore, the Ace-K-microbiome interaction led to a dose-dependent decrease in Caco-2 epithelial integrity, possibly due to the release of sulfated metabolites. This study provides evidence of the potential risk of Ace-K consumption based on its metabolism by the human gut microbiome.
Additional Links: PMID-42012901
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@article {pmid42012901,
year = {2026},
author = {Bellanco, A and Yépez-Notario, C and Lozano, M and Martínez-Cuesta, MC and Requena, T},
title = {Human Gut Microbiome Can Degrade the Sweetener Acesulfame K with Potential Damaging Effects in the Intestinal Barrier Function.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c16498},
pmid = {42012901},
issn = {1520-5118},
abstract = {Acesulfame K (Ace-K) is a commonly consumed sweetener, although knowledge about the Ace-K-gut microbiota interaction remains limited. This study evaluates dose-dependent effects of Ace-K on metataxonomics, metagenomics, and metabolic activity of children gut microbiota developed in a dynamic gut simulator. An Ace-K-dose dependent increase in Anaerostipes, Coprococcus, Subdoligranulum, Blautia, Sutterella wadsworthensis, Alistipes, and Bacteroides thetaiotaomicron was observed. Butyrate showed a dose-response increase that correlated with Ace-K consumption, suggesting its microbial metabolism. Increasing bacterial taxa showed sulfatase and amidase activities potentially capable of degrading Ace-K, releasing sulfamate and acetoacetate, which species such as Anaerostipes hadrus and Intestinimonas can metabolize to produce butyrate via the butanoyl-CoA pathway. Furthermore, the Ace-K-microbiome interaction led to a dose-dependent decrease in Caco-2 epithelial integrity, possibly due to the release of sulfated metabolites. This study provides evidence of the potential risk of Ace-K consumption based on its metabolism by the human gut microbiome.},
}
RevDate: 2026-04-21
The naked mole-rat microbiome is associated with healthy aging and social structure.
Cell reports, 45(4):117265 pii:S2211-1247(26)00343-8 [Epub ahead of print].
The naked mole-rat (NMR), Heterocephalus glaber, is an unusual mammal that lives underground in eusocial colonies. NMRs show remarkable longevity and are resistant to cancer, neurodegeneration, and cardiovascular disease. The gut microbiome is known to modulate human health and disease; here, we investigate the microbiome of NMRs, comparing fecal samples from individuals over different social ranks and over a span of more than three decades. In contrast to a cohort of C57BL6/J mice, which showed extensive age-related changes, we found little difference in the microbiota of NMRs from different age cohorts. Only the archaea Methanomassiliicoccus intestinalis, which was present in the NMR gut but not the murine gut, showed an increased proportion with older age. Pregnant queens were found to have higher microbial diversity, potentially a consequence of their aggressive coprophagia. Overall, these findings provide a rich and dynamic picture of the NMR microbiome and starting points for future investigation.
Additional Links: PMID-42012979
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@article {pmid42012979,
year = {2026},
author = {Tanes, C and Wilson, NG and Smith, M and Patel, TT and Merenstein, C and Bushman, FD and Bittinger, K and Buffenstein, R},
title = {The naked mole-rat microbiome is associated with healthy aging and social structure.},
journal = {Cell reports},
volume = {45},
number = {4},
pages = {117265},
doi = {10.1016/j.celrep.2026.117265},
pmid = {42012979},
issn = {2211-1247},
abstract = {The naked mole-rat (NMR), Heterocephalus glaber, is an unusual mammal that lives underground in eusocial colonies. NMRs show remarkable longevity and are resistant to cancer, neurodegeneration, and cardiovascular disease. The gut microbiome is known to modulate human health and disease; here, we investigate the microbiome of NMRs, comparing fecal samples from individuals over different social ranks and over a span of more than three decades. In contrast to a cohort of C57BL6/J mice, which showed extensive age-related changes, we found little difference in the microbiota of NMRs from different age cohorts. Only the archaea Methanomassiliicoccus intestinalis, which was present in the NMR gut but not the murine gut, showed an increased proportion with older age. Pregnant queens were found to have higher microbial diversity, potentially a consequence of their aggressive coprophagia. Overall, these findings provide a rich and dynamic picture of the NMR microbiome and starting points for future investigation.},
}
RevDate: 2026-04-21
A New approach and conceptual model for understanding systemic sclerosis-associated gastrointestinal symptoms.
Expert review of clinical immunology [Epub ahead of print].
INTRODUCTION: Our understanding of the pathogenesis of systemic sclerosis-associated gastrointestinal (SSc-GI) disease is limited. This has hindered progress in the management of SSc-GI disease as objective measures to assess extent of disease and monitor treatment response are lacking. We propose a conceptual model for understanding pathogenic mechanisms of SSc-GI symptoms. A multi-dimensional model of understanding the etiology of symptoms may enable an improved understanding of patients' symptom experience and opportunities for development of therapies.
AREAS COVERED: We reviewed literature from the past 5 years pertaining to SSc-GI symptoms and their etiology. When gaps in data were identified, we evaluated research from general gastroenterology and inflammatory bowel disease. We describe evolving concepts of pathologic mechanisms of SSc-GI disease, including motility, the gut-brain axis, diet, the microbiome and pelvic floor dysfunction.
EXPERT OPINION: A broad understanding of factors that contribute to symptoms is necessary to understand the experience of SSc-GI disease and develop targeted therapies that modify the SSc-GI disease course. Due to a lack of objective clinical outcome measures in SSc-GI disease, qualitative research methodologies are essential for deepening our understanding of these patient experiences and developing new outcome measures to enable trials to establish an evidence-based approach to SSc-GI disease.
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@article {pmid42012987,
year = {2026},
author = {Good, SD and Volkmann, ER and Basnayake, C and Ross, L},
title = {A New approach and conceptual model for understanding systemic sclerosis-associated gastrointestinal symptoms.},
journal = {Expert review of clinical immunology},
volume = {},
number = {},
pages = {},
doi = {10.1080/1744666X.2026.2663044},
pmid = {42012987},
issn = {1744-8409},
abstract = {INTRODUCTION: Our understanding of the pathogenesis of systemic sclerosis-associated gastrointestinal (SSc-GI) disease is limited. This has hindered progress in the management of SSc-GI disease as objective measures to assess extent of disease and monitor treatment response are lacking. We propose a conceptual model for understanding pathogenic mechanisms of SSc-GI symptoms. A multi-dimensional model of understanding the etiology of symptoms may enable an improved understanding of patients' symptom experience and opportunities for development of therapies.
AREAS COVERED: We reviewed literature from the past 5 years pertaining to SSc-GI symptoms and their etiology. When gaps in data were identified, we evaluated research from general gastroenterology and inflammatory bowel disease. We describe evolving concepts of pathologic mechanisms of SSc-GI disease, including motility, the gut-brain axis, diet, the microbiome and pelvic floor dysfunction.
EXPERT OPINION: A broad understanding of factors that contribute to symptoms is necessary to understand the experience of SSc-GI disease and develop targeted therapies that modify the SSc-GI disease course. Due to a lack of objective clinical outcome measures in SSc-GI disease, qualitative research methodologies are essential for deepening our understanding of these patient experiences and developing new outcome measures to enable trials to establish an evidence-based approach to SSc-GI disease.},
}
RevDate: 2026-04-21
Incremental value of a gut microbiome score (M-score) for predicting stroke-associated pneumonia beyond the clinical A2DS2 score: A nested case-control study.
Acta microbiologica et immunologica Hungarica pii:030.2026.02907 [Epub ahead of print].
Stroke-associated pneumonia (SAP) is a major complication of acute ischemic stroke. The brain-gut-lung axis suggests that post-stroke gut dysbiosis may offer independent risk information beyond clinical scores like A2DS2. The aim of this study was to evaluate the incremental predictive value of early post-stroke gut microbiome biomarkers for SAP and to construct a simplified microbiome risk score (M-score). In a prospective nested case-control study, we identified 63 SAP cases from a cohort of 551 patients with acute ischemic stroke and stool samples were collected 24-72 h post-admission. Cases were matched 1:2 (age, sex) to 126 controls. Gut microbiota was profiled via 16S rRNA sequencing. Three differentially abundant genera (prevalence ≥20%, FDR q < 0.10) were used to construct an M-score via bootstrapped regression. Independent associations were assessed with conditional logistic regression. Incremental value over the A2DS2 score was evaluated using AUC, continuous net reclassification improvement (NRI), and the Brier score. SAP cases exhibited reduced α-diversity and distinct β-diversity (both P < 0.01). Cases had higher Enterococcus and Streptococcus and lower Faecalibacterium levels (all q < 0.05). The M-score was independently associated with SAP (adjusted OR per 1-SD: 1.76, 95% CI: 1.30-2.39, P = 0.001). Adding the M-score to A2DS2 significantly improved prediction: AUC increased from 0.76 to 0.84 (ΔAUC = 0.08, P = 0.009), NRI was 0.31 (95% CI: 0.12-0.51), and the Brier score decreased from 0.18 to 0.16. Results were robust in sensitivity analyses. A gut microbiome score based on three genera provides significant independent and incremental predictive value for SAP over the A2DS2 score, enabling more precise early risk stratification after stroke.
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@article {pmid42013360,
year = {2026},
author = {Zhang, Y and Dong, Q and Li, W},
title = {Incremental value of a gut microbiome score (M-score) for predicting stroke-associated pneumonia beyond the clinical A2DS2 score: A nested case-control study.},
journal = {Acta microbiologica et immunologica Hungarica},
volume = {},
number = {},
pages = {},
doi = {10.1556/030.2026.02907},
pmid = {42013360},
issn = {1588-2640},
abstract = {Stroke-associated pneumonia (SAP) is a major complication of acute ischemic stroke. The brain-gut-lung axis suggests that post-stroke gut dysbiosis may offer independent risk information beyond clinical scores like A2DS2. The aim of this study was to evaluate the incremental predictive value of early post-stroke gut microbiome biomarkers for SAP and to construct a simplified microbiome risk score (M-score). In a prospective nested case-control study, we identified 63 SAP cases from a cohort of 551 patients with acute ischemic stroke and stool samples were collected 24-72 h post-admission. Cases were matched 1:2 (age, sex) to 126 controls. Gut microbiota was profiled via 16S rRNA sequencing. Three differentially abundant genera (prevalence ≥20%, FDR q < 0.10) were used to construct an M-score via bootstrapped regression. Independent associations were assessed with conditional logistic regression. Incremental value over the A2DS2 score was evaluated using AUC, continuous net reclassification improvement (NRI), and the Brier score. SAP cases exhibited reduced α-diversity and distinct β-diversity (both P < 0.01). Cases had higher Enterococcus and Streptococcus and lower Faecalibacterium levels (all q < 0.05). The M-score was independently associated with SAP (adjusted OR per 1-SD: 1.76, 95% CI: 1.30-2.39, P = 0.001). Adding the M-score to A2DS2 significantly improved prediction: AUC increased from 0.76 to 0.84 (ΔAUC = 0.08, P = 0.009), NRI was 0.31 (95% CI: 0.12-0.51), and the Brier score decreased from 0.18 to 0.16. Results were robust in sensitivity analyses. A gut microbiome score based on three genera provides significant independent and incremental predictive value for SAP over the A2DS2 score, enabling more precise early risk stratification after stroke.},
}
RevDate: 2026-04-21
Data Science at the Interface of Air Pollution and Lung Health: Toward Precision Health.
Annual review of biomedical data science [Epub ahead of print].
Air pollution is a leading cause of death, commonly linked to respiratory diseases, such as asthma, chronic obstructive pulmonary disease, and lung cancer. With a view toward precision health, efforts have been made to ascertain the relationships between air pollution and molecular dysregulation to direct risk management and prevention of pollution-promoted respiratory diseases. To this end, there have been several analyses aimed at uncovering how air pollution drives disease through dysregulation of the methylome, transcriptome, metabolome, proteome, genome, and microbiome. Here we review these studies, assess their current limitations, and discuss their contributions to research at the interface of air pollution and lung health. We highlight how large-scale analyses have elucidated the role of air pollution in dysregulating genomic stability, inflammation, and apoptotic pathways to promote respiratory diseases. Finally, we summarize opportunities for future research that may be facilitated by ongoing improvements in exposure estimates and multiomic integration strategies.
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@article {pmid42013465,
year = {2026},
author = {Ofori-Amanfo, K and Dustin, M and Lim, EL},
title = {Data Science at the Interface of Air Pollution and Lung Health: Toward Precision Health.},
journal = {Annual review of biomedical data science},
volume = {},
number = {},
pages = {},
doi = {10.1146/annurev-biodatasci-092724-061536},
pmid = {42013465},
issn = {2574-3414},
abstract = {Air pollution is a leading cause of death, commonly linked to respiratory diseases, such as asthma, chronic obstructive pulmonary disease, and lung cancer. With a view toward precision health, efforts have been made to ascertain the relationships between air pollution and molecular dysregulation to direct risk management and prevention of pollution-promoted respiratory diseases. To this end, there have been several analyses aimed at uncovering how air pollution drives disease through dysregulation of the methylome, transcriptome, metabolome, proteome, genome, and microbiome. Here we review these studies, assess their current limitations, and discuss their contributions to research at the interface of air pollution and lung health. We highlight how large-scale analyses have elucidated the role of air pollution in dysregulating genomic stability, inflammation, and apoptotic pathways to promote respiratory diseases. Finally, we summarize opportunities for future research that may be facilitated by ongoing improvements in exposure estimates and multiomic integration strategies.},
}
RevDate: 2026-04-21
Microbiome and metabolomics provide insights into the metamorphosis and settlement in the jellyfish Aurelia coerulea inhibited by Bacillus pacificus.
Marine pollution bulletin, 229:119760 pii:S0025-326X(26)00547-3 [Epub ahead of print].
Jellyfish outbreaks threaten coastal ecosystems and demand urgent control strategies, the potential for microbial-based interventions remains largely unexplored even though the key role of microbiota in marine invertebrate development. Bacillus pacificus SG15 inhibits settlement and metamorphosis of Aurelia coerulea planulae, although the underlying mechanism remains unclear. Here, we employed a combination of co-culture experiments, high-throughput sequencing, and metabolomics analyses to elucidate these mechanisms. Our results indicated that strain SG15 inhibited planulae settlement and metamorphosis and induced developmental abnormalities. Inoculation with strain SG15 reduced the abundance of Neptuniibacter, a reported potential probiotic for jellyfish, and decreased metabolites critical for metamorphosis, including all-trans-4-Oxoretinoic acid, indole-3-acetamide and indole-3-carbinol. Functional analysis revealed that strain SG15 inoculation interfered with metabolic pathways related to calcium signaling, gap junction, and nervous system development. Additionally, polyp tissues exhibited an accumulation of L-tryptophan, L-phenylalanine, and L-leucine, alongside a marked decline in the tryptophan-derived metabolite indole-3-acetamide, suggesting impaired host metabolic capacity. These metabolic shifts showed a significant correlation with changes in the abundance of Bacillus, Neptuniibacter, Marivita, Ruegeria, and Sulfitobacter. Collectively, our findings revealed that strain SG15 disrupts key host metabolic functions by altering the microbial community, thereby depriving planulae of essential compounds required for settlement and metamorphosis, providing a foundation for novel strategies to mitigate jellyfish blooms and their ecological effects.
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@article {pmid42013483,
year = {2026},
author = {Guo, X and Li, M and Ahmad, M and Liu, X and Zhang, S and Yu, Z and Zhao, Y and Sun, H and Zhang, Y},
title = {Microbiome and metabolomics provide insights into the metamorphosis and settlement in the jellyfish Aurelia coerulea inhibited by Bacillus pacificus.},
journal = {Marine pollution bulletin},
volume = {229},
number = {},
pages = {119760},
doi = {10.1016/j.marpolbul.2026.119760},
pmid = {42013483},
issn = {1879-3363},
abstract = {Jellyfish outbreaks threaten coastal ecosystems and demand urgent control strategies, the potential for microbial-based interventions remains largely unexplored even though the key role of microbiota in marine invertebrate development. Bacillus pacificus SG15 inhibits settlement and metamorphosis of Aurelia coerulea planulae, although the underlying mechanism remains unclear. Here, we employed a combination of co-culture experiments, high-throughput sequencing, and metabolomics analyses to elucidate these mechanisms. Our results indicated that strain SG15 inhibited planulae settlement and metamorphosis and induced developmental abnormalities. Inoculation with strain SG15 reduced the abundance of Neptuniibacter, a reported potential probiotic for jellyfish, and decreased metabolites critical for metamorphosis, including all-trans-4-Oxoretinoic acid, indole-3-acetamide and indole-3-carbinol. Functional analysis revealed that strain SG15 inoculation interfered with metabolic pathways related to calcium signaling, gap junction, and nervous system development. Additionally, polyp tissues exhibited an accumulation of L-tryptophan, L-phenylalanine, and L-leucine, alongside a marked decline in the tryptophan-derived metabolite indole-3-acetamide, suggesting impaired host metabolic capacity. These metabolic shifts showed a significant correlation with changes in the abundance of Bacillus, Neptuniibacter, Marivita, Ruegeria, and Sulfitobacter. Collectively, our findings revealed that strain SG15 disrupts key host metabolic functions by altering the microbial community, thereby depriving planulae of essential compounds required for settlement and metamorphosis, providing a foundation for novel strategies to mitigate jellyfish blooms and their ecological effects.},
}
RevDate: 2026-04-21
Impact of spray-dried Lactiplantibacillus plantarum CIDCA 83114 on a murine model of giardiasis.
Revista Argentina de microbiologia, 58(3):100721 pii:S0325-7541(26)00031-3 [Epub ahead of print].
This study investigates the efficacy of spray-dried Lactiplantibacillus plantarum CIDCA 83114 in a murine model of giardiasis. Mice (C57BL/6) were divided into four groups: control, Giardia-only, probiotic-only, and a combined (probiotic+Giardia, PG) group. Probiotic treatment started one week pre-infection with Giardia intestinalis H7 and continued throughout the study. Infection was monitored through trophozoite counts, intestinal histology, cytokine expression and microbiome analysis. Histology revealed that the administration of strain CIDCA 83114 prior to infection, increases villus/crypt ratios compared with control infected animals. In addition, trophozoite counts in the small intestine were lower in probiotic-treated mice than in infected control animals. Probiotic-treated infected mice showed significantly higher IL-10 expression than untreated controls. Expression of the IL-12 gene was diminished in animals administered with strain CIDCA 83114 (both infected and non-infected with Giardia). In addition, Giardia infection led to a decrease in IFN-γ expression, even when the probiotic-treated animals. Expression of TNF-α increased in the groups treated only with strain CIDCA 83114 and in infected animals. Notably, the PG group exhibited lower values of TNF-α expression, potentially due to the elevated IL-10 levels detected in this group. Dysbiosis associated with Giardia infection led to an increase in Epsilonproteobacteria and Clostridium. These changes were abrogated in the group that received the probiotic strain, which, as expected, showed an increase in Lactobacillaceae. This study demonstrates that spray-dried probiotic L. plantarum CIDCA 83114 has a positive impact on key aspects of Giardia infection, supporting its potential as a preventive or therapeutic strategy for giardiasis.
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@article {pmid42013659,
year = {2026},
author = {Teijeiro, M and De Antoni, GL and Golowczyc, MA and Pérez, PF},
title = {Impact of spray-dried Lactiplantibacillus plantarum CIDCA 83114 on a murine model of giardiasis.},
journal = {Revista Argentina de microbiologia},
volume = {58},
number = {3},
pages = {100721},
doi = {10.1016/j.ram.2026.100721},
pmid = {42013659},
issn = {0325-7541},
abstract = {This study investigates the efficacy of spray-dried Lactiplantibacillus plantarum CIDCA 83114 in a murine model of giardiasis. Mice (C57BL/6) were divided into four groups: control, Giardia-only, probiotic-only, and a combined (probiotic+Giardia, PG) group. Probiotic treatment started one week pre-infection with Giardia intestinalis H7 and continued throughout the study. Infection was monitored through trophozoite counts, intestinal histology, cytokine expression and microbiome analysis. Histology revealed that the administration of strain CIDCA 83114 prior to infection, increases villus/crypt ratios compared with control infected animals. In addition, trophozoite counts in the small intestine were lower in probiotic-treated mice than in infected control animals. Probiotic-treated infected mice showed significantly higher IL-10 expression than untreated controls. Expression of the IL-12 gene was diminished in animals administered with strain CIDCA 83114 (both infected and non-infected with Giardia). In addition, Giardia infection led to a decrease in IFN-γ expression, even when the probiotic-treated animals. Expression of TNF-α increased in the groups treated only with strain CIDCA 83114 and in infected animals. Notably, the PG group exhibited lower values of TNF-α expression, potentially due to the elevated IL-10 levels detected in this group. Dysbiosis associated with Giardia infection led to an increase in Epsilonproteobacteria and Clostridium. These changes were abrogated in the group that received the probiotic strain, which, as expected, showed an increase in Lactobacillaceae. This study demonstrates that spray-dried probiotic L. plantarum CIDCA 83114 has a positive impact on key aspects of Giardia infection, supporting its potential as a preventive or therapeutic strategy for giardiasis.},
}
RevDate: 2026-04-21
When "biodegradable" is not benign: Microplastic-driven disruption of soil processes and plant-microbe interactions.
Journal of hazardous materials, 510:142138 pii:S0304-3894(26)01116-7 [Epub ahead of print].
The increasing use of biodegradable plastics (BPs) as alternatives to conventional plastics (CPs) is leading to the accumulation of biodegradable microplastics (BMPs) in terrestrial environments. Contrary to assumptions of rapid degradation, BMPs can persist in soil long enough to interact with key biological processes. This review advances the field by proposing a mechanistic framework linking BMP aging and degradation, soil physicochemical transformations, plastisphere assembly, rhizosphere interactions, and plant responses, and by critically evaluating the sources of inconsistency across studies. We show that divergent effects of BMPs can be best explained by four interacting determinants: polymer chemistry and additive composition, aging-driven surface transformations, soil physicochemical properties, and rhizosphere processes including plant-mediated effects. Through these coupled pathways, BMPs can alter aggregation, pore architecture, pH, enzyme activity, and carbon and nutrient cycling, thereby reshaping the soil environment in which microorganisms and roots interact. BMP surfaces can also act as dynamic microbial niches that promote biofilm formation, shift microbial community composition and function, and under certain conditions may facilitate pollutant transport, pathogen persistence, and horizontal gene transfer. Plant responses to BMPs are predominantly indirect and emerge from rhizosphere-mediated processes, which helps explain the wide variability in reported plant responses, ranging from subtle metabolic changes to pronounced growth inhibition. However, current evidence is constrained by short-term studies and insufficient consideration of aged materials. Biodegradability should therefore not be equated with low ecological risk in soils. Progress in this field requires integrative approaches linking BMP properties, plastisphere dynamics, and plant-soil interactions over time.
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@article {pmid42013709,
year = {2026},
author = {Pelko, T and Jemec Kokalj, A and Regvar, M and Dermastia, M and Vogel-Mikuš, K},
title = {When "biodegradable" is not benign: Microplastic-driven disruption of soil processes and plant-microbe interactions.},
journal = {Journal of hazardous materials},
volume = {510},
number = {},
pages = {142138},
doi = {10.1016/j.jhazmat.2026.142138},
pmid = {42013709},
issn = {1873-3336},
abstract = {The increasing use of biodegradable plastics (BPs) as alternatives to conventional plastics (CPs) is leading to the accumulation of biodegradable microplastics (BMPs) in terrestrial environments. Contrary to assumptions of rapid degradation, BMPs can persist in soil long enough to interact with key biological processes. This review advances the field by proposing a mechanistic framework linking BMP aging and degradation, soil physicochemical transformations, plastisphere assembly, rhizosphere interactions, and plant responses, and by critically evaluating the sources of inconsistency across studies. We show that divergent effects of BMPs can be best explained by four interacting determinants: polymer chemistry and additive composition, aging-driven surface transformations, soil physicochemical properties, and rhizosphere processes including plant-mediated effects. Through these coupled pathways, BMPs can alter aggregation, pore architecture, pH, enzyme activity, and carbon and nutrient cycling, thereby reshaping the soil environment in which microorganisms and roots interact. BMP surfaces can also act as dynamic microbial niches that promote biofilm formation, shift microbial community composition and function, and under certain conditions may facilitate pollutant transport, pathogen persistence, and horizontal gene transfer. Plant responses to BMPs are predominantly indirect and emerge from rhizosphere-mediated processes, which helps explain the wide variability in reported plant responses, ranging from subtle metabolic changes to pronounced growth inhibition. However, current evidence is constrained by short-term studies and insufficient consideration of aged materials. Biodegradability should therefore not be equated with low ecological risk in soils. Progress in this field requires integrative approaches linking BMP properties, plastisphere dynamics, and plant-soil interactions over time.},
}
RevDate: 2026-04-21
Biochemical and molecular mechanisms of resilience in the response of prokaryotes of an active volcano to cadmium-induced stress.
Microbiological research, 309:128529 pii:S0944-5013(26)00093-5 [Epub ahead of print].
The crater lake of the active volcano "El Chichón" in Mexico, represents an ecosystem characterized by changing conditions of salinity, acidity, temperature, and the concentration of different heavy metals, posing significant challenges to the abundance and diversity of microorganisms. In this study, anaerobic mesophilic and hyperthermophilic prokaryotic microbiomes isolated from the volcano-lake were evaluated to elucidate the molecular and biochemical mechanisms involved in Cd[2+] bioremoval. Cultures consumed actively carbohydrates, triacetylglycerol, acetate and methanol; the hyperthermophilic microbiome produced 50% more biomass than mesophiles at the end of the growth curve; however, the presence of Cd[2+] stimulated the biomass and methane production in the mesophilic microbiome. The relative abundance of the 16S rRNA metabarcoding analysis showed dominance of Firmicutes and Euryarchaeota in both microbiomes. The constitutive synthesis of biofilm and the overproduction of polyphosphates and thiol group molecules were protection mechanisms against Cd[2+] toxicity. Such mechanisms allowed 68-74% of Cd[2+] bioremoval (biosorption plus accumulation) at concentrations up to 500 µM CdCl2. Data suggested that the prokaryotic microbiome isolated from the extreme environment of the "El Chichón" volcano is forming a complex metabolic resilient network involving methanogenesis with phosphate and sulfur metabolism that is capable of thriving under extreme conditions of pH, temperature, and the ability for the Cd[2+] removal. This work provides for the first time, information on the mechanisms of tolerance to poly-extreme conditions; moreover, microbiomes studied here may be a promising strategy for biotechnological applications under extreme conditions.
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@article {pmid42013750,
year = {2026},
author = {Ruíz-Valdiviezo, VM and Hernández-Lira, KV and Silva-Flores, M and Gutiérrez-Sarmiento, W and Ovando-Ovando, CI and Peña-Ocaña, BA and Jasso-Chávez, R},
title = {Biochemical and molecular mechanisms of resilience in the response of prokaryotes of an active volcano to cadmium-induced stress.},
journal = {Microbiological research},
volume = {309},
number = {},
pages = {128529},
doi = {10.1016/j.micres.2026.128529},
pmid = {42013750},
issn = {1618-0623},
abstract = {The crater lake of the active volcano "El Chichón" in Mexico, represents an ecosystem characterized by changing conditions of salinity, acidity, temperature, and the concentration of different heavy metals, posing significant challenges to the abundance and diversity of microorganisms. In this study, anaerobic mesophilic and hyperthermophilic prokaryotic microbiomes isolated from the volcano-lake were evaluated to elucidate the molecular and biochemical mechanisms involved in Cd[2+] bioremoval. Cultures consumed actively carbohydrates, triacetylglycerol, acetate and methanol; the hyperthermophilic microbiome produced 50% more biomass than mesophiles at the end of the growth curve; however, the presence of Cd[2+] stimulated the biomass and methane production in the mesophilic microbiome. The relative abundance of the 16S rRNA metabarcoding analysis showed dominance of Firmicutes and Euryarchaeota in both microbiomes. The constitutive synthesis of biofilm and the overproduction of polyphosphates and thiol group molecules were protection mechanisms against Cd[2+] toxicity. Such mechanisms allowed 68-74% of Cd[2+] bioremoval (biosorption plus accumulation) at concentrations up to 500 µM CdCl2. Data suggested that the prokaryotic microbiome isolated from the extreme environment of the "El Chichón" volcano is forming a complex metabolic resilient network involving methanogenesis with phosphate and sulfur metabolism that is capable of thriving under extreme conditions of pH, temperature, and the ability for the Cd[2+] removal. This work provides for the first time, information on the mechanisms of tolerance to poly-extreme conditions; moreover, microbiomes studied here may be a promising strategy for biotechnological applications under extreme conditions.},
}
RevDate: 2026-04-21
An infant nasal microbial gene atlas uncovers intervention-driven microbiome shifts and salt-resistant pathogen expansion.
Cell host & microbe pii:S1931-3128(26)00127-7 [Epub ahead of print].
Functional studies of how early-life interventions shape the airway microbiome remain scarce. Here, we performed metagenomic sequencing of 704 longitudinal nasal swabs from infants with and without cystic fibrosis (CF) to construct and characterize a non-redundant gene atlas of the infant nasal microbiome. We aimed to determine how the nasal microbiome is perturbed by early therapies, as CF is commonly treated with inhaled hypertonic saline to improve mucociliary clearance. We found functional and compositional microbiome changes linked to inhalation therapy, including an expansion of salt-associated transporter genes and a community shift toward CF-associated microbial opportunists, including Haemophilus influenzae and fungi, carrying the identified salt-associated transporter genes with high sequence and structural identity. Hypertonic, compared with isotonic, saline accelerates H. influenzae growth and induces efflux pumps linked to antibiotic tolerance in vitro. This study establishes a reference framework for functional airway microbiome research, enabling the examination of therapeutic perturbations and their impact on microbial adaptation.
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@article {pmid42013836,
year = {2026},
author = {Steinberg, R and Pust, MM and Arias-Rojas, A and Pishchany, G and Ramsey, KA and Kieninger, E and Moeller, A and Casaulta, C and Hilty, M and Latzin, P and , and , and Korten, I and Xavier, RJ},
title = {An infant nasal microbial gene atlas uncovers intervention-driven microbiome shifts and salt-resistant pathogen expansion.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.019},
pmid = {42013836},
issn = {1934-6069},
abstract = {Functional studies of how early-life interventions shape the airway microbiome remain scarce. Here, we performed metagenomic sequencing of 704 longitudinal nasal swabs from infants with and without cystic fibrosis (CF) to construct and characterize a non-redundant gene atlas of the infant nasal microbiome. We aimed to determine how the nasal microbiome is perturbed by early therapies, as CF is commonly treated with inhaled hypertonic saline to improve mucociliary clearance. We found functional and compositional microbiome changes linked to inhalation therapy, including an expansion of salt-associated transporter genes and a community shift toward CF-associated microbial opportunists, including Haemophilus influenzae and fungi, carrying the identified salt-associated transporter genes with high sequence and structural identity. Hypertonic, compared with isotonic, saline accelerates H. influenzae growth and induces efflux pumps linked to antibiotic tolerance in vitro. This study establishes a reference framework for functional airway microbiome research, enabling the examination of therapeutic perturbations and their impact on microbial adaptation.},
}
RevDate: 2026-04-21
Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments.
Cell host & microbe pii:S1931-3128(26)00128-9 [Epub ahead of print].
Chronic antipsychotic use is associated with neuronal damage and cognitive impairment, with the gut microbiome increasingly implicated. However, the specific microbial metabolites and mechanisms involved remain unknown. Here, we demonstrate that chronic olanzapine treatment induces gut microbial dysbiosis, compromises intestinal barrier integrity, and causes cognitive deficits in mice. Multi-omics analyses reveal profound depletion of the microbiota-associated metabolite ergothioneine in blood and brain, a finding validated in the blood of olanzapine-treated patients and risperidone- and clozapine-treated mice. This deficiency correlates with a loss of ergothioneine-producing bacteria (Cyanobacteria and subordinate taxa). Fecal microbiota transplantation from olanzapine-treated mice confers cognitive impairment, while ergothioneine supplementation mitigates it. Mechanistically, ergothioneine attenuates hippocampal oxidative stress and inhibits the redox-sensitive phosphatase protein tyrosine phosphatase 1B (PTP1B). Furthermore, hippocampal neuronal-specific PTP1B deletion abolishes olanzapine-induced synaptic and cognitive deficits. Our findings identify depletion of microbiota-derived ergothioneine as a mechanism underlying antipsychotic-induced cognitive impairment, highlighting therapeutic strategies to mitigate this side effect.
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@article {pmid42013837,
year = {2026},
author = {Zheng, M and Yan, H and Hao, W and An, H and Chen, X and Wu, Q and Ge, X and Ye, H and Zhou, M and Zhou, G and Yang, X and Hu, M and Zhang, P and Pan, W and Tang, R and Zheng, K and Huang, XF and Yu, Y},
title = {Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.020},
pmid = {42013837},
issn = {1934-6069},
abstract = {Chronic antipsychotic use is associated with neuronal damage and cognitive impairment, with the gut microbiome increasingly implicated. However, the specific microbial metabolites and mechanisms involved remain unknown. Here, we demonstrate that chronic olanzapine treatment induces gut microbial dysbiosis, compromises intestinal barrier integrity, and causes cognitive deficits in mice. Multi-omics analyses reveal profound depletion of the microbiota-associated metabolite ergothioneine in blood and brain, a finding validated in the blood of olanzapine-treated patients and risperidone- and clozapine-treated mice. This deficiency correlates with a loss of ergothioneine-producing bacteria (Cyanobacteria and subordinate taxa). Fecal microbiota transplantation from olanzapine-treated mice confers cognitive impairment, while ergothioneine supplementation mitigates it. Mechanistically, ergothioneine attenuates hippocampal oxidative stress and inhibits the redox-sensitive phosphatase protein tyrosine phosphatase 1B (PTP1B). Furthermore, hippocampal neuronal-specific PTP1B deletion abolishes olanzapine-induced synaptic and cognitive deficits. Our findings identify depletion of microbiota-derived ergothioneine as a mechanism underlying antipsychotic-induced cognitive impairment, highlighting therapeutic strategies to mitigate this side effect.},
}
RevDate: 2026-04-21
Sex-biased intratumoral microbiome influences tumor molecular and immune landscape and disease outcomes.
Cell reports. Medicine pii:S2666-3791(26)00174-6 [Epub ahead of print].
The intratumoral microbiome is increasingly recognized as a regulator of cancer biology, yet sex-specific patterns and their relevance to cancer disparities remain poorly understood. We perform a multi-kingdom analysis of more than 5,000 tumors from seven datasets to identify sex-differential microbial taxa across aerodigestive and gastrointestinal cancers. We identify and validate 22 taxa with consistent sex-biased abundance, including in real-world cohort. These microbes show cancer-type- and microbe-specific associations with tumor transcriptomes, oncogenic pathways, and immune cell infiltration. Female-enriched microbes are linked to increased estrogen signaling and interferon responses, whereas male-enriched taxa show opposing patterns. In gastric cancer, intratumoral Epstein-Barr virus is enriched in males and associated with higher CD8[+] T cell infiltration and improved survival. Functional co-culture experiments demonstrate that sex-biased microbes modulate chemotherapy sensitivity. Together, these findings reveal a sex-biased intratumoral microbiome axis that shapes tumor phenotypes and disease outcomes, highlighting opportunities for microbiota-guided, sex-aware approaches in oncology.
Additional Links: PMID-42013847
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@article {pmid42013847,
year = {2026},
author = {Shan, Y and Huang, Y and Lee, A and Elmorsi, RM and Phan, T and Chaudhury, I and Corbiere, T and Collins, LB and Hirsch, EB and Weinberg, BA and Johnson, JM and Antonarakis, ES and Lou, E and Huang, RS},
title = {Sex-biased intratumoral microbiome influences tumor molecular and immune landscape and disease outcomes.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102757},
doi = {10.1016/j.xcrm.2026.102757},
pmid = {42013847},
issn = {2666-3791},
abstract = {The intratumoral microbiome is increasingly recognized as a regulator of cancer biology, yet sex-specific patterns and their relevance to cancer disparities remain poorly understood. We perform a multi-kingdom analysis of more than 5,000 tumors from seven datasets to identify sex-differential microbial taxa across aerodigestive and gastrointestinal cancers. We identify and validate 22 taxa with consistent sex-biased abundance, including in real-world cohort. These microbes show cancer-type- and microbe-specific associations with tumor transcriptomes, oncogenic pathways, and immune cell infiltration. Female-enriched microbes are linked to increased estrogen signaling and interferon responses, whereas male-enriched taxa show opposing patterns. In gastric cancer, intratumoral Epstein-Barr virus is enriched in males and associated with higher CD8[+] T cell infiltration and improved survival. Functional co-culture experiments demonstrate that sex-biased microbes modulate chemotherapy sensitivity. Together, these findings reveal a sex-biased intratumoral microbiome axis that shapes tumor phenotypes and disease outcomes, highlighting opportunities for microbiota-guided, sex-aware approaches in oncology.},
}
RevDate: 2026-04-21
Distinct signatures in the human gut and oral microbiomes of gastric cancer.
Cell reports. Medicine pii:S2666-3791(26)00178-3 [Epub ahead of print].
Microbiome dysbiosis is increasingly recognized as a hallmark of gastric cancer (GC). Here, we analyzed gut and oral shotgun metagenomic data from 317 individuals across two independent cohorts, with validation in a Harbin cohort. We identify 20 oral-gut shared species enriched in the gut of GC, predominantly lactic acid bacteria (LAB). While most gut microbial markers are abundant in saliva, none are significantly altered in GC. Strain-level analysis of 87 matched saliva-stool metagenomes confirms oral-gut transmission of Streptococcus species. GC-enriched LAB form robust co-abundance networks in oral and gut microbiomes, suggesting synergistic interactions. Functional analysis reveals enriched lactate fermentation pathways in GC stool, aligning with LAB dominance and previous findings on gastric microbiota. Moreover, microbiome-based classifiers achieve high predictive accuracy (area under receiver operating characteristic curve [AUROC] = 0.85 for stool, 0.87 for saliva) for GC diagnosis, highlighting translational potential. Collectively, these findings underscore the critical role of the oral-gut microbiome axis in GC.
Additional Links: PMID-42013850
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@article {pmid42013850,
year = {2026},
author = {Qin, Y and Zhang, YX and Liu, LP and Xie, YH and Ma, XY and Hao, Y and Zhao, LC and Dong, JJ and He, Y and Sun, K and Zhong, H and Zhu, S and Liu, M and Fang, JY and Zhou, CB},
title = {Distinct signatures in the human gut and oral microbiomes of gastric cancer.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102761},
doi = {10.1016/j.xcrm.2026.102761},
pmid = {42013850},
issn = {2666-3791},
abstract = {Microbiome dysbiosis is increasingly recognized as a hallmark of gastric cancer (GC). Here, we analyzed gut and oral shotgun metagenomic data from 317 individuals across two independent cohorts, with validation in a Harbin cohort. We identify 20 oral-gut shared species enriched in the gut of GC, predominantly lactic acid bacteria (LAB). While most gut microbial markers are abundant in saliva, none are significantly altered in GC. Strain-level analysis of 87 matched saliva-stool metagenomes confirms oral-gut transmission of Streptococcus species. GC-enriched LAB form robust co-abundance networks in oral and gut microbiomes, suggesting synergistic interactions. Functional analysis reveals enriched lactate fermentation pathways in GC stool, aligning with LAB dominance and previous findings on gastric microbiota. Moreover, microbiome-based classifiers achieve high predictive accuracy (area under receiver operating characteristic curve [AUROC] = 0.85 for stool, 0.87 for saliva) for GC diagnosis, highlighting translational potential. Collectively, these findings underscore the critical role of the oral-gut microbiome axis in GC.},
}
RevDate: 2026-04-21
A 15-layer multi-omics analysis of gastric cancer ecotypes provides therapeutic insights.
Cell reports. Medicine pii:S2666-3791(26)00173-4 [Epub ahead of print].
Gastric cancer is marked by profound molecular and microenvironmental heterogeneity that limits therapeutic progress. Here, we present a 15-layer multi-omics atlas that integrates genomics, epigenomics, transcriptomics, proteomics, multiple post-translational modifications (PTMs), protein-protein interactions, metabolomics, and microbiome profiles from 159 primary gastric adenocarcinomas and 30 matched normal adjacent tissues. Using cell-state deconvolution, we define tumor ecotypes that refine genomic and histological subtypes by capturing distinct tumor microenvironment architectures linked to clinical outcomes and potential associations with immunotherapy response. Multi-omics integration prioritizes genomic and epigenomic aberrations and their associated vulnerabilities; defines ecotype-specific transcriptional programs, signaling pathways, PTMs, protein interaction networks, and metabolic regulation; and identifies microbiome features linked to ecotypes and resistance pathways. We further prioritize ecotype-, genomic subtype-, and cell type-specific targetable proteins using proteomic and PTM analyses within a tumor microenvironment context. This comprehensive atlas provides a systems-level blueprint for decoding gastric cancer heterogeneity and advancing precision oncology.
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@article {pmid42013851,
year = {2026},
author = {Wang, Y and Olsen, LK and Jiao, F and Wang, C and Jiang, KX and Dou, Y and Hu, Y and Jiao, L and Chen, W and Elizarraras, JM and Khare, P and Yu, N and Zhu, H and Chen, L and Lih, TM and Eser, PÖ and Martins Rodrigues, F and Shi, Z and Zhang, C and Yu, C and Heiman, DI and Liao, Y and Shafer, PW and Choi, S and Choi, JM and Savage, SR and Jaehnig, EJ and Lei, JT and Sun, Y and Peng, CW and Sun, Z and Morenkov, P and Zhang, K and Geffen, Y and Hess, J and Kumar-Sinha, C and Mani, DR and Ding, L and Getz, G and Li, QK and Omenn, GS and Le, A and Hostetter, G and Newton, CJ and Cai, S and Ketchum, KA and Robles, AI and Mesri, M and Minoo, P and Camargo, MC and An, E and Hruban, RH and Liu, Z and Thiagarajan, M and Dohlman, AB and Jin, RU and Huang, L and Chan, DW and Zhang, H and Zhang, B and , },
title = {A 15-layer multi-omics analysis of gastric cancer ecotypes provides therapeutic insights.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102756},
doi = {10.1016/j.xcrm.2026.102756},
pmid = {42013851},
issn = {2666-3791},
abstract = {Gastric cancer is marked by profound molecular and microenvironmental heterogeneity that limits therapeutic progress. Here, we present a 15-layer multi-omics atlas that integrates genomics, epigenomics, transcriptomics, proteomics, multiple post-translational modifications (PTMs), protein-protein interactions, metabolomics, and microbiome profiles from 159 primary gastric adenocarcinomas and 30 matched normal adjacent tissues. Using cell-state deconvolution, we define tumor ecotypes that refine genomic and histological subtypes by capturing distinct tumor microenvironment architectures linked to clinical outcomes and potential associations with immunotherapy response. Multi-omics integration prioritizes genomic and epigenomic aberrations and their associated vulnerabilities; defines ecotype-specific transcriptional programs, signaling pathways, PTMs, protein interaction networks, and metabolic regulation; and identifies microbiome features linked to ecotypes and resistance pathways. We further prioritize ecotype-, genomic subtype-, and cell type-specific targetable proteins using proteomic and PTM analyses within a tumor microenvironment context. This comprehensive atlas provides a systems-level blueprint for decoding gastric cancer heterogeneity and advancing precision oncology.},
}
RevDate: 2026-04-21
Genetic modification of intractable bacterial clones by heat shock-facilitated phage transduction.
Cell reports methods pii:S2667-2375(26)00106-2 [Epub ahead of print].
Increasing recognition of commensal bacteria as essential for microbiome integrity and pathogen exclusion underscores the urgency of molecularly characterizing commensal interactions. However, many commensals cannot be transformed using available methodologies due to barriers imposed by restriction-modification (RM) systems. We developed a method for introducing plasmid DNA into otherwise intractable non-Staphylococcus aureus (NAS) staphylococci, important commensals of the human nasal and skin microbiomes, via phage transduction. We demonstrate that exposing recipient bacteria to a pulse of elevated temperature prior to phage exposure renders NAS isolates effectively and transiently amenable to transduction. Transduction of NAS mutants lacking RM systems did not respond to heat shock, indicating that transient deactivation of RM enzymes enables transduction. Our method also facilitates the transduction of representatives from other Bacillota and Actinomycetota taxa, suggesting that this approach will support research on diverse bacterial groups across a range of ecosystems.
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@article {pmid42013857,
year = {2026},
author = {Schulze, L and Stahl, J and Knoedlseder, NJ and Krauss, S and Harbig, T and Nieselt, K and Brueggemann, H and Krismer, B and Peschel, A},
title = {Genetic modification of intractable bacterial clones by heat shock-facilitated phage transduction.},
journal = {Cell reports methods},
volume = {},
number = {},
pages = {101406},
doi = {10.1016/j.crmeth.2026.101406},
pmid = {42013857},
issn = {2667-2375},
abstract = {Increasing recognition of commensal bacteria as essential for microbiome integrity and pathogen exclusion underscores the urgency of molecularly characterizing commensal interactions. However, many commensals cannot be transformed using available methodologies due to barriers imposed by restriction-modification (RM) systems. We developed a method for introducing plasmid DNA into otherwise intractable non-Staphylococcus aureus (NAS) staphylococci, important commensals of the human nasal and skin microbiomes, via phage transduction. We demonstrate that exposing recipient bacteria to a pulse of elevated temperature prior to phage exposure renders NAS isolates effectively and transiently amenable to transduction. Transduction of NAS mutants lacking RM systems did not respond to heat shock, indicating that transient deactivation of RM enzymes enables transduction. Our method also facilitates the transduction of representatives from other Bacillota and Actinomycetota taxa, suggesting that this approach will support research on diverse bacterial groups across a range of ecosystems.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-21
Testosterone administration partially modulates gut microbiota responses to severe energy deficit.
American journal of physiology. Endocrinology and metabolism, 330(5):E606-E626.
Severe diet- and exercise-induced energy deficit (SED) suppresses androgen production in healthy men, altering metabolism and driving muscle loss. The gut microbiota modulates host metabolism, yet the community's response to SED and any role of androgen hormones are unclear. Herein, healthy, physically active men were randomized to receive 200 mg/wk testosterone enanthate (n = 24) or placebo (n = 26) during a 28-day residential intervention that restricted energy intake and increased energy expenditure inducing a ∼2,000 kcal/day SED. Multiomic analyses revealed altered gut microbiota composition, reduced fecal short-chain fatty acids (SCFA), and shifts in bacterial metabolic pathways toward lipid utilization and mucin degradation during SED, suggesting adverse effects of SED on gut microbiota metabolic functions. Testosterone administration preserved certain SCFA-producing taxa and bioenergetic pathways without fully counteracting the effects of SED indicating a limited but potentially important interplay between androgen status and the gut microbiota under conditions of SED.NEW & NOTEWORTHY This study is the first to demonstrate that testosterone administration partially preserves gut microbiota composition and metabolic function during severe energy deficit in healthy men. Using a multiomic approach, we show that testosterone modulates short-chain fatty acid-producing taxa and microbial pathways linked to host energy metabolism. These findings reveal a novel role for androgens in shaping host-microbiome interactions during catabolic stress and may inform strategies to maintain metabolic resilience.
Additional Links: PMID-41874457
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@article {pmid41874457,
year = {2026},
author = {Mohr, AE and Berryman, CE and Harris, MN and Lawrence, AB and Chakraborty, N and Campbell, R and Dimitrov, GI and Gautam, A and Hammamieh, R and Lieberman, HR and Rood, JC and Pasiakos, SM and Karl, JP},
title = {Testosterone administration partially modulates gut microbiota responses to severe energy deficit.},
journal = {American journal of physiology. Endocrinology and metabolism},
volume = {330},
number = {5},
pages = {E606-E626},
doi = {10.1152/ajpendo.00291.2025},
pmid = {41874457},
issn = {1522-1555},
support = {W81XWH-14-1-0335//DOD | OSD | Defense Technical Information Center (ADD)/ ; W81XWH-17-2-0026//DOD | OSD | Defense Technical Information Center (ADD)/ ; Joint Program Committee-5//Military Operational Medicine Research Program (MOMRP)/ ; //DOE | Oak Ridge Institute for Science and Education (ORISE)/ ; T32DK137525//HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Male ; *Testosterone/pharmacology/analogs & derivatives/administration & dosage ; *Energy Metabolism/drug effects ; Adult ; Fatty Acids, Volatile/metabolism ; Feces/chemistry/microbiology ; Young Adult ; Exercise/physiology ; *Androgens/pharmacology/administration & dosage ; Energy Intake/drug effects ; Double-Blind Method ; },
abstract = {Severe diet- and exercise-induced energy deficit (SED) suppresses androgen production in healthy men, altering metabolism and driving muscle loss. The gut microbiota modulates host metabolism, yet the community's response to SED and any role of androgen hormones are unclear. Herein, healthy, physically active men were randomized to receive 200 mg/wk testosterone enanthate (n = 24) or placebo (n = 26) during a 28-day residential intervention that restricted energy intake and increased energy expenditure inducing a ∼2,000 kcal/day SED. Multiomic analyses revealed altered gut microbiota composition, reduced fecal short-chain fatty acids (SCFA), and shifts in bacterial metabolic pathways toward lipid utilization and mucin degradation during SED, suggesting adverse effects of SED on gut microbiota metabolic functions. Testosterone administration preserved certain SCFA-producing taxa and bioenergetic pathways without fully counteracting the effects of SED indicating a limited but potentially important interplay between androgen status and the gut microbiota under conditions of SED.NEW & NOTEWORTHY This study is the first to demonstrate that testosterone administration partially preserves gut microbiota composition and metabolic function during severe energy deficit in healthy men. Using a multiomic approach, we show that testosterone modulates short-chain fatty acid-producing taxa and microbial pathways linked to host energy metabolism. These findings reveal a novel role for androgens in shaping host-microbiome interactions during catabolic stress and may inform strategies to maintain metabolic resilience.},
}
MeSH Terms:
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Humans
*Gastrointestinal Microbiome/drug effects
Male
*Testosterone/pharmacology/analogs & derivatives/administration & dosage
*Energy Metabolism/drug effects
Adult
Fatty Acids, Volatile/metabolism
Feces/chemistry/microbiology
Young Adult
Exercise/physiology
*Androgens/pharmacology/administration & dosage
Energy Intake/drug effects
Double-Blind Method
RevDate: 2026-04-21
CmpDate: 2026-04-21
TrIdent - An R package to automate transductomics analysis of virus-like particle mediated DNA mobilization.
bioRxiv : the preprint server for biology.
BACKGROUND: Transduction is a form of horizontal gene transfer in which bacterial DNA is packaged and transferred by virus-like particles (VLPs). Transductomics is a sequencing-based method used to detect DNA carried by VLPs. During transductomics analysis, reads from a sample's ultra-purified VLPs are mapped to metagenomic contigs assembled from the same sample's whole-community. The read mapping produces coverage patterns that require a time-consuming manual inspection and classification process which makes the method's use unfeasible for datasets with many samples.
RESULTS: We developed a novel algorithm, TrIdent (Transduction Identification), that uses pattern-matching to automate the transductomics data analysis and that is available as an R package (https://jlmaier12.github.io/TrIdent/). There is no software equivalent to TrIdent so we compared TrIdent's classifications of transductomics datasets to classifications made by human classifiers. TrIdent's classifications were generally comparable to the manual classifications on a previously generated, manually classified transductomics dataset. When applied to newly generated transductomics data from the murine microbiota, TrIdent agreed with two independent human classifiers as much as the two independent human classifications agreed with each other. TrIdent classified transductomics datasets in a fraction of the time needed by human classifiers, and the classifications produced by TrIdent are fully reproducible. We used TrIdent to explore three murine gut transductomes and found that bacterial DNA associated with the Oscillospiraceae and Turicibacteraceae families was highly enriched in the DNA packaged by VLPs as compared to the whole community metagenomes.
CONCLUSIONS: The TrIdent software is a more accessible, more efficient, and more reproducible alternative to the manual inspection of read coverage patterns previously required for transductomics data analysis. To demonstrate the application of TrIdent, we analyzed transductomics datasets from murine fecal pellets and showed that specific low abundance bacterial families appear to be heavily involved in transduction.
Additional Links: PMID-41959403
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@article {pmid41959403,
year = {2026},
author = {Maier, J and Gin, C and Rabasco, J and Bass, A and Spencer, W and Duerkop, BA and Callahan, B and Kleiner, M},
title = {TrIdent - An R package to automate transductomics analysis of virus-like particle mediated DNA mobilization.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {41959403},
issn = {2692-8205},
support = {R01 AI171046/AI/NIAID NIH HHS/United States ; R35 GM138362/GM/NIGMS NIH HHS/United States ; },
abstract = {BACKGROUND: Transduction is a form of horizontal gene transfer in which bacterial DNA is packaged and transferred by virus-like particles (VLPs). Transductomics is a sequencing-based method used to detect DNA carried by VLPs. During transductomics analysis, reads from a sample's ultra-purified VLPs are mapped to metagenomic contigs assembled from the same sample's whole-community. The read mapping produces coverage patterns that require a time-consuming manual inspection and classification process which makes the method's use unfeasible for datasets with many samples.
RESULTS: We developed a novel algorithm, TrIdent (Transduction Identification), that uses pattern-matching to automate the transductomics data analysis and that is available as an R package (https://jlmaier12.github.io/TrIdent/). There is no software equivalent to TrIdent so we compared TrIdent's classifications of transductomics datasets to classifications made by human classifiers. TrIdent's classifications were generally comparable to the manual classifications on a previously generated, manually classified transductomics dataset. When applied to newly generated transductomics data from the murine microbiota, TrIdent agreed with two independent human classifiers as much as the two independent human classifications agreed with each other. TrIdent classified transductomics datasets in a fraction of the time needed by human classifiers, and the classifications produced by TrIdent are fully reproducible. We used TrIdent to explore three murine gut transductomes and found that bacterial DNA associated with the Oscillospiraceae and Turicibacteraceae families was highly enriched in the DNA packaged by VLPs as compared to the whole community metagenomes.
CONCLUSIONS: The TrIdent software is a more accessible, more efficient, and more reproducible alternative to the manual inspection of read coverage patterns previously required for transductomics data analysis. To demonstrate the application of TrIdent, we analyzed transductomics datasets from murine fecal pellets and showed that specific low abundance bacterial families appear to be heavily involved in transduction.},
}
RevDate: 2026-04-18
Tracking antibiotic resistance genes and microbiome shifts under reclaimed wastewater irrigation: Root-associated selective modulation.
Journal of environmental management, 405:129707 pii:S0301-4797(26)01167-9 [Epub ahead of print].
The reuse of treated wastewater (TWW) for crop irrigation reduces pressure on freshwater resources but may also disseminate antimicrobial resistance (AMR) through the presence of antibiotics, resistant bacteria and antibiotic resistant genes (ARGs). While many studies have examined the impact of water quality on dissemination of AMR in soils, the role of plants in filtering or accumulating AMR within the soil-plant continuum remains unclear. Here, we investigated the influence of irrigation water quality, plant species, and microbial compartments (soil, rhizosphere, roots) on bacterial communities and selected ARGs under controlled mesocosm conditions. Lettuce and leek were irrigated over two consecutive years with drinking water (DW), TWW, or raw wastewater (RWW). We monitored the abundance of ARGs sul1, ermB, and intI1 and characterized bacterial community composition by 16S rRNA sequencing. Soil microbiomes were influenced by water type and probably irrigation volume, and bacterial enrichment associated with DW, TWW, and RWW were identified. Plant-specific effects on soil microbiome were observed but were minor compared to the effect of water quality. Root microbiomes appeared more resilient than soils, as most taxa enriched in TWW- or RWW-irrigated soils were less or not amplified in roots, suggesting a potential barrier effect or at least selective processes at the root interface. Only Tahibacter and Rhodanobacteraceae increased in roots, while RWW irrigation also promoted the growth of the plant-pathogen Rhizorhapis. ARGs rose significantly in soils under TWW and RWW irrigation, with distinct year-to-year dynamics, but these shifts were not observed in root communities. Overall, our results indicate that root-associated compartments may contribute to modulate the dissemination of sul1, ermB, and intI1 ARGs in the plants irrigated with TWW.
Additional Links: PMID-42000489
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@article {pmid42000489,
year = {2026},
author = {Della-Negra, O and Bru-Adan, V and Patureau, D and Ait-Mouheb, N and Wéry, N},
title = {Tracking antibiotic resistance genes and microbiome shifts under reclaimed wastewater irrigation: Root-associated selective modulation.},
journal = {Journal of environmental management},
volume = {405},
number = {},
pages = {129707},
doi = {10.1016/j.jenvman.2026.129707},
pmid = {42000489},
issn = {1095-8630},
abstract = {The reuse of treated wastewater (TWW) for crop irrigation reduces pressure on freshwater resources but may also disseminate antimicrobial resistance (AMR) through the presence of antibiotics, resistant bacteria and antibiotic resistant genes (ARGs). While many studies have examined the impact of water quality on dissemination of AMR in soils, the role of plants in filtering or accumulating AMR within the soil-plant continuum remains unclear. Here, we investigated the influence of irrigation water quality, plant species, and microbial compartments (soil, rhizosphere, roots) on bacterial communities and selected ARGs under controlled mesocosm conditions. Lettuce and leek were irrigated over two consecutive years with drinking water (DW), TWW, or raw wastewater (RWW). We monitored the abundance of ARGs sul1, ermB, and intI1 and characterized bacterial community composition by 16S rRNA sequencing. Soil microbiomes were influenced by water type and probably irrigation volume, and bacterial enrichment associated with DW, TWW, and RWW were identified. Plant-specific effects on soil microbiome were observed but were minor compared to the effect of water quality. Root microbiomes appeared more resilient than soils, as most taxa enriched in TWW- or RWW-irrigated soils were less or not amplified in roots, suggesting a potential barrier effect or at least selective processes at the root interface. Only Tahibacter and Rhodanobacteraceae increased in roots, while RWW irrigation also promoted the growth of the plant-pathogen Rhizorhapis. ARGs rose significantly in soils under TWW and RWW irrigation, with distinct year-to-year dynamics, but these shifts were not observed in root communities. Overall, our results indicate that root-associated compartments may contribute to modulate the dissemination of sul1, ermB, and intI1 ARGs in the plants irrigated with TWW.},
}
RevDate: 2026-04-18
Natural recovery trajectory of soil chemistry and microbiome after low-temperature thermal desorption remediation.
Journal of environmental management, 405:129700 pii:S0301-4797(26)01160-6 [Epub ahead of print].
Urban soil contamination from historical industrial activities hinders sustainable redevelopment. Low-temperature thermal desorption is a common soil remediation strategy, offering efficient removal of volatile pollutants while limiting soil disruption. However, its ecological legacy and the potential for natural microbial recovery remain poorly understood. We tracked chemical and microbial recovery in an isolated urban brownfield for two years following remediation. Soil chemistry improved naturally over time: pH decreased from 9.1 to 8.2, total organic carbon rose from 2.3 to 5.4 g kg[-1], and carbon-to-nitrogen ratio increased from year 1 to year 2 post-remediation, although all remained below nearby urban greenspace soil (city park) soil levels. In contrast, salinity emerged as a new stressor in year 2, with electrical conductivity rising to 1.13 mS cm[-1], higher than both year 1 (0.41 mS cm[-1]) and the park (0.21 mS cm[-1]), likely due to the gradual weathering of quicklime additives applied during the thermal desorption process to enhance organic pollutant volatilization. Microbial abundance, measured by qPCR of total 16S rRNA genes, remained three orders of magnitude lower in remediated soils than park soils, but the microbial communities increased in diversity and network complexity. Functional annotations revealed a trajectory from mainly chemoheterotrophy in year 1 to a broader suite of metabolisms in year 2, though still distinct from park soils with substantially more nitrifying taxa. Collectively, these findings show that although qPCR-based microbial abundance suggests non appreciable recovery at first glance, the underlying communities exhibited clear post-remediation restructuring over two years. Persistent salinity and carbon limitation remain barriers, offering opportunities for targeted interventions-organic carbon replenishment, salinity management, and nitrogen-cycling taxa stimulation-to accelerate convergence toward resilient, multifunctional urban soils.
Additional Links: PMID-42000492
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@article {pmid42000492,
year = {2026},
author = {Zhao, X and Zhang, S and Lai, X and Shi, D and Yang, C and Yu, H},
title = {Natural recovery trajectory of soil chemistry and microbiome after low-temperature thermal desorption remediation.},
journal = {Journal of environmental management},
volume = {405},
number = {},
pages = {129700},
doi = {10.1016/j.jenvman.2026.129700},
pmid = {42000492},
issn = {1095-8630},
abstract = {Urban soil contamination from historical industrial activities hinders sustainable redevelopment. Low-temperature thermal desorption is a common soil remediation strategy, offering efficient removal of volatile pollutants while limiting soil disruption. However, its ecological legacy and the potential for natural microbial recovery remain poorly understood. We tracked chemical and microbial recovery in an isolated urban brownfield for two years following remediation. Soil chemistry improved naturally over time: pH decreased from 9.1 to 8.2, total organic carbon rose from 2.3 to 5.4 g kg[-1], and carbon-to-nitrogen ratio increased from year 1 to year 2 post-remediation, although all remained below nearby urban greenspace soil (city park) soil levels. In contrast, salinity emerged as a new stressor in year 2, with electrical conductivity rising to 1.13 mS cm[-1], higher than both year 1 (0.41 mS cm[-1]) and the park (0.21 mS cm[-1]), likely due to the gradual weathering of quicklime additives applied during the thermal desorption process to enhance organic pollutant volatilization. Microbial abundance, measured by qPCR of total 16S rRNA genes, remained three orders of magnitude lower in remediated soils than park soils, but the microbial communities increased in diversity and network complexity. Functional annotations revealed a trajectory from mainly chemoheterotrophy in year 1 to a broader suite of metabolisms in year 2, though still distinct from park soils with substantially more nitrifying taxa. Collectively, these findings show that although qPCR-based microbial abundance suggests non appreciable recovery at first glance, the underlying communities exhibited clear post-remediation restructuring over two years. Persistent salinity and carbon limitation remain barriers, offering opportunities for targeted interventions-organic carbon replenishment, salinity management, and nitrogen-cycling taxa stimulation-to accelerate convergence toward resilient, multifunctional urban soils.},
}
RevDate: 2026-04-18
Heteroaggregation with microalgae masks charge-dependent accumulation but amplifies charge-dependent toxicity of nanoplastics in mussels.
Journal of hazardous materials, 510:142121 pii:S0304-3894(26)01099-X [Epub ahead of print].
In natural waters, nanoplastics (NPLs) often form heteroaggregates (HAs) with microalgae. Despite surface charge being a primary driver of NPL behavior, its role in governing HA toxicokinetics and impacts in bivalves remains largely unknown. Here, the effects of positively charged polystyrene NPLs (NPL+), their negative charged counterparts (NPL-), and the pre-formed HAs (HA+ and HA-) with the microalga Chlorella salina were evaluated in the green mussel (Perna viridis) during a 21-day exposure followed by 7-day elimination. HA+ and HA- enhanced NPL uptake in digestive gland and peripheral tissues, with uptake rate constants 1.5 - 4.0 times those of NPLs alone. Although 70 - 95% of accumulated NPLs were eliminated within 24 h, higher initial burdens under HA+ and HA- produced greater residual levels. NPL+ showed stronger uptake than NPL- due to greater electrostatic affinity with negatively charged epithelial surfaces. However, this charge-related uptake advantage was attenuated in HAs, concurrent with algal-like ζ-potentials of the heteroaggregates. Biological responses paralleled toxicokinetics, with HA+ inducing the strongest effects, including hemocyte dysfunction, oxidative stress, and fungal community disruption. Overall, HAs and surface charge jointly regulated NPL accumulation and toxicity in P. viridis, highlighting the need for ecological risk assessments to consider charge effects and HA formation to avoid underestimating NPLs hazards in filter-feeding bivalves.
Additional Links: PMID-42000498
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@article {pmid42000498,
year = {2026},
author = {Wu, F and Deng, Y and Wu, Q and Chen, H and Mu, J and Zhang, Y and Meng, W and Li, N and Xie, L},
title = {Heteroaggregation with microalgae masks charge-dependent accumulation but amplifies charge-dependent toxicity of nanoplastics in mussels.},
journal = {Journal of hazardous materials},
volume = {510},
number = {},
pages = {142121},
doi = {10.1016/j.jhazmat.2026.142121},
pmid = {42000498},
issn = {1873-3336},
abstract = {In natural waters, nanoplastics (NPLs) often form heteroaggregates (HAs) with microalgae. Despite surface charge being a primary driver of NPL behavior, its role in governing HA toxicokinetics and impacts in bivalves remains largely unknown. Here, the effects of positively charged polystyrene NPLs (NPL+), their negative charged counterparts (NPL-), and the pre-formed HAs (HA+ and HA-) with the microalga Chlorella salina were evaluated in the green mussel (Perna viridis) during a 21-day exposure followed by 7-day elimination. HA+ and HA- enhanced NPL uptake in digestive gland and peripheral tissues, with uptake rate constants 1.5 - 4.0 times those of NPLs alone. Although 70 - 95% of accumulated NPLs were eliminated within 24 h, higher initial burdens under HA+ and HA- produced greater residual levels. NPL+ showed stronger uptake than NPL- due to greater electrostatic affinity with negatively charged epithelial surfaces. However, this charge-related uptake advantage was attenuated in HAs, concurrent with algal-like ζ-potentials of the heteroaggregates. Biological responses paralleled toxicokinetics, with HA+ inducing the strongest effects, including hemocyte dysfunction, oxidative stress, and fungal community disruption. Overall, HAs and surface charge jointly regulated NPL accumulation and toxicity in P. viridis, highlighting the need for ecological risk assessments to consider charge effects and HA formation to avoid underestimating NPLs hazards in filter-feeding bivalves.},
}
RevDate: 2026-04-18
Enantioselective alteration of soil bacterial community assembly and keystone taxa under chiral triadimefon stress.
Journal of hazardous materials, 510:142063 pii:S0304-3894(26)01041-1 [Epub ahead of print].
Triadimefon, a representative chiral triazole fungicide, is ubiquitously applied as a racemic mixture and exhibits negative effects on microbiome in agroecosystems. However, its enantioselective effects on soil microbial community structure and assembly processes remain undefined. In this study, we investigated how bacteriome assembly responds to triadimefon at the enantiomeric level. It was found that the R- and S-enantiomers exerted distinct effects on bacterial diversity and community structure. Furthermore, deterministic processes dominated bacterial community assembly under chiral triadimefon. Co-occurrence network analysis revealed a distinct shift in microbial network across the chiral triadimefon treatments, revealing enantiomeric disparity in network organization to different enantiomers. Importantly, we identified 12 and 6 distinct key amplicon sequence variants (ASVs), respectively, selected by R- and S-enantiomers. These stereoselective key taxa are closely associated with bacterial community recombination trajectories. Overall, our research provides novel insights into understanding the enantioselective response of microbiome under chiral triadimefon and ideal targets to manipulate for contaminated situations. SYNOPSIS: Soil microbial community assembly exhibited striking differences in response to the R- and S-enantiomers of triadimefon, which are governed by the stereospecific selection imposed on the keystone taxa.
Additional Links: PMID-42000502
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PubMed:
Citation:
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@article {pmid42000502,
year = {2026},
author = {Wang, Z and Wang, P and Yin, B and Gao, R and Dai, P and Lin, X and Sun, C},
title = {Enantioselective alteration of soil bacterial community assembly and keystone taxa under chiral triadimefon stress.},
journal = {Journal of hazardous materials},
volume = {510},
number = {},
pages = {142063},
doi = {10.1016/j.jhazmat.2026.142063},
pmid = {42000502},
issn = {1873-3336},
abstract = {Triadimefon, a representative chiral triazole fungicide, is ubiquitously applied as a racemic mixture and exhibits negative effects on microbiome in agroecosystems. However, its enantioselective effects on soil microbial community structure and assembly processes remain undefined. In this study, we investigated how bacteriome assembly responds to triadimefon at the enantiomeric level. It was found that the R- and S-enantiomers exerted distinct effects on bacterial diversity and community structure. Furthermore, deterministic processes dominated bacterial community assembly under chiral triadimefon. Co-occurrence network analysis revealed a distinct shift in microbial network across the chiral triadimefon treatments, revealing enantiomeric disparity in network organization to different enantiomers. Importantly, we identified 12 and 6 distinct key amplicon sequence variants (ASVs), respectively, selected by R- and S-enantiomers. These stereoselective key taxa are closely associated with bacterial community recombination trajectories. Overall, our research provides novel insights into understanding the enantioselective response of microbiome under chiral triadimefon and ideal targets to manipulate for contaminated situations. SYNOPSIS: Soil microbial community assembly exhibited striking differences in response to the R- and S-enantiomers of triadimefon, which are governed by the stereospecific selection imposed on the keystone taxa.},
}
RevDate: 2026-04-18
Secondary chlorination enhanced the role of pipe materials in shaping chlorine-resistant microbiome and antibiotic resistome in secondary water supply systems.
Journal of hazardous materials, 510:142114 pii:S0304-3894(26)01092-7 [Epub ahead of print].
Secondary chlorination is often strategically applied in secondary water supply systems (SWSSs) with insufficient disinfectant residuals to suppress microbial regrowth. However, the associated risks posed by chlorine-resistant bacteria (CRB) and antibiotic resistance genes (ARGs) remain unclear. Herein, simulated SWSSs with different pipe materials and chlorine levels were operated for 220 days. Biomass in biofilms and bulk water was markedly reduced following chlorination, and extracellular polymeric substances responded more strongly in stainless steel (SS) pipes, with polysaccharides (70.28%) exhibiting a greater reduction than proteins (37.44%). Meanwhile, chlorination reduced bacterial diversity and reshaped community structure, boosting the contributions of biofilm and particulate phases to waterborne bacteria by 11.47%-15.60% and 17.52%-22.82%, respectively. Chlorination promoted the CRB enrichment (e.g., Nevskia and Sphingomonas), with higher relative abundance in polyvinyl chloride (PVC) pipes and more taxa in SS pipes. The decline in Legionella mitigated potentially pathogenic risks, particularly in chlorinated PVC pipes, despite nine of 13 potential pathogens being chlorine-resistant. Moreover, chlorination generally reduced the ARG absolute abundance but increased their relative abundance, with sulfonamide- and multidrug-ARGs being predominant. Regarding the ARG bacterial hosts, potential pathogens (e.g., Pseudomonas and Enterobacter) posed the highest risk, followed by non-pathogenic CRB (e.g., Herbaspirillum and Sediminibacterium) and chlorine-sensitive bacteria (e.g., Runella and Isosphaera). Vertical gene transfer dominated ARG transmission, while horizontal gene transfer occurred more readily in the water phase and was promoted in chlorinated PVC pipes. These findings provide novel insights into the microbial risk and antibiotic resistome, and may guide pipe material selection and disinfection optimization within SWSSs.
Additional Links: PMID-42000515
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PubMed:
Citation:
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@article {pmid42000515,
year = {2026},
author = {Qiu, Y and Yang, Y and Li, N and Li, X and Lu, Z and Zhou, Z and Feng, S and Liu, Y},
title = {Secondary chlorination enhanced the role of pipe materials in shaping chlorine-resistant microbiome and antibiotic resistome in secondary water supply systems.},
journal = {Journal of hazardous materials},
volume = {510},
number = {},
pages = {142114},
doi = {10.1016/j.jhazmat.2026.142114},
pmid = {42000515},
issn = {1873-3336},
abstract = {Secondary chlorination is often strategically applied in secondary water supply systems (SWSSs) with insufficient disinfectant residuals to suppress microbial regrowth. However, the associated risks posed by chlorine-resistant bacteria (CRB) and antibiotic resistance genes (ARGs) remain unclear. Herein, simulated SWSSs with different pipe materials and chlorine levels were operated for 220 days. Biomass in biofilms and bulk water was markedly reduced following chlorination, and extracellular polymeric substances responded more strongly in stainless steel (SS) pipes, with polysaccharides (70.28%) exhibiting a greater reduction than proteins (37.44%). Meanwhile, chlorination reduced bacterial diversity and reshaped community structure, boosting the contributions of biofilm and particulate phases to waterborne bacteria by 11.47%-15.60% and 17.52%-22.82%, respectively. Chlorination promoted the CRB enrichment (e.g., Nevskia and Sphingomonas), with higher relative abundance in polyvinyl chloride (PVC) pipes and more taxa in SS pipes. The decline in Legionella mitigated potentially pathogenic risks, particularly in chlorinated PVC pipes, despite nine of 13 potential pathogens being chlorine-resistant. Moreover, chlorination generally reduced the ARG absolute abundance but increased their relative abundance, with sulfonamide- and multidrug-ARGs being predominant. Regarding the ARG bacterial hosts, potential pathogens (e.g., Pseudomonas and Enterobacter) posed the highest risk, followed by non-pathogenic CRB (e.g., Herbaspirillum and Sediminibacterium) and chlorine-sensitive bacteria (e.g., Runella and Isosphaera). Vertical gene transfer dominated ARG transmission, while horizontal gene transfer occurred more readily in the water phase and was promoted in chlorinated PVC pipes. These findings provide novel insights into the microbial risk and antibiotic resistome, and may guide pipe material selection and disinfection optimization within SWSSs.},
}
RevDate: 2026-04-18
Multi-kingdom profiling reveals altered gut phage-bacteria-metabolite interactions in MASLD.
Nature communications pii:10.1038/s41467-026-71981-0 [Epub ahead of print].
Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly linked to gut microbial dysbiosis, but most studies have focused on bacteria, neglecting viruses and fungi, and their interactions. Here we show that MASLD is characterized by coordinated disruption of bacterial, viral and fungal communities and by a disturbed phage-bacteria-metabolite axis associated with disease-related bile acid changes. Integrating shotgun metagenomics, fungal ITS2 sequencing, fecal metabolomics and clinical profiling in 210 patients with MASLD and 210 age- and gender-matched healthy controls, we find reduced microbial diversity and extensive remodeling of cross-kingdom ecological networks in MASLD. Ruminococcus gnavus emerges as an enriched central hub, while Faecalibacterium prausnitzii and its associated bacteriophages are depleted. Phage-host analyses further reveal reduced lytic activity against R. gnavus and loss of sulfur amino acid metabolism-related auxiliary metabolic genes, which may impair F. prausnitzii fitness. Diminished phage control may facilitate R. gnavus expansion, alongside increased fecal isodeoxycholic acid, a secondary bile acid implicated in hepatic steatosis. A diagnostic classifier integrating bacterial and viral features with clinical parameters distinguish MASLD from controls in our cohort and maintain predictive performance in two external datasets. Together, these findings uncover a disrupted phage-bacteria-metabolite axis in MASLD and provide a multi-kingdom framework for non-invasive biomarker discovery and microbiome-targeted therapies.
Additional Links: PMID-42000726
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PubMed:
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@article {pmid42000726,
year = {2026},
author = {Zhou, X and Zhou, D and Pu, Y and Kim, H and Sun, Z and Qi, W and Jin, J and Zhang, W and Xia, M and Wang, C and Hong, S and Nguyen, LH and Jiao, N and Zheng, Y and Liu, T},
title = {Multi-kingdom profiling reveals altered gut phage-bacteria-metabolite interactions in MASLD.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-71981-0},
pmid = {42000726},
issn = {2041-1723},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly linked to gut microbial dysbiosis, but most studies have focused on bacteria, neglecting viruses and fungi, and their interactions. Here we show that MASLD is characterized by coordinated disruption of bacterial, viral and fungal communities and by a disturbed phage-bacteria-metabolite axis associated with disease-related bile acid changes. Integrating shotgun metagenomics, fungal ITS2 sequencing, fecal metabolomics and clinical profiling in 210 patients with MASLD and 210 age- and gender-matched healthy controls, we find reduced microbial diversity and extensive remodeling of cross-kingdom ecological networks in MASLD. Ruminococcus gnavus emerges as an enriched central hub, while Faecalibacterium prausnitzii and its associated bacteriophages are depleted. Phage-host analyses further reveal reduced lytic activity against R. gnavus and loss of sulfur amino acid metabolism-related auxiliary metabolic genes, which may impair F. prausnitzii fitness. Diminished phage control may facilitate R. gnavus expansion, alongside increased fecal isodeoxycholic acid, a secondary bile acid implicated in hepatic steatosis. A diagnostic classifier integrating bacterial and viral features with clinical parameters distinguish MASLD from controls in our cohort and maintain predictive performance in two external datasets. Together, these findings uncover a disrupted phage-bacteria-metabolite axis in MASLD and provide a multi-kingdom framework for non-invasive biomarker discovery and microbiome-targeted therapies.},
}
RevDate: 2026-04-18
Exploring the characteristics of gut microbiome changes in lung cancer patients and healthy controls.
Scientific reports pii:10.1038/s41598-026-48560-w [Epub ahead of print].
Lung cancer is among the most prevalent and lethal malignant neoplasms worldwide. Although the role of the pulmonary microbiome in the pathogenesis of lung cancer has been examined, the structure, diversity, and composition of the gut microbiome in lung cancer remain largely unclear. The present study is chiefly concerned with the analysis of the characteristics and alterations of the gut microbiome in lung cancer patients and healthy individuals, and with the exploration of potential characteristic gut microbiome in lung cancer patients. Stool samples were collected from 40 patients with lung cancer and 20 healthy controls at the Lung Cancer Center of West China Hospital, Sichuan University. The samples were analysed using 16S rRNA gene amplicon sequencing to investigate differences in the relative and absolute abundance, diversity, and functionality of the gut microbiome between the two groups. The predominant gut microbiome communities in lung cancer patients and healthy controls were found to comprise Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria. The F/B (Firmicutes/Bacteroidetes) ratio in the lung cancer group (0.73) was lower than that in the healthy control group (0.96). We found that there was no significant difference in α-diversity between LC patients and the control group (p > 0.05), whereas β-diversity of the gut microbiome revealed differences in microbial community structure between the patient and control groups (stress < 0.2). The healthy controls exhibited higher abundances of Bacteroidetes and Firmicutes as dominant bacterial groups, whereas the characteristic bacterial groups in lung cancer patients were the Ruminococcus_gnavus_group and the Prevotellaceae NK3B31 group. Studies have demonstrated that the gut microbiome of patients with lung cancer patients undergoes changes, and characteristic gut microbiome profiles may serve as potential diagnostic markers for lung cancer. Furthermore, we have revealed that impairments in normal gut microbiome function may be associated with the development and progression of lung cancer, providing valuable insights for the early prevention, diagnosis, and targeted intervention of lung cancer.
Additional Links: PMID-42000796
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PubMed:
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@article {pmid42000796,
year = {2026},
author = {Xu, P and Chen, J and Lu, X and Luo, H},
title = {Exploring the characteristics of gut microbiome changes in lung cancer patients and healthy controls.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-48560-w},
pmid = {42000796},
issn = {2045-2322},
abstract = {Lung cancer is among the most prevalent and lethal malignant neoplasms worldwide. Although the role of the pulmonary microbiome in the pathogenesis of lung cancer has been examined, the structure, diversity, and composition of the gut microbiome in lung cancer remain largely unclear. The present study is chiefly concerned with the analysis of the characteristics and alterations of the gut microbiome in lung cancer patients and healthy individuals, and with the exploration of potential characteristic gut microbiome in lung cancer patients. Stool samples were collected from 40 patients with lung cancer and 20 healthy controls at the Lung Cancer Center of West China Hospital, Sichuan University. The samples were analysed using 16S rRNA gene amplicon sequencing to investigate differences in the relative and absolute abundance, diversity, and functionality of the gut microbiome between the two groups. The predominant gut microbiome communities in lung cancer patients and healthy controls were found to comprise Bacteroidetes, Firmicutes, Proteobacteria, and Actinobacteria. The F/B (Firmicutes/Bacteroidetes) ratio in the lung cancer group (0.73) was lower than that in the healthy control group (0.96). We found that there was no significant difference in α-diversity between LC patients and the control group (p > 0.05), whereas β-diversity of the gut microbiome revealed differences in microbial community structure between the patient and control groups (stress < 0.2). The healthy controls exhibited higher abundances of Bacteroidetes and Firmicutes as dominant bacterial groups, whereas the characteristic bacterial groups in lung cancer patients were the Ruminococcus_gnavus_group and the Prevotellaceae NK3B31 group. Studies have demonstrated that the gut microbiome of patients with lung cancer patients undergoes changes, and characteristic gut microbiome profiles may serve as potential diagnostic markers for lung cancer. Furthermore, we have revealed that impairments in normal gut microbiome function may be associated with the development and progression of lung cancer, providing valuable insights for the early prevention, diagnosis, and targeted intervention of lung cancer.},
}
RevDate: 2026-04-18
Study on the diversity, structure, and function of endophytic bacteria in seeds of genuine medicinal plants in gansu province.
BMC plant biology pii:10.1186/s12870-026-08767-5 [Epub ahead of print].
Additional Links: PMID-42001039
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PubMed:
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@article {pmid42001039,
year = {2026},
author = {Li, S and White, JF and Zhai, Y and Li, X and Wang, K},
title = {Study on the diversity, structure, and function of endophytic bacteria in seeds of genuine medicinal plants in gansu province.},
journal = {BMC plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12870-026-08767-5},
pmid = {42001039},
issn = {1471-2229},
support = {25YFFA043//Gansu Provincial Key Research and Development Program/ ; },
}
RevDate: 2026-04-18
Dihydromyricetin exerts neuroprotective effects in acute spinal cord injury by inhibiting NLRP3/Caspase-1 inflammasome through gut microbiome modeling.
Journal of inflammation (London, England) pii:10.1186/s12950-026-00499-5 [Epub ahead of print].
Additional Links: PMID-42001079
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PubMed:
Citation:
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@article {pmid42001079,
year = {2026},
author = {Yang, Y and Kang, C and Pang, R and Huang, S and He, X and Gou, X and Yang, Y and Yan, Y and Ma, X},
title = {Dihydromyricetin exerts neuroprotective effects in acute spinal cord injury by inhibiting NLRP3/Caspase-1 inflammasome through gut microbiome modeling.},
journal = {Journal of inflammation (London, England)},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12950-026-00499-5},
pmid = {42001079},
issn = {1476-9255},
support = {2024060//Chengdu Municipal Health Commission Medical Research Project/ ; 25MSZX488//Sichuan Provincial Administration of Traditional Chinese Medicine Research Project/ ; },
}
RevDate: 2026-04-18
Microbiome and plasmidome shifts drive carbon, nitrogen, and greenhouse gas dynamics within transitioning permafrost.
Environmental microbiome pii:10.1186/s40793-026-00892-w [Epub ahead of print].
Thermokarst lakes contribute to greenhouse gas emissions but often experience constraints on available nitrogen. However, the interactions between carbon and nitrogen cycles in these systems, especially along the terrestrial-aquatic continuum, remain poorly understood. The increased soil-water connectivity in those systems affects organic matter processing, nutrient availability, and microbial transport. In Nunavik (Quebec, Canada), we sampled along a transect from a palsa (permafrost remnant) through an emerging thermokarst lake to peatland soils and mature lake. Using hybrid metagenome co-assemblies with gene-, plasmid-, and genome-centric approaches, we explored key biogeochemical cycles and the role of plasmids in microbial adaptation along the transect. Gene annotation, metagenome-assembled genome (MAG) reconstruction, and network analysis revealed a shift from potential for anaerobic ammonium oxidation (anammox) in palsa and emerging lake to potential for nitrification in mature lake. Potential for methanogenesis transitions from hydrogenotrophic in the palsa to methylotrophic in lakes, likely driven by a bacterial consortium degrading aromatic, peat-derived compounds. Sediments may support methane production via both hydrogenotrophic and acetoclastic potential for methanogenesis, partially fueled by the action of polysaccharide lyases. Anaerobic methane oxidation (AOM) potential seems important in both peat and the mature lake; and can be coupled with nitrification and sulfate-reducing partners through extracellular electron transfer, with cytochromes playing a central role. Notably, plasmidome shifts preceded metagenomic changes, especially in genes related to carbon and methane cycling, suggesting a role for plasmids in microbial adaptation to permafrost thaw. These findings highlight the complex microbial and plasmid dynamics that drive carbon, nitrogen, and greenhouse gas cycles in permafrost ecosystems.
Additional Links: PMID-42001152
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PubMed:
Citation:
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@article {pmid42001152,
year = {2026},
author = {Leroy, M and Cyriaque, V and Rattei, T and Laurion, I and Comte, J},
title = {Microbiome and plasmidome shifts drive carbon, nitrogen, and greenhouse gas dynamics within transitioning permafrost.},
journal = {Environmental microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40793-026-00892-w},
pmid = {42001152},
issn = {2524-6372},
support = {2021-PR-284297//Fonds de recherche du Québec - Nature et technologie/ ; RGPIN-2020-06876//Natural Sciences and Engineering Research Council - Discovery and Northern Research Programs/ ; RGPIN-2020-06874//Natural Sciences and Engineering Research Council - Discovery and Northern Research Programs/ ; 2021-PR-284297//Fonds de recherche du Québec - Nature et technologies/ ; },
abstract = {Thermokarst lakes contribute to greenhouse gas emissions but often experience constraints on available nitrogen. However, the interactions between carbon and nitrogen cycles in these systems, especially along the terrestrial-aquatic continuum, remain poorly understood. The increased soil-water connectivity in those systems affects organic matter processing, nutrient availability, and microbial transport. In Nunavik (Quebec, Canada), we sampled along a transect from a palsa (permafrost remnant) through an emerging thermokarst lake to peatland soils and mature lake. Using hybrid metagenome co-assemblies with gene-, plasmid-, and genome-centric approaches, we explored key biogeochemical cycles and the role of plasmids in microbial adaptation along the transect. Gene annotation, metagenome-assembled genome (MAG) reconstruction, and network analysis revealed a shift from potential for anaerobic ammonium oxidation (anammox) in palsa and emerging lake to potential for nitrification in mature lake. Potential for methanogenesis transitions from hydrogenotrophic in the palsa to methylotrophic in lakes, likely driven by a bacterial consortium degrading aromatic, peat-derived compounds. Sediments may support methane production via both hydrogenotrophic and acetoclastic potential for methanogenesis, partially fueled by the action of polysaccharide lyases. Anaerobic methane oxidation (AOM) potential seems important in both peat and the mature lake; and can be coupled with nitrification and sulfate-reducing partners through extracellular electron transfer, with cytochromes playing a central role. Notably, plasmidome shifts preceded metagenomic changes, especially in genes related to carbon and methane cycling, suggesting a role for plasmids in microbial adaptation to permafrost thaw. These findings highlight the complex microbial and plasmid dynamics that drive carbon, nitrogen, and greenhouse gas cycles in permafrost ecosystems.},
}
RevDate: 2026-04-19
Periodontal Medicine Rewired: Mechanisms Linking Periodontitis to Systemic Diseases.
Journal of periodontal research [Epub ahead of print].
Periodontitis is now recognized not merely as a localized oral condition but as a systemic disease linked to over 70 communicable and non-communicable conditions. This Review explores the key mechanistic pathways-or "gum-shots"-underpinning the systemic impact of periodontitis. Seven interwoven mechanisms are identified. The first, microbial translocation, involves oral pathobionts and virulence factors breaching anatomical barriers and gaining systemic access via hematological, respiratory, and enteral routes, contributing to tissue damage at extra-oral sites. The second, systemic (meta)inflammation, implicates both the spillover of inflammatory mediators from periodontal tissues into circulation and the immune response to translocated pathogens, fueling pro-inflammatory processes. The third, maladaptive myelopoiesis, involves the periodontitis-associated maladaptive trained immunity and aging-related clonal hematopoiesis of indeterminate potential in the bone marrow, leading to myeloid cells with heightened proinflammatory potential. The fourth, immune players trafficking, centers on the systemic repercussions of periodontally generated autoantibodies, translocated orally primed inflammatory cells, and other local immune events. The fifth, masticatory dysfunction-mediated dietary alterations, involves compromised chewing efficiency that alters dietary intake, resulting in nutritional and metabolic imbalances. The sixth, functional dysregulation of the oral microbiome, describes how periodontitis alters the metabolic activity of this densely populated microbial "superorganism", with downstream effects on both oral and systemic physiology. The final mechanism, shared underlying vulnerabilities, refers to background entities-such as biological aging, oxidative stress, psychosocial stress, (epi)genetic predispositions, certain viral infections, and potentially other as-yet-unknown contributors-that drive multi-morbidity, including periodontitis. By dissecting these interconnected pathways, this critical Review challenges the traditional dichotomy of direct versus indirect mechanisms, revealing a more intricate and dynamic interplay.
Additional Links: PMID-42001319
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PubMed:
Citation:
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@article {pmid42001319,
year = {2026},
author = {Romandini, M and Hajishengallis, G and Curtis, M and Baima, G},
title = {Periodontal Medicine Rewired: Mechanisms Linking Periodontitis to Systemic Diseases.},
journal = {Journal of periodontal research},
volume = {},
number = {},
pages = {},
doi = {10.1111/jre.70099},
pmid = {42001319},
issn = {1600-0765},
abstract = {Periodontitis is now recognized not merely as a localized oral condition but as a systemic disease linked to over 70 communicable and non-communicable conditions. This Review explores the key mechanistic pathways-or "gum-shots"-underpinning the systemic impact of periodontitis. Seven interwoven mechanisms are identified. The first, microbial translocation, involves oral pathobionts and virulence factors breaching anatomical barriers and gaining systemic access via hematological, respiratory, and enteral routes, contributing to tissue damage at extra-oral sites. The second, systemic (meta)inflammation, implicates both the spillover of inflammatory mediators from periodontal tissues into circulation and the immune response to translocated pathogens, fueling pro-inflammatory processes. The third, maladaptive myelopoiesis, involves the periodontitis-associated maladaptive trained immunity and aging-related clonal hematopoiesis of indeterminate potential in the bone marrow, leading to myeloid cells with heightened proinflammatory potential. The fourth, immune players trafficking, centers on the systemic repercussions of periodontally generated autoantibodies, translocated orally primed inflammatory cells, and other local immune events. The fifth, masticatory dysfunction-mediated dietary alterations, involves compromised chewing efficiency that alters dietary intake, resulting in nutritional and metabolic imbalances. The sixth, functional dysregulation of the oral microbiome, describes how periodontitis alters the metabolic activity of this densely populated microbial "superorganism", with downstream effects on both oral and systemic physiology. The final mechanism, shared underlying vulnerabilities, refers to background entities-such as biological aging, oxidative stress, psychosocial stress, (epi)genetic predispositions, certain viral infections, and potentially other as-yet-unknown contributors-that drive multi-morbidity, including periodontitis. By dissecting these interconnected pathways, this critical Review challenges the traditional dichotomy of direct versus indirect mechanisms, revealing a more intricate and dynamic interplay.},
}
RevDate: 2026-04-21
CmpDate: 2026-04-19
Therapeutic Remodeling of the Gut Microbiome as a Strategy to Restore Immune Tolerance in Autoimmunity.
MicrobiologyOpen, 15(2):e70294.
Autoimmune diseases happen when the immune system, which is supposed to defend the body from infections and other harmful things, starts to attack the body's own cells by mistake. In the last few years, they seem to be getting more public, and the reasons are quite complicated. It is usually not just one factor, but a mix of genes and environmental influences, such as diet, infections, or even stress. The gut microbiome, the vast community of bacteria and other tiny organisms living in our intestines, plays an important role in shaping how the immune system behaves. When this gut microbiota becomes unstable (a state called dysbiosis), it can be associated with the onset or worsening of various autoimmune diseases. In this review, we discuss the close relationship between the gut microbiome and autoimmune disorders and focus on how the microbiome can affect immune activation, immune tolerance, and inflammation at the molecular level. The general idea is that, if we understand these interactions better, we might be able in the future to design new ways to manage autoimmune diseases earlier and maybe in a more personalized way. In the end, the review suggests that if we understand better how the microbiome is involved in autoimmune diseases, it might be possible in the future to design more personalized therapies that change gut bacteria in a smart way and hopefully improve patient outcomes.
Additional Links: PMID-42001402
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@article {pmid42001402,
year = {2026},
author = {Boroumand, B and Jaberi, A and Zamani, G and Zandi, E and Zare, F and Vahedinezhad, M and Abdollahi, E and KarkonShayan, S and GhazanfarAhari, S and Sattar, M},
title = {Therapeutic Remodeling of the Gut Microbiome as a Strategy to Restore Immune Tolerance in Autoimmunity.},
journal = {MicrobiologyOpen},
volume = {15},
number = {2},
pages = {e70294},
pmid = {42001402},
issn = {2045-8827},
mesh = {*Gastrointestinal Microbiome/immunology ; Humans ; *Autoimmune Diseases/therapy/immunology/microbiology ; *Dysbiosis/immunology/therapy/microbiology ; *Immune Tolerance ; *Autoimmunity ; Animals ; },
abstract = {Autoimmune diseases happen when the immune system, which is supposed to defend the body from infections and other harmful things, starts to attack the body's own cells by mistake. In the last few years, they seem to be getting more public, and the reasons are quite complicated. It is usually not just one factor, but a mix of genes and environmental influences, such as diet, infections, or even stress. The gut microbiome, the vast community of bacteria and other tiny organisms living in our intestines, plays an important role in shaping how the immune system behaves. When this gut microbiota becomes unstable (a state called dysbiosis), it can be associated with the onset or worsening of various autoimmune diseases. In this review, we discuss the close relationship between the gut microbiome and autoimmune disorders and focus on how the microbiome can affect immune activation, immune tolerance, and inflammation at the molecular level. The general idea is that, if we understand these interactions better, we might be able in the future to design new ways to manage autoimmune diseases earlier and maybe in a more personalized way. In the end, the review suggests that if we understand better how the microbiome is involved in autoimmune diseases, it might be possible in the future to design more personalized therapies that change gut bacteria in a smart way and hopefully improve patient outcomes.},
}
MeSH Terms:
show MeSH Terms
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*Gastrointestinal Microbiome/immunology
Humans
*Autoimmune Diseases/therapy/immunology/microbiology
*Dysbiosis/immunology/therapy/microbiology
*Immune Tolerance
*Autoimmunity
Animals
RevDate: 2026-04-19
DRHIN: An Integrated and Interactive Web Server for Drug Repositioning.
Journal of chemical information and modeling [Epub ahead of print].
Drug repositioning (DR) identifies new therapeutic uses for approved drugs, reducing development burdens and offering safer treatment options for patients. While high-throughput technologies generate complex, large-scale multiomics data, existing DR tools struggle to comprehensively analyze the resulting biological networks. To address this challenge, we present DRHIN, an integrated, interactive web server for DR over heterogeneous information networks (HINs) using advanced deep learning techniques. DRHIN integrates transcriptomics, proteomics, and microbiome data, incorporating eight biological entities and 19 association types to build diverse HINs and elucidate the underlying molecular mechanisms. It includes 19 state-of-the-art graph representation algorithms, enabling flexible training, comparison, and evaluation of heterogeneous network data. The platform provides a code-free portal supporting three key predictive tasks: discovering drug-disease associations, repurposing existing drugs for new indications, and identifying potential therapies for specific diseases, making analyses accessible and reproducible. Leveraging high-performance computing, DRHIN efficiently processes million-scale networks, ensuring practical applicability in real-world scenarios. The web server is freely accessible at http://drhin.tianshanzw.cn.
Additional Links: PMID-42001407
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@article {pmid42001407,
year = {2026},
author = {Zhao, B and Li, D and Yang, Y and Hou, T and Hu, L},
title = {DRHIN: An Integrated and Interactive Web Server for Drug Repositioning.},
journal = {Journal of chemical information and modeling},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jcim.6c00311},
pmid = {42001407},
issn = {1549-960X},
abstract = {Drug repositioning (DR) identifies new therapeutic uses for approved drugs, reducing development burdens and offering safer treatment options for patients. While high-throughput technologies generate complex, large-scale multiomics data, existing DR tools struggle to comprehensively analyze the resulting biological networks. To address this challenge, we present DRHIN, an integrated, interactive web server for DR over heterogeneous information networks (HINs) using advanced deep learning techniques. DRHIN integrates transcriptomics, proteomics, and microbiome data, incorporating eight biological entities and 19 association types to build diverse HINs and elucidate the underlying molecular mechanisms. It includes 19 state-of-the-art graph representation algorithms, enabling flexible training, comparison, and evaluation of heterogeneous network data. The platform provides a code-free portal supporting three key predictive tasks: discovering drug-disease associations, repurposing existing drugs for new indications, and identifying potential therapies for specific diseases, making analyses accessible and reproducible. Leveraging high-performance computing, DRHIN efficiently processes million-scale networks, ensuring practical applicability in real-world scenarios. The web server is freely accessible at http://drhin.tianshanzw.cn.},
}
RevDate: 2026-04-19
Mutation studies on degradation of 3-phenoxybenzoic acid by Lacticaseibacillus paracasei - human gut microbiome in controlling risk for Parkinson's disease using molecular simulation dynamics.
Journal of biomolecular structure & dynamics [Epub ahead of print].
Parkinson's disease (PD) is a debilitating neurodegenerative disease affecting millions worldwide, especially the elderly. Pesticides, particularly pyrethroids like Cypermethrin, have been linked to the development of PD. Cypermethrin, when ingested, is broken down into 3-phenoxybenzoic acid (3PBA), which can lead to the dysfunction or death of dopaminergic neurons. Catechol-2,3-dioxygenase is an enzyme that breaks down 3PBA into catechol, that can further be processed and excreted by the human body. This enzyme is produced by the bacteria Lacticaseibacillus paracasei, a naturally present human gut microbe. Mutation studies were done to study the potential of the human gut microbiome in pesticide degradation improve the activity of the wild-type enzymes in degrading pesticides. The mutations were induced in two subunits of Catechol-2,3-dioxygenase using the WGS sequence of the gene coding for the same. Two subunits of the same protein i.e. Catechol-2,3-dioxygenase and NAD(+) reductase, were subjected to mutations using PyMol v3.1.0, and the crystal structures of the wild-type and mutant were docked against the ligand, 3-Phenoxybenzoic acid, using PyRx v0.8, and visualised using BIOVIA Discovery Studio Visualiser v24.1.0.23298, PyMol v3.1.0 and LigPlot + v2.2.9. The effects of mutation were further studied by analyzing the results of the molecular dynamics simulations conducted using the GROMACS software. Simulation trajectories like RMSD, RMSF, Inter and Intramolecular H-bonds, SASA, RG, PCA, FEL and FEP, all indicated better binding of the ligand (3PBA) to the active site.
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@article {pmid42001412,
year = {2026},
author = {Maria Lewis, B and Prashanth, A and Ramachandran, N and Sabat, S},
title = {Mutation studies on degradation of 3-phenoxybenzoic acid by Lacticaseibacillus paracasei - human gut microbiome in controlling risk for Parkinson's disease using molecular simulation dynamics.},
journal = {Journal of biomolecular structure & dynamics},
volume = {},
number = {},
pages = {1-28},
doi = {10.1080/07391102.2026.2653065},
pmid = {42001412},
issn = {1538-0254},
abstract = {Parkinson's disease (PD) is a debilitating neurodegenerative disease affecting millions worldwide, especially the elderly. Pesticides, particularly pyrethroids like Cypermethrin, have been linked to the development of PD. Cypermethrin, when ingested, is broken down into 3-phenoxybenzoic acid (3PBA), which can lead to the dysfunction or death of dopaminergic neurons. Catechol-2,3-dioxygenase is an enzyme that breaks down 3PBA into catechol, that can further be processed and excreted by the human body. This enzyme is produced by the bacteria Lacticaseibacillus paracasei, a naturally present human gut microbe. Mutation studies were done to study the potential of the human gut microbiome in pesticide degradation improve the activity of the wild-type enzymes in degrading pesticides. The mutations were induced in two subunits of Catechol-2,3-dioxygenase using the WGS sequence of the gene coding for the same. Two subunits of the same protein i.e. Catechol-2,3-dioxygenase and NAD(+) reductase, were subjected to mutations using PyMol v3.1.0, and the crystal structures of the wild-type and mutant were docked against the ligand, 3-Phenoxybenzoic acid, using PyRx v0.8, and visualised using BIOVIA Discovery Studio Visualiser v24.1.0.23298, PyMol v3.1.0 and LigPlot + v2.2.9. The effects of mutation were further studied by analyzing the results of the molecular dynamics simulations conducted using the GROMACS software. Simulation trajectories like RMSD, RMSF, Inter and Intramolecular H-bonds, SASA, RG, PCA, FEL and FEP, all indicated better binding of the ligand (3PBA) to the active site.},
}
RevDate: 2026-04-19
CmpDate: 2026-04-19
Characterization of the Oral Bacteria in Patients With Neuroendocrine Tumors of the Pancreas.
Cancer medicine, 15(4):e71840.
The primary objective of this study was to investigate dysbiosis in the oral microbiota of patients with pancreatic neuroendocrine tumors (pNETs) and to identify potential biomarkers for clinical diagnosis and prognostic evaluation of pNETs. Healthy controls and pNETs patients were recruited from our hospital. Salivary flora were profiled in healthy subjects (HS group) and pNETs patients (PS group) using 16S rRNA gene sequencing. Microbial diversity was assessed by α-diversity (Tukey test) and β-diversity (Partial Least Squares Discriminant Analysis, PLS-DA). Taxonomic differences between groups were evaluated using linear discriminant analysis effect size (LEfSe). The salivary microbiota of pNETs patients showed higher abundance and diversity compared to healthy controls. Dominant bacterial phyla in both groups include Proteobacteria, Firmicutes, Bacteroidota, Actinobacteriota, Fusobacteriota, Cyanobacteria, and Campilobacterota. At the genus level, Leptotrichia, Actinobacillus, and Granulicatella were more abundant in the PS group. LEfSe analysis further indicated a greater abundance of Rothia, Chloroplast, Leptotrichia, Actinomyces, and Granulicatella in the PS group. Our findings offer initial evidence suggesting a potential link between oral microbiome dysbiosis and pNETs, and identify microbial features that could be evaluated in future studies as potential biomarkers for clinical diagnosis and prognosis.
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@article {pmid42001450,
year = {2026},
author = {Yao, J and Fei, C and Wu, H and Zhang, Z and Jiang, Z},
title = {Characterization of the Oral Bacteria in Patients With Neuroendocrine Tumors of the Pancreas.},
journal = {Cancer medicine},
volume = {15},
number = {4},
pages = {e71840},
doi = {10.1002/cam4.71840},
pmid = {42001450},
issn = {2045-7634},
support = {YKK20108//Nanjing health science and technology development special fund project plan/ ; NMUB2019134//Science and Technology Development Project of Nanjing Medical University/ ; },
mesh = {Humans ; Male ; *Pancreatic Neoplasms/microbiology ; Female ; *Neuroendocrine Tumors/microbiology/diagnosis ; Middle Aged ; RNA, Ribosomal, 16S/genetics ; *Dysbiosis/microbiology ; *Microbiota ; *Bacteria/genetics/classification/isolation & purification ; Adult ; *Saliva/microbiology ; Aged ; Case-Control Studies ; Prognosis ; *Mouth/microbiology ; },
abstract = {The primary objective of this study was to investigate dysbiosis in the oral microbiota of patients with pancreatic neuroendocrine tumors (pNETs) and to identify potential biomarkers for clinical diagnosis and prognostic evaluation of pNETs. Healthy controls and pNETs patients were recruited from our hospital. Salivary flora were profiled in healthy subjects (HS group) and pNETs patients (PS group) using 16S rRNA gene sequencing. Microbial diversity was assessed by α-diversity (Tukey test) and β-diversity (Partial Least Squares Discriminant Analysis, PLS-DA). Taxonomic differences between groups were evaluated using linear discriminant analysis effect size (LEfSe). The salivary microbiota of pNETs patients showed higher abundance and diversity compared to healthy controls. Dominant bacterial phyla in both groups include Proteobacteria, Firmicutes, Bacteroidota, Actinobacteriota, Fusobacteriota, Cyanobacteria, and Campilobacterota. At the genus level, Leptotrichia, Actinobacillus, and Granulicatella were more abundant in the PS group. LEfSe analysis further indicated a greater abundance of Rothia, Chloroplast, Leptotrichia, Actinomyces, and Granulicatella in the PS group. Our findings offer initial evidence suggesting a potential link between oral microbiome dysbiosis and pNETs, and identify microbial features that could be evaluated in future studies as potential biomarkers for clinical diagnosis and prognosis.},
}
MeSH Terms:
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Humans
Male
*Pancreatic Neoplasms/microbiology
Female
*Neuroendocrine Tumors/microbiology/diagnosis
Middle Aged
RNA, Ribosomal, 16S/genetics
*Dysbiosis/microbiology
*Microbiota
*Bacteria/genetics/classification/isolation & purification
Adult
*Saliva/microbiology
Aged
Case-Control Studies
Prognosis
*Mouth/microbiology
RevDate: 2026-04-19
Human microbiome influence on head and neck cancer.
Cancer treatment and research communications, 47:101218 pii:S2468-2942(26)00129-2 [Epub ahead of print].
Recent breakthroughs in microbiome research have identified the gut microbiota as an important regulator of systemic immunity, inflammation, and carcinogenesis. Although established risk factors for head and neck cancer (HNC) include tobacco use, alcohol use, and human papillomavirus (HPV) infection, growing data suggest that gut microbial dysbiosis may also play a role in its etiology. Changes in gut microbiota composition can have a distal influence on the head and neck region by modulating immune function, producing microbial metabolites, and disrupting epithelial barrier integrity, influencing tumor initiation, development, and therapeutic response. New research suggests that the gut microbiome plays an important role in regulating the success and toxicity of traditional HNC treatments such as chemoradiation and immunotherapy. This review focuses on current evidence linking alterations in the gut microbiome to HNC development and progression, emphasizing underlying mechanisms, diagnostic potential, and emerging microbiome-based therapeutic strategies.
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@article {pmid42001830,
year = {2026},
author = {Vijayakumar, V and Rathinam, T and Deenadhayalan, SS and Edwin, ER},
title = {Human microbiome influence on head and neck cancer.},
journal = {Cancer treatment and research communications},
volume = {47},
number = {},
pages = {101218},
doi = {10.1016/j.ctarc.2026.101218},
pmid = {42001830},
issn = {2468-2942},
abstract = {Recent breakthroughs in microbiome research have identified the gut microbiota as an important regulator of systemic immunity, inflammation, and carcinogenesis. Although established risk factors for head and neck cancer (HNC) include tobacco use, alcohol use, and human papillomavirus (HPV) infection, growing data suggest that gut microbial dysbiosis may also play a role in its etiology. Changes in gut microbiota composition can have a distal influence on the head and neck region by modulating immune function, producing microbial metabolites, and disrupting epithelial barrier integrity, influencing tumor initiation, development, and therapeutic response. New research suggests that the gut microbiome plays an important role in regulating the success and toxicity of traditional HNC treatments such as chemoradiation and immunotherapy. This review focuses on current evidence linking alterations in the gut microbiome to HNC development and progression, emphasizing underlying mechanisms, diagnostic potential, and emerging microbiome-based therapeutic strategies.},
}
RevDate: 2026-04-19
Antibacterial immunity in teleost fish: Integrating innate and adaptive responses for sustainable aquaculture.
Veterinary immunology and immunopathology, 297:111113 pii:S0165-2427(26)00052-8 [Epub ahead of print].
Bacterial infections are currently the most significant hindrance to the worldwide adoption of sustainable aquaculture, causing unprecedented economical losses and challenges to food security. Teleosts have an extremely well-developed innate and adaptive immune system, but the functional integrity of these immune systems is adversely affected under universal aquaculture-related stress factors. The current review critically and comprehensively synthesizes the two most important challenges, addressing immune resilience, which include: (1) the complex functional interactions between innate and adaptive immune mechanisms, and (2) the combined modulation of these immune mechanisms under environmental factors mentioned above. Our focus primarily centers on the role of major stressors such as temperature change, water quality measures, (physiological) chronic stressing, and microbiome diversity on innate host immunity and resistance to bacterially infected diseases. Finally, we not only conclude the current state regarding the latest research progress on the role and mechanisms utilized in the transition phase from the latent to chronic infection phase based on autophagy-related responses but also emphasize the need to adopt an integrated research area named 'Eco-Immunology' to measure and develop effective interventions against fish diseases. It is the prime requirement to improve the host's resistance to diverse farming conditions to develop sustainable and effective aquaculture. This review uniquely integrates innate-adaptive immune crosstalk with environmentally driven immune reprogramming and autophagy-mediated control of chronic bacterial infections, framing teleost antibacterial immunity within an eco-immunological perspective relevant to sustainable aquaculture.
Additional Links: PMID-42001862
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@article {pmid42001862,
year = {2026},
author = {Özcan, F and Arserim, NB},
title = {Antibacterial immunity in teleost fish: Integrating innate and adaptive responses for sustainable aquaculture.},
journal = {Veterinary immunology and immunopathology},
volume = {297},
number = {},
pages = {111113},
doi = {10.1016/j.vetimm.2026.111113},
pmid = {42001862},
issn = {1873-2534},
abstract = {Bacterial infections are currently the most significant hindrance to the worldwide adoption of sustainable aquaculture, causing unprecedented economical losses and challenges to food security. Teleosts have an extremely well-developed innate and adaptive immune system, but the functional integrity of these immune systems is adversely affected under universal aquaculture-related stress factors. The current review critically and comprehensively synthesizes the two most important challenges, addressing immune resilience, which include: (1) the complex functional interactions between innate and adaptive immune mechanisms, and (2) the combined modulation of these immune mechanisms under environmental factors mentioned above. Our focus primarily centers on the role of major stressors such as temperature change, water quality measures, (physiological) chronic stressing, and microbiome diversity on innate host immunity and resistance to bacterially infected diseases. Finally, we not only conclude the current state regarding the latest research progress on the role and mechanisms utilized in the transition phase from the latent to chronic infection phase based on autophagy-related responses but also emphasize the need to adopt an integrated research area named 'Eco-Immunology' to measure and develop effective interventions against fish diseases. It is the prime requirement to improve the host's resistance to diverse farming conditions to develop sustainable and effective aquaculture. This review uniquely integrates innate-adaptive immune crosstalk with environmentally driven immune reprogramming and autophagy-mediated control of chronic bacterial infections, framing teleost antibacterial immunity within an eco-immunological perspective relevant to sustainable aquaculture.},
}
RevDate: 2026-04-19
Pre-Crohn's Disease Stool from Discordant Siblings Promotes the Development of Colitis in Germ-Free Mice.
Gastroenterology pii:S0016-5085(26)00345-8 [Epub ahead of print].
BACKGROUND AND AIMS: The gut microbiome is implicated in Crohn's disease (CD) development. However, human microbiome studies need experimental evidence to demonstrate if specific microbial differences promote CD pathogenesis. This study aims to determine if the gut microbiome from individuals who later developed CD promotes colitis in germ-free recipient mice.
METHODS: Germ-free mice were colonized with fecal samples from 12 pairs of discordant siblings: where one sibling later developed CD (pre-CD), while the other remained a healthy matched control (HMC). After colonization, colitis was induced by T-cell transfer to assess effect of stool on multiple measures of colitis severity. Comparative analysis with human donor metadata explored transferred pathogenic traits.
RESULTS: Mice receiving pre-CD stool exhibited increased weight loss, fecal lipocalin-2, and intestinal histological damage compared to mice receiving HMC stool. Fecal metabolomic analysis revealed differences in 40 metabolites between pre-CD and HMC colonized mice. Furthermore, two metabolic pathways were shared between pre-CD participants and mice. Notably, sphingolipids showed a positive correlation between humans and mice, associated with increased colitis in mice.
CONCLUSION: This study functionally demonstrates that the stool microbiome of individuals susceptible to CD is altered years before diagnosis, exhibiting greater inflammatory potential when transferred to susceptible mice.
Additional Links: PMID-42002154
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@article {pmid42002154,
year = {2026},
author = {Dang, CP and Chen-Liaw, A and Xue, M and Luchak, A and Mu, K and Li, Q and Ren, MY and Lee, SH and Moayyedi, P and Griffiths, AM and Deslandres, C and Murthy, SK and Steinhart, AH and Otley, A and Dieleman, LA and Jacobson, K and Rubin, DT and Panaccione, R and Feagan, BG and Streutker, C and Mogno, I and Britton, GJ and Faith, JJ and , and Croitoru, K and Turpin, W},
title = {Pre-Crohn's Disease Stool from Discordant Siblings Promotes the Development of Colitis in Germ-Free Mice.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2026.03.023},
pmid = {42002154},
issn = {1528-0012},
abstract = {BACKGROUND AND AIMS: The gut microbiome is implicated in Crohn's disease (CD) development. However, human microbiome studies need experimental evidence to demonstrate if specific microbial differences promote CD pathogenesis. This study aims to determine if the gut microbiome from individuals who later developed CD promotes colitis in germ-free recipient mice.
METHODS: Germ-free mice were colonized with fecal samples from 12 pairs of discordant siblings: where one sibling later developed CD (pre-CD), while the other remained a healthy matched control (HMC). After colonization, colitis was induced by T-cell transfer to assess effect of stool on multiple measures of colitis severity. Comparative analysis with human donor metadata explored transferred pathogenic traits.
RESULTS: Mice receiving pre-CD stool exhibited increased weight loss, fecal lipocalin-2, and intestinal histological damage compared to mice receiving HMC stool. Fecal metabolomic analysis revealed differences in 40 metabolites between pre-CD and HMC colonized mice. Furthermore, two metabolic pathways were shared between pre-CD participants and mice. Notably, sphingolipids showed a positive correlation between humans and mice, associated with increased colitis in mice.
CONCLUSION: This study functionally demonstrates that the stool microbiome of individuals susceptible to CD is altered years before diagnosis, exhibiting greater inflammatory potential when transferred to susceptible mice.},
}
RevDate: 2026-04-20
Iron plaque on wetland plant roots serves as a hotspot at the rhizosphere and a barrier within the endosphere for antibiotic resistance gene dissemination.
Bioresource technology, 453:134648 pii:S0960-8524(26)00730-3 [Epub ahead of print].
The iron plaque (IP) on wetland plant roots provides a crucial microenvironment for pollutant transport and transformation, yet its influence on the migration and dissemination of antibiotic resistance genes (ARGs) remains unexplored. Plasmid conjugation greatly contributes to ARG spreads. This study investigated the effect of IP formation on the plasmid-mediated ARG transfer across rhizosphere-iron plaque-root endosphere continuum and identified the key factors driving this process. Both the quantification of target genes and visual evidence demonstrated that conjugation frequencies within IP increased in a dose-dependent manner with the amount of IP formed on the root surface. In contrast, conjugation frequencies in the endosphere declined significantly as IP increased. The elevated IP content enhanced cell membrane permeability, raised reactive oxygen species (ROS) levels, and increased the activities of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT). A significant positive correlation was observed between ROS levels and conjugation frequencies, as well as between the activities of antioxidant enzymes (SOD and CAT) and IP formation. The bacterial community structure was significantly shaped in root compartments. The transconjugal pool was phylogenetically constrained, dominated by Gammaproteobacteria such as Escherichia and Pseudomonas, which accounted for over 70% of transfer events despite representing less than 3% of the total bacterial community. Our findings imply that IP functions as both a hotspot for ARG transfer on root surfaces and a barrier against their entry into the root interior, which guide and optimize the application of IP in the phytoremediation of emerging contaminants including ARGs.
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@article {pmid42002159,
year = {2026},
author = {Liu, X and Li, S and Huang, C and Liu, Y and Dong, Y and Gong, H and Zhou, G},
title = {Iron plaque on wetland plant roots serves as a hotspot at the rhizosphere and a barrier within the endosphere for antibiotic resistance gene dissemination.},
journal = {Bioresource technology},
volume = {453},
number = {},
pages = {134648},
doi = {10.1016/j.biortech.2026.134648},
pmid = {42002159},
issn = {1873-2976},
abstract = {The iron plaque (IP) on wetland plant roots provides a crucial microenvironment for pollutant transport and transformation, yet its influence on the migration and dissemination of antibiotic resistance genes (ARGs) remains unexplored. Plasmid conjugation greatly contributes to ARG spreads. This study investigated the effect of IP formation on the plasmid-mediated ARG transfer across rhizosphere-iron plaque-root endosphere continuum and identified the key factors driving this process. Both the quantification of target genes and visual evidence demonstrated that conjugation frequencies within IP increased in a dose-dependent manner with the amount of IP formed on the root surface. In contrast, conjugation frequencies in the endosphere declined significantly as IP increased. The elevated IP content enhanced cell membrane permeability, raised reactive oxygen species (ROS) levels, and increased the activities of antioxidant enzymes including superoxide dismutase (SOD) and catalase (CAT). A significant positive correlation was observed between ROS levels and conjugation frequencies, as well as between the activities of antioxidant enzymes (SOD and CAT) and IP formation. The bacterial community structure was significantly shaped in root compartments. The transconjugal pool was phylogenetically constrained, dominated by Gammaproteobacteria such as Escherichia and Pseudomonas, which accounted for over 70% of transfer events despite representing less than 3% of the total bacterial community. Our findings imply that IP functions as both a hotspot for ARG transfer on root surfaces and a barrier against their entry into the root interior, which guide and optimize the application of IP in the phytoremediation of emerging contaminants including ARGs.},
}
RevDate: 2026-04-19
Fecal Microbiota Transplantation for gastrointestinal complications after Allogeneic Hematopoietic Cell Transplantation: a systematic review and narrative synthesis.
Transplantation and cellular therapy pii:S2666-6367(26)00303-9 [Epub ahead of print].
BACKGROUND: Following allogeneic hematopoietic stem cell transplantation (allo-HSCT), patients frequently develop gastrointestinal complications, including microbiota dysbiosis, infectious syndromes, and graft-versus-host disease (GVHD), which remain major contributors to post-transplant morbidity and mortality. In recent years, several studies have explored microbiome-based interventions, particularly fecal microbiota transplantation (FMT), as a therapeutic strategy for these complications in this highly immunocompromised population. However, substantial variability exists across studies with respect to clinical indications, FMT protocols, and reported outcomes.
OBJECTIVES: To systematically evaluate the reported clinical use of FMT for gastrointestinal complications following allo-HSCT, including microbiota dysbiosis, infectious complications, and GVHD. The aim was to characterize study populations, treatment protocols, and reported clinical outcomes, and to synthesize evidence regarding efficacy and safety, with a focus on indication-specific patterns and potential translational relevance for patient management in this highly immunocompromised population.
STUDY DESIGN: We conducted a PRISMA-compliant systematic review of studies evaluating FMT as a treatment in patients after allo-HSCT. PubMed, Embase, Web of Science, and the Cochrane Library were searched through October 2025. Eligible studies included randomized controlled trials, cohort studies, and prospective or retrospective single-arm studies reporting clinical outcomes following FMT. Given the marked heterogeneity in clinical indications, FMT administration strategies, and outcome definitions, study findings were synthesized using a structured narrative approach, with quantitative data summarized descriptively where appropriate.
RESULTS: Twenty studies including patients after allo-HSCT were analyzed. FMT demonstrated high and consistent response rates in non-GVHD indications, whereas GVHD cohorts exhibited more variable responses, with median CR and ORR ranging 50-55% in steroid-refractory cases. One-year overall survival was generally favorable in dysbiosis and infection groups (>70%), but more heterogeneous in GVHD. FMT was well tolerated, with predominantly mild gastrointestinal adverse events; serious events were infrequent and mostly disease-related.
CONCLUSIONS: Current evidence indicates that FMT has been explored as a context-dependent therapy for selected gastrointestinal complications following allo-HSCT, particularly in patients with aGVHD. Nevertheless, substantial heterogeneity in study design, clinical indications, and outcome assessment limits definitive conclusions regarding efficacy. Well-designed prospective studies with standardized treatment indications, outcome measures, and careful consideration of concurrent immunosuppressive therapies are required to better define the optimal role, timing, and patient selection for FMT in the post-transplant treatment setting.
Additional Links: PMID-42002228
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@article {pmid42002228,
year = {2026},
author = {Liu, S and Huang, Z and Guo, Z},
title = {Fecal Microbiota Transplantation for gastrointestinal complications after Allogeneic Hematopoietic Cell Transplantation: a systematic review and narrative synthesis.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.04.016},
pmid = {42002228},
issn = {2666-6367},
abstract = {BACKGROUND: Following allogeneic hematopoietic stem cell transplantation (allo-HSCT), patients frequently develop gastrointestinal complications, including microbiota dysbiosis, infectious syndromes, and graft-versus-host disease (GVHD), which remain major contributors to post-transplant morbidity and mortality. In recent years, several studies have explored microbiome-based interventions, particularly fecal microbiota transplantation (FMT), as a therapeutic strategy for these complications in this highly immunocompromised population. However, substantial variability exists across studies with respect to clinical indications, FMT protocols, and reported outcomes.
OBJECTIVES: To systematically evaluate the reported clinical use of FMT for gastrointestinal complications following allo-HSCT, including microbiota dysbiosis, infectious complications, and GVHD. The aim was to characterize study populations, treatment protocols, and reported clinical outcomes, and to synthesize evidence regarding efficacy and safety, with a focus on indication-specific patterns and potential translational relevance for patient management in this highly immunocompromised population.
STUDY DESIGN: We conducted a PRISMA-compliant systematic review of studies evaluating FMT as a treatment in patients after allo-HSCT. PubMed, Embase, Web of Science, and the Cochrane Library were searched through October 2025. Eligible studies included randomized controlled trials, cohort studies, and prospective or retrospective single-arm studies reporting clinical outcomes following FMT. Given the marked heterogeneity in clinical indications, FMT administration strategies, and outcome definitions, study findings were synthesized using a structured narrative approach, with quantitative data summarized descriptively where appropriate.
RESULTS: Twenty studies including patients after allo-HSCT were analyzed. FMT demonstrated high and consistent response rates in non-GVHD indications, whereas GVHD cohorts exhibited more variable responses, with median CR and ORR ranging 50-55% in steroid-refractory cases. One-year overall survival was generally favorable in dysbiosis and infection groups (>70%), but more heterogeneous in GVHD. FMT was well tolerated, with predominantly mild gastrointestinal adverse events; serious events were infrequent and mostly disease-related.
CONCLUSIONS: Current evidence indicates that FMT has been explored as a context-dependent therapy for selected gastrointestinal complications following allo-HSCT, particularly in patients with aGVHD. Nevertheless, substantial heterogeneity in study design, clinical indications, and outcome assessment limits definitive conclusions regarding efficacy. Well-designed prospective studies with standardized treatment indications, outcome measures, and careful consideration of concurrent immunosuppressive therapies are required to better define the optimal role, timing, and patient selection for FMT in the post-transplant treatment setting.},
}
RevDate: 2026-04-19
CmpDate: 2026-04-19
Mechanisms Underlying Bioactive Compounds Decline in Medicinal Blaps rhynchopetera During Artificial Rearing.
Environmental microbiology, 28(4):e70304.
Artificial rearing is essential for sustainable utilization of medicinal insects, yet its impact on bioactive compound production remains poorly understood. Here we provide preliminary evidence that rearing of the medicinal beetle Blaps rhynchopetera reshapes its gut microbiota and metabolome, beyond mere environmental effects. Metabolomic analysis revealed 727 significantly altered metabolites, with 436 compounds, many linked to analgesic and anti-inflammatory activities, markedly reduced under rearing. Network pharmacology analysis suggested that this metabolic remodelling alters the overall regulatory landscape, with reduced network complexity compared to wild counterparts. Metagenomic profiling uncovered a decline in Pseudomonadota, a phylum positively correlated with multiple bioactive metabolites. Preliminary reintroduction of four Pseudomonadota strains suggested their potential involvement in terpenoid backbone biosynthesis, a key pathway for natural product synthesis. These findings reveal an intrinsic trade-off between rearing-driven microbial homogenization and preservation of medicinal potency, highlighting the need for microbiome-informed rearing strategies.
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@article {pmid42002296,
year = {2026},
author = {Yang, X and Zhang, L and Zhou, S and Wang, Z and Lv, Q and Zhao, M and Wang, C},
title = {Mechanisms Underlying Bioactive Compounds Decline in Medicinal Blaps rhynchopetera During Artificial Rearing.},
journal = {Environmental microbiology},
volume = {28},
number = {4},
pages = {e70304},
doi = {10.1111/1462-2920.70304},
pmid = {42002296},
issn = {1462-2920},
support = {2022YFC2602500//National Key Research and Development Program of China/ ; JiaoWaiSiYa[2020]619//Lancang-Mekong Cooperation Special Fund Projects/ ; SAJC202402//Chinese Academy of Sciences/ ; 2025YKZY002//Yunnan Characteristic Plant Extraction Laboratory/ ; 202449CE340005//Yunnan Provincial Science and Technology Department/ ; 202305AH340007//Yunnan Provincial Science and Technology Department/ ; },
mesh = {Animals ; *Coleoptera/microbiology/metabolism/growth & development ; *Gastrointestinal Microbiome ; Bacteria/metabolism/genetics/classification/isolation & purification ; Metabolome ; Biological Products/metabolism ; },
abstract = {Artificial rearing is essential for sustainable utilization of medicinal insects, yet its impact on bioactive compound production remains poorly understood. Here we provide preliminary evidence that rearing of the medicinal beetle Blaps rhynchopetera reshapes its gut microbiota and metabolome, beyond mere environmental effects. Metabolomic analysis revealed 727 significantly altered metabolites, with 436 compounds, many linked to analgesic and anti-inflammatory activities, markedly reduced under rearing. Network pharmacology analysis suggested that this metabolic remodelling alters the overall regulatory landscape, with reduced network complexity compared to wild counterparts. Metagenomic profiling uncovered a decline in Pseudomonadota, a phylum positively correlated with multiple bioactive metabolites. Preliminary reintroduction of four Pseudomonadota strains suggested their potential involvement in terpenoid backbone biosynthesis, a key pathway for natural product synthesis. These findings reveal an intrinsic trade-off between rearing-driven microbial homogenization and preservation of medicinal potency, highlighting the need for microbiome-informed rearing strategies.},
}
MeSH Terms:
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Animals
*Coleoptera/microbiology/metabolism/growth & development
*Gastrointestinal Microbiome
Bacteria/metabolism/genetics/classification/isolation & purification
Metabolome
Biological Products/metabolism
RevDate: 2026-04-19
CmpDate: 2026-04-19
A fructan-type polysaccharide from Lycium ruthenicum attenuates liver fibrosis via microbiota-dependent ferroptosis inhibition.
Carbohydrate polymers, 382:125243.
Plant-derived polysaccharides represent promising candidates for hepatic fibrosis (HF) therapy through the gut-liver axis. This study investigated the structural characteristics, anti-fibrotic efficacy, and mechanisms of LRMP1, a novel polysaccharide from Lycium ruthenicum Murr. LRMP1 was identified as a homogeneous inulin-type fructan (3.055 kDa) with a → 1)-β-D-Fruf-(2 → backbone terminated by α-D-Glcp-(1 → 2)-β-D-Fruf linkages (DP 4-20). Integrated multi-omics analysis combining hepatic transcriptomics, serum metabolomics, and gut microbiome profiling revealed that LRMP1 ameliorates HF via a gut microbiota-postbiotics-ferroptosis regulatory axis. In both CCl4-induced and MCD diet-induced chronic fibrosis models, LRMP1 significantly attenuated liver injury, fibrosis, inflammation, and oxidative stress, while restoring intestinal barrier integrity. These protective effects correlated with enrichment of beneficial bacteria (Akkermansia muciniphila, Lactobacillus spp.) and pathogen depletion. Mechanistically, LRMP1 suppressed TGF-β signaling and inhibited hepatocyte ferroptosis by restoring the GPX4/SLC7A11 antioxidant system and reducing lipid peroxidation. Serum metabolomics further revealed elevated anti-ferroptotic metabolites and suppressed pro-inflammatory lipids. Crucially, antibiotic depletion abolished LRMP1's efficacy, whereas fecal microbiota transplantation and fermentation supernatant experiments confirmed that microbiota-derived postbiotics selectively protect hepatocytes from ferroptosis. These findings establish LRMP1 as a promising microbiota-targeted polysaccharide for HF intervention through the gut-liver axis.
Additional Links: PMID-42002330
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PubMed:
Citation:
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@article {pmid42002330,
year = {2026},
author = {Zhao, Y and Qiao, M and Ma, C and Hou, Q and Hu, J and Yang, J},
title = {A fructan-type polysaccharide from Lycium ruthenicum attenuates liver fibrosis via microbiota-dependent ferroptosis inhibition.},
journal = {Carbohydrate polymers},
volume = {382},
number = {},
pages = {125243},
doi = {10.1016/j.carbpol.2026.125243},
pmid = {42002330},
issn = {1879-1344},
mesh = {Animals ; *Liver Cirrhosis/drug therapy/metabolism/pathology/chemically induced ; *Gastrointestinal Microbiome/drug effects ; *Lycium/chemistry ; *Ferroptosis/drug effects ; Mice ; Male ; *Polysaccharides/pharmacology/chemistry ; Mice, Inbred C57BL ; *Fructans/pharmacology/chemistry ; Liver/drug effects/metabolism/pathology ; Oxidative Stress/drug effects ; },
abstract = {Plant-derived polysaccharides represent promising candidates for hepatic fibrosis (HF) therapy through the gut-liver axis. This study investigated the structural characteristics, anti-fibrotic efficacy, and mechanisms of LRMP1, a novel polysaccharide from Lycium ruthenicum Murr. LRMP1 was identified as a homogeneous inulin-type fructan (3.055 kDa) with a → 1)-β-D-Fruf-(2 → backbone terminated by α-D-Glcp-(1 → 2)-β-D-Fruf linkages (DP 4-20). Integrated multi-omics analysis combining hepatic transcriptomics, serum metabolomics, and gut microbiome profiling revealed that LRMP1 ameliorates HF via a gut microbiota-postbiotics-ferroptosis regulatory axis. In both CCl4-induced and MCD diet-induced chronic fibrosis models, LRMP1 significantly attenuated liver injury, fibrosis, inflammation, and oxidative stress, while restoring intestinal barrier integrity. These protective effects correlated with enrichment of beneficial bacteria (Akkermansia muciniphila, Lactobacillus spp.) and pathogen depletion. Mechanistically, LRMP1 suppressed TGF-β signaling and inhibited hepatocyte ferroptosis by restoring the GPX4/SLC7A11 antioxidant system and reducing lipid peroxidation. Serum metabolomics further revealed elevated anti-ferroptotic metabolites and suppressed pro-inflammatory lipids. Crucially, antibiotic depletion abolished LRMP1's efficacy, whereas fecal microbiota transplantation and fermentation supernatant experiments confirmed that microbiota-derived postbiotics selectively protect hepatocytes from ferroptosis. These findings establish LRMP1 as a promising microbiota-targeted polysaccharide for HF intervention through the gut-liver axis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Liver Cirrhosis/drug therapy/metabolism/pathology/chemically induced
*Gastrointestinal Microbiome/drug effects
*Lycium/chemistry
*Ferroptosis/drug effects
Mice
Male
*Polysaccharides/pharmacology/chemistry
Mice, Inbred C57BL
*Fructans/pharmacology/chemistry
Liver/drug effects/metabolism/pathology
Oxidative Stress/drug effects
RevDate: 2026-04-19
Linking microbial function and remote sensing for understanding drylands.
Trends in ecology & evolution pii:S0169-5347(26)00075-3 [Epub ahead of print].
Drylands, covering over 40% of Earth's land surface, are expanding due to accelerating aridification and vegetation loss. Their microbial communities sustain essential processes such as carbon fixation, nitrogen cycling, and trace gas regulation; yet they remain largely invisible to global models. While microbiome studies reveal mechanistic details at local scales, environmental monitoring requires spatial continuity. We argue that advances in remote sensing, with its increasing resolutions, now allow microbial processes to be observed, scaled, and modeled across regions. Linking omics and spectral data can reveal microbial 'sentinels' of ecosystem change, transforming microbial ecology into a spatially predictive science. This integration provides a foundation for early-warning systems of biodiversity loss and land degradation, positioning microbes as measurable actors in Earth system dynamics.
Additional Links: PMID-42002450
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PubMed:
Citation:
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@article {pmid42002450,
year = {2026},
author = {Coleine, C and Obermeier, W and Lehnert, L and Leung, PM and Donati, C},
title = {Linking microbial function and remote sensing for understanding drylands.},
journal = {Trends in ecology & evolution},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tree.2026.04.002},
pmid = {42002450},
issn = {1872-8383},
abstract = {Drylands, covering over 40% of Earth's land surface, are expanding due to accelerating aridification and vegetation loss. Their microbial communities sustain essential processes such as carbon fixation, nitrogen cycling, and trace gas regulation; yet they remain largely invisible to global models. While microbiome studies reveal mechanistic details at local scales, environmental monitoring requires spatial continuity. We argue that advances in remote sensing, with its increasing resolutions, now allow microbial processes to be observed, scaled, and modeled across regions. Linking omics and spectral data can reveal microbial 'sentinels' of ecosystem change, transforming microbial ecology into a spatially predictive science. This integration provides a foundation for early-warning systems of biodiversity loss and land degradation, positioning microbes as measurable actors in Earth system dynamics.},
}
RevDate: 2026-04-19
Corrigendum to "Microbiome and gartynecologic cancer" [Cancer Lett. 636 (2026) 217940].
Additional Links: PMID-42002490
Publisher:
PubMed:
Citation:
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@article {pmid42002490,
year = {2026},
author = {Liao, B and Chen, L and Ruan, J and Wang, R and Hu, B and Long, R and Li, Y and Zhang, G and Yu, J and Ming Zhang, and Zhang, Y and Liao, S},
title = {Corrigendum to "Microbiome and gartynecologic cancer" [Cancer Lett. 636 (2026) 217940].},
journal = {Cancer letters},
volume = {},
number = {},
pages = {218519},
doi = {10.1016/j.canlet.2026.218519},
pmid = {42002490},
issn = {1872-7980},
}
RevDate: 2026-04-19
Influence of seasonal humidity and nitrogen on soil ciliate and bacterial diversity beneath the canopy of Neltuma laevigata.
International microbiology : the official journal of the Spanish Society for Microbiology [Epub ahead of print].
Additional Links: PMID-42002654
PubMed:
Citation:
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@article {pmid42002654,
year = {2026},
author = {Martínez-Reyes, CM and González-Macedo, M and Rojas-Oropeza, M and Rodríguez-Zaragoza, S and Cabirol, N},
title = {Influence of seasonal humidity and nitrogen on soil ciliate and bacterial diversity beneath the canopy of Neltuma laevigata.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42002654},
issn = {1618-1905},
support = {PhD Grant//Secretaría de Ciencia, Humanidades, Tecnología e Innovación/ ; PAPIIT IN224716//Dirección General de Asuntos del Personal Académico, Universidad Nacional Autónoma de México/ ; },
}
RevDate: 2026-04-19
CmpDate: 2026-04-19
Dietary N-acetylcysteine enhances sperm motility by remodeling the rumen microbiome and its metabolic axis in goats.
Journal of animal science and biotechnology, 17(1):.
BACKGROUND: Enhancing sperm motility is crucial for improving male fertility in ruminants. The rumen microbiota, central to nutrient metabolism of ruminants, represents a promising yet underexplored target for dietary intervention. This study investigated whether N-acetylcysteine (NAC) improves sperm motility via modulating the rumen microbiota-metabolite axis.
RESULTS: Dietary NAC supplementation significantly enhanced sperm motility in goats (P < 0.05), with the optimal effect observed at 0.3%, which coincided with improvements in sperm membrane integrity, antioxidant capacity, and mitochondrial function. Functional analysis revealed that NAC-induced microbial remodeling enriched KEGG pathways involved in antioxidant, energy, and lipid metabolism. Correspondingly, beneficial bacteria such as Pediococcus pentosaceus, Bacteroides acidifaciens, and Akkermansia, among others, were significantly enriched (P < 0.05). Notably, metabolic alterations in these pathways were consistently reflected in both the rumen fluid and plasma metabolomes, as evidenced by 25 conserved pathways and 2 overlapping metabolites. Collectively, these metabolic alterations ultimately enhanced sperm motility by improving sperm antioxidant status, energy supply, and lipid homeostasis.
CONCLUSIONS: Our study thus reveals that NAC enhances sperm motility via a rumen microbiome-mediated "rumen-plasma-sperm" axis. This novel insight broadens the understanding of how NAC-and potentially other antioxidants-regulates sperm motility, highlighting the promise of NAC-based dietary interventions for improving reproductive performance.
Additional Links: PMID-42002801
PubMed:
Citation:
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@article {pmid42002801,
year = {2026},
author = {Luo, J and Wang, X and Ju, Y and Ji, Q and Li, R and Ruan, Y and Zhao, J and Long, Q and Shang, Y and Li, P and Cao, M and Chen, X},
title = {Dietary N-acetylcysteine enhances sperm motility by remodeling the rumen microbiome and its metabolic axis in goats.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42002801},
issn = {1674-9782},
support = {2021YFD1200403//National Key Research and Development Program/ ; GZNYJGHX-2023006//Guizhou Province Mountainous Agriculture Key Research Program/ ; Qian Kehe Platform Talent-CXTD[2023]025//Guizhou Province Mutton Sheep Genetic Improvement and Innovative Utilization Science and Technology Innovation Talent Team Project/ ; GCC[2022]021-1//Guizhou Province High-level Innovative"Hundred" Level Talent Project/ ; },
abstract = {BACKGROUND: Enhancing sperm motility is crucial for improving male fertility in ruminants. The rumen microbiota, central to nutrient metabolism of ruminants, represents a promising yet underexplored target for dietary intervention. This study investigated whether N-acetylcysteine (NAC) improves sperm motility via modulating the rumen microbiota-metabolite axis.
RESULTS: Dietary NAC supplementation significantly enhanced sperm motility in goats (P < 0.05), with the optimal effect observed at 0.3%, which coincided with improvements in sperm membrane integrity, antioxidant capacity, and mitochondrial function. Functional analysis revealed that NAC-induced microbial remodeling enriched KEGG pathways involved in antioxidant, energy, and lipid metabolism. Correspondingly, beneficial bacteria such as Pediococcus pentosaceus, Bacteroides acidifaciens, and Akkermansia, among others, were significantly enriched (P < 0.05). Notably, metabolic alterations in these pathways were consistently reflected in both the rumen fluid and plasma metabolomes, as evidenced by 25 conserved pathways and 2 overlapping metabolites. Collectively, these metabolic alterations ultimately enhanced sperm motility by improving sperm antioxidant status, energy supply, and lipid homeostasis.
CONCLUSIONS: Our study thus reveals that NAC enhances sperm motility via a rumen microbiome-mediated "rumen-plasma-sperm" axis. This novel insight broadens the understanding of how NAC-and potentially other antioxidants-regulates sperm motility, highlighting the promise of NAC-based dietary interventions for improving reproductive performance.},
}
RevDate: 2026-04-19
CmpDate: 2026-04-19
Global research on the crosstalk between microbiota - intratumoral microorganisms and liver cancer: a visualization analysis.
Infectious agents and cancer, 21(1):.
BACKGROUND: In the past few decades, the field of microbiota research has experienced rapid development and growth. We have employed bibliometric methods to comprehensively visualize and analyze the global knowledge and hotspots in the field of microbiome-intratumoral microbiota in liver cancer.
METHOD: The relevant literature in this field from 2009 to 2025 was extracted from the Web of Science Core Collection Database. After the data was extracted, it was analyzed and visualized using CiteSpace, VOSviewer and R (bibliometrix) software.
RESULT: A total of 1001 publications on microbiome - intratumoral microbiota and liver cancer were published during the period 2009–2025. Among these, China had the highest number of publications (n = 495). The most prolific institution publishing on microbiome - intratumoral microbiota and liver cancer was Huazhong University of Science and Technology, China (n = 29). The author with the most publications on this topic was Yu, Jun (n = 14, 1.4%). The journal with the highest number of publications on this subject was Cancers (n = 41, 4.1%). The top seven keywords with a frequency of 100 or more include: gut microbiota, hepatocellular carcinoma, nonalcoholic fatty liver disease, fatty liver disease, cancer, inflammation, bile acids, liver cancer, cell, and insulin resistance. Recent emerging topics include “intratumoral microbiota” (since 2024) and “tumor microenvironment.”
CONCLUSION: Current research in this field primarily investigates the mechanistic associations between gut microbiota and hepatic malignancies, with particular emphasis on hepatocellular carcinoma. The scientific frontier has progressively evolved to encompass the exploration of intratumoral microbiota and its multifaceted interactions within the tumor microenvironment.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13027-026-00750-x.
Additional Links: PMID-42002816
PubMed:
Citation:
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@article {pmid42002816,
year = {2026},
author = {Jiang, H and Cui, Y and Lei, J},
title = {Global research on the crosstalk between microbiota - intratumoral microorganisms and liver cancer: a visualization analysis.},
journal = {Infectious agents and cancer},
volume = {21},
number = {1},
pages = {},
pmid = {42002816},
issn = {1750-9378},
support = {2020-XG-40//Lanzhou Science and Technology Bureau Project, 2020-XG-40: Development of an Intelligent Image-Assisted Diagnosis System for Early Detection and Quantitative Assessment of Therapeutic Efficacy in COVID-19 Using Deep Learning Technology and Its Clinical Application./ ; },
abstract = {BACKGROUND: In the past few decades, the field of microbiota research has experienced rapid development and growth. We have employed bibliometric methods to comprehensively visualize and analyze the global knowledge and hotspots in the field of microbiome-intratumoral microbiota in liver cancer.
METHOD: The relevant literature in this field from 2009 to 2025 was extracted from the Web of Science Core Collection Database. After the data was extracted, it was analyzed and visualized using CiteSpace, VOSviewer and R (bibliometrix) software.
RESULT: A total of 1001 publications on microbiome - intratumoral microbiota and liver cancer were published during the period 2009–2025. Among these, China had the highest number of publications (n = 495). The most prolific institution publishing on microbiome - intratumoral microbiota and liver cancer was Huazhong University of Science and Technology, China (n = 29). The author with the most publications on this topic was Yu, Jun (n = 14, 1.4%). The journal with the highest number of publications on this subject was Cancers (n = 41, 4.1%). The top seven keywords with a frequency of 100 or more include: gut microbiota, hepatocellular carcinoma, nonalcoholic fatty liver disease, fatty liver disease, cancer, inflammation, bile acids, liver cancer, cell, and insulin resistance. Recent emerging topics include “intratumoral microbiota” (since 2024) and “tumor microenvironment.”
CONCLUSION: Current research in this field primarily investigates the mechanistic associations between gut microbiota and hepatic malignancies, with particular emphasis on hepatocellular carcinoma. The scientific frontier has progressively evolved to encompass the exploration of intratumoral microbiota and its multifaceted interactions within the tumor microenvironment.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s13027-026-00750-x.},
}
RevDate: 2026-04-19
CmpDate: 2026-04-20
Longitudinal gut microbiome dynamics are associated with clinical outcome and toxicity during ibrutinib therapy.
Gut microbes, 18(1):2659397.
Accumulating evidence indicates that the gut microbiome influences therapeutic efficacy and toxicity across cancer treatments; however, its longitudinal dynamics during targeted therapies remain poorly characterized. Here, we performed whole-genome shotgun metagenomic sequencing of 291 longitudinal stool samples collected over one year from 30 patients with hematologic malignancies treated with ibrutinib. Overall gut microbial diversity remained stable at the population level but exhibited markedly divergent temporal trajectories according to clinical outcome, with progressive recovery in responders and blunted or delayed restoration in non-responders. Longitudinal modeling revealed distinct species- and pathway-level microbial dynamics between patients with treatment response or nonresponse, including enrichment of saccharolytic, short-chain fatty acid-associated taxa and metabolic pathways in responders, and expansion of bile acid-modifying, proteolytic, and inflammation-associated microbial features in non-responders. Functional profiling further demonstrated opposing temporal trends in pathways related to carbohydrate fermentation, amino-acid metabolism, and secondary bile acid synthesis. In addition, both baseline microbiome composition and longitudinal remodeling were associated with the development of ibrutinib-associated diarrhea. Together, these findings reveal coordinated, outcome-specific remodeling of the gut microbiome during ibrutinib therapy and highlight longitudinal microbiome trajectories, rather than static baseline features, as potential biomarkers of treatment response and toxicity, as well as targets for microbiome-directed interventions. In conclusion, our findings highlight a potential role of gut microbiome dynamics in modulating response to BTK inhibition and support the need for larger, prospective studies to validate these observations.
Additional Links: PMID-42002835
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PubMed:
Citation:
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@article {pmid42002835,
year = {2026},
author = {Morineau, N and Tessoulin, B and Guimard, T and Papin, M and Roquilly, A and Le Gouill, S and Montassier, E},
title = {Longitudinal gut microbiome dynamics are associated with clinical outcome and toxicity during ibrutinib therapy.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2659397},
doi = {10.1080/19490976.2026.2659397},
pmid = {42002835},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Piperidines/adverse effects/therapeutic use ; *Adenine/analogs & derivatives/adverse effects/therapeutic use ; Male ; Female ; Middle Aged ; Aged ; Longitudinal Studies ; *Bacteria/classification/genetics/isolation & purification/metabolism/drug effects ; Feces/microbiology ; Treatment Outcome ; *Antineoplastic Agents/adverse effects/therapeutic use ; Adult ; },
abstract = {Accumulating evidence indicates that the gut microbiome influences therapeutic efficacy and toxicity across cancer treatments; however, its longitudinal dynamics during targeted therapies remain poorly characterized. Here, we performed whole-genome shotgun metagenomic sequencing of 291 longitudinal stool samples collected over one year from 30 patients with hematologic malignancies treated with ibrutinib. Overall gut microbial diversity remained stable at the population level but exhibited markedly divergent temporal trajectories according to clinical outcome, with progressive recovery in responders and blunted or delayed restoration in non-responders. Longitudinal modeling revealed distinct species- and pathway-level microbial dynamics between patients with treatment response or nonresponse, including enrichment of saccharolytic, short-chain fatty acid-associated taxa and metabolic pathways in responders, and expansion of bile acid-modifying, proteolytic, and inflammation-associated microbial features in non-responders. Functional profiling further demonstrated opposing temporal trends in pathways related to carbohydrate fermentation, amino-acid metabolism, and secondary bile acid synthesis. In addition, both baseline microbiome composition and longitudinal remodeling were associated with the development of ibrutinib-associated diarrhea. Together, these findings reveal coordinated, outcome-specific remodeling of the gut microbiome during ibrutinib therapy and highlight longitudinal microbiome trajectories, rather than static baseline features, as potential biomarkers of treatment response and toxicity, as well as targets for microbiome-directed interventions. In conclusion, our findings highlight a potential role of gut microbiome dynamics in modulating response to BTK inhibition and support the need for larger, prospective studies to validate these observations.},
}
MeSH Terms:
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hide MeSH Terms
Humans
*Gastrointestinal Microbiome/drug effects
*Piperidines/adverse effects/therapeutic use
*Adenine/analogs & derivatives/adverse effects/therapeutic use
Male
Female
Middle Aged
Aged
Longitudinal Studies
*Bacteria/classification/genetics/isolation & purification/metabolism/drug effects
Feces/microbiology
Treatment Outcome
*Antineoplastic Agents/adverse effects/therapeutic use
Adult
RevDate: 2026-04-20
Impact of Portulaca oleracea L. extract in patients with irritable bowel syndrome.
Intestinal research pii:ir.2025.00200 [Epub ahead of print].
BACKGROUND/AIMS: Portulaca oleracea is known to have anti-inflammatory and immunoregulatory effects, and also showed positive effect on complete spontaneous bowel movement and bowel symptoms in patients with chronic constipation in a previous study. Thus, we aimed to investigate the impact of P. oleracea in patients with irritable bowel syndrome (IBS).
METHODS: Patients with IBS defined by ROME IV criteria were enrolled between July 2022 and April 2023. Patients were randomly assigned to P. oleracea or placebo group and took drugs for 8 weeks. Clinical data including gastrointestinal and IBS symptoms, laboratory tests including inflammatory and immunologic laboratory markers, and stool tests including fecal calprotectin and stool microbial analysis were evaluated at the baseline, week 4, and week 8.
RESULTS: A total of 108 patients were initially enrolled and 101 patients were finally included in the analysis. There was significant improvement during 8 weeks in P. oleracea group compared to placebo group in the aspect of gastrointestinal and IBS-related bowel symptoms (Gastrointestinal Symptom Rating Scale total score: from 44.1 to 31.7 vs. from 41.4 to 39.9; IBS-Symptom Severity Score total score: from 232.0 to 120.6 vs. from 202.7 to 178.2), especially in the aspect of abdominal pain. Interleukin-6 (IL-6) was significantly decreased during 8 weeks in P. oleracea group, although there was no significant difference between 2 groups. In addition, increase in IL-6 during study period was significantly associated with dysbiosis in stool microbial analysis. There was no significant adverse event.
CONCLUSIONS: P. oleracea has positive impact in patients with IBS showing improvement of immunologic cytokine and stool microbiome.
Additional Links: PMID-42002973
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PubMed:
Citation:
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@article {pmid42002973,
year = {2026},
author = {Nam, K and Choi, JH and Kim, YS and Lee, S and Park, JH and Kim, H and Lee, S and Lee, Y and Lee, D and Ryou, S and Shin, JE},
title = {Impact of Portulaca oleracea L. extract in patients with irritable bowel syndrome.},
journal = {Intestinal research},
volume = {},
number = {},
pages = {},
doi = {10.5217/ir.2025.00200},
pmid = {42002973},
issn = {1598-9100},
abstract = {BACKGROUND/AIMS: Portulaca oleracea is known to have anti-inflammatory and immunoregulatory effects, and also showed positive effect on complete spontaneous bowel movement and bowel symptoms in patients with chronic constipation in a previous study. Thus, we aimed to investigate the impact of P. oleracea in patients with irritable bowel syndrome (IBS).
METHODS: Patients with IBS defined by ROME IV criteria were enrolled between July 2022 and April 2023. Patients were randomly assigned to P. oleracea or placebo group and took drugs for 8 weeks. Clinical data including gastrointestinal and IBS symptoms, laboratory tests including inflammatory and immunologic laboratory markers, and stool tests including fecal calprotectin and stool microbial analysis were evaluated at the baseline, week 4, and week 8.
RESULTS: A total of 108 patients were initially enrolled and 101 patients were finally included in the analysis. There was significant improvement during 8 weeks in P. oleracea group compared to placebo group in the aspect of gastrointestinal and IBS-related bowel symptoms (Gastrointestinal Symptom Rating Scale total score: from 44.1 to 31.7 vs. from 41.4 to 39.9; IBS-Symptom Severity Score total score: from 232.0 to 120.6 vs. from 202.7 to 178.2), especially in the aspect of abdominal pain. Interleukin-6 (IL-6) was significantly decreased during 8 weeks in P. oleracea group, although there was no significant difference between 2 groups. In addition, increase in IL-6 during study period was significantly associated with dysbiosis in stool microbial analysis. There was no significant adverse event.
CONCLUSIONS: P. oleracea has positive impact in patients with IBS showing improvement of immunologic cytokine and stool microbiome.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
Resveratrol as a Multi-Domain Modulator of Oxidative Stress, Gut Dysbiosis, and Epigenetic Remodeling in Obesity: A Systems Biology Interpretation.
Journal of biochemical and molecular toxicology, 40(5):e70846.
Obesity is increasingly recognized as a chronic inflammatory redox disorder sustained by gut dysbiosis and maladaptive epigenetic programming. A "lock-in" model describes how gut dysbiosis induced reactive oxygen species (ROS) stabilize inflammatory signaling and establish epigenetic metabolic scars in adipose tissue, thereby perpetuating obesity even after the initial triggers subside. Resveratrol, a dietary stilbenoid, acts as a tri-axis therapeutic candidate by: (1) Restoring redox balance via Nrf2 activation and SIRT1 signaling, (2) Reshaping the gut microbiota to enhance SCFA production and barrier integrity, and (3) Reprogramming obesity-associated epigenetic alterations, including DNA methylation and miRNA dysregulation. By targeting oxidative, microbial, and epigenetic dimensions simultaneously, resveratrol offers a novel strategy to erase metabolic memory and disrupt obesity chronicity.
Additional Links: PMID-42003036
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PubMed:
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@article {pmid42003036,
year = {2026},
author = {Ganamurali, N and Sabarathinam, S},
title = {Resveratrol as a Multi-Domain Modulator of Oxidative Stress, Gut Dysbiosis, and Epigenetic Remodeling in Obesity: A Systems Biology Interpretation.},
journal = {Journal of biochemical and molecular toxicology},
volume = {40},
number = {5},
pages = {e70846},
doi = {10.1002/jbt.70846},
pmid = {42003036},
issn = {1099-0461},
mesh = {*Resveratrol/pharmacology/therapeutic use ; *Obesity/drug therapy/metabolism/genetics/microbiology/pathology ; Humans ; *Epigenesis, Genetic/drug effects ; *Oxidative Stress/drug effects ; *Dysbiosis/drug therapy/metabolism ; *Gastrointestinal Microbiome/drug effects ; Animals ; *Systems Biology ; },
abstract = {Obesity is increasingly recognized as a chronic inflammatory redox disorder sustained by gut dysbiosis and maladaptive epigenetic programming. A "lock-in" model describes how gut dysbiosis induced reactive oxygen species (ROS) stabilize inflammatory signaling and establish epigenetic metabolic scars in adipose tissue, thereby perpetuating obesity even after the initial triggers subside. Resveratrol, a dietary stilbenoid, acts as a tri-axis therapeutic candidate by: (1) Restoring redox balance via Nrf2 activation and SIRT1 signaling, (2) Reshaping the gut microbiota to enhance SCFA production and barrier integrity, and (3) Reprogramming obesity-associated epigenetic alterations, including DNA methylation and miRNA dysregulation. By targeting oxidative, microbial, and epigenetic dimensions simultaneously, resveratrol offers a novel strategy to erase metabolic memory and disrupt obesity chronicity.},
}
MeSH Terms:
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*Resveratrol/pharmacology/therapeutic use
*Obesity/drug therapy/metabolism/genetics/microbiology/pathology
Humans
*Epigenesis, Genetic/drug effects
*Oxidative Stress/drug effects
*Dysbiosis/drug therapy/metabolism
*Gastrointestinal Microbiome/drug effects
Animals
*Systems Biology
RevDate: 2026-04-20
Lactobacillus plantarum as a Novel Modulator of Immune and Behavioral Recovery in Substance Use Disorders: A Hypothesis.
Substance Use Disorders (SUDs) are increasingly recognized as conditions driven by neuroimmune dysfunction, leading to neuroinflammation and immune dysregulation. Growing evidence highlights the microbiota-gut-brain axis as a critical regulator of central nervous system activity, particularly through the modulation of glial cells such as microglia and astrocytes. The gut microbiome provides key immunomodulatory signals, and its therapeutic exploitation through probiotics offers a promising avenue. In this study, we hypothesize that supplementation with Lactobacillus plantarum can attenuate neuroinflammation and improve immune tolerance in SUDs by restoring microbial balance and modulating neuroimmune activity via the gut-brain axis. Using an established animal model of SUD, we propose to investigate the impact of L. plantarum on gut microbial composition, systemic and central inflammatory markers, glial cell activation, and behavioral outcomes. We further suggest that probiotics containing Lactobacillus species, including L. plantarum, could serve as a transformative approach not only for SUD-associated neuroinflammation but also for other neurological disorders. Such interventions may represent a breakthrough in non-drug discovery strategies by reducing reliance on conventional pharmacological treatments. Importantly, probiotic-based therapies could enhance overall survival and quality of life in individuals with SUDs, as Lactobacillus species have been shown to suppress inflammatory pathways from early developmental stages. Lactobacillus species could regulate the gut-brain axis and impact neurodegenerative diseases. If validated, this work could position L. plantarum and related probiotic strains as novel microbiome-based adjuncts for managing SUDs and open broader therapeutic possibilities for neuropsychiatric and neurodegenerative conditions.
Additional Links: PMID-42003076
Publisher:
PubMed:
Citation:
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@article {pmid42003076,
year = {2026},
author = {Malik, JA},
title = {Lactobacillus plantarum as a Novel Modulator of Immune and Behavioral Recovery in Substance Use Disorders: A Hypothesis.},
journal = {Current drug research reviews},
volume = {},
number = {},
pages = {},
doi = {10.2174/0125899775442579260409073358},
pmid = {42003076},
issn = {2589-9783},
abstract = {Substance Use Disorders (SUDs) are increasingly recognized as conditions driven by neuroimmune dysfunction, leading to neuroinflammation and immune dysregulation. Growing evidence highlights the microbiota-gut-brain axis as a critical regulator of central nervous system activity, particularly through the modulation of glial cells such as microglia and astrocytes. The gut microbiome provides key immunomodulatory signals, and its therapeutic exploitation through probiotics offers a promising avenue. In this study, we hypothesize that supplementation with Lactobacillus plantarum can attenuate neuroinflammation and improve immune tolerance in SUDs by restoring microbial balance and modulating neuroimmune activity via the gut-brain axis. Using an established animal model of SUD, we propose to investigate the impact of L. plantarum on gut microbial composition, systemic and central inflammatory markers, glial cell activation, and behavioral outcomes. We further suggest that probiotics containing Lactobacillus species, including L. plantarum, could serve as a transformative approach not only for SUD-associated neuroinflammation but also for other neurological disorders. Such interventions may represent a breakthrough in non-drug discovery strategies by reducing reliance on conventional pharmacological treatments. Importantly, probiotic-based therapies could enhance overall survival and quality of life in individuals with SUDs, as Lactobacillus species have been shown to suppress inflammatory pathways from early developmental stages. Lactobacillus species could regulate the gut-brain axis and impact neurodegenerative diseases. If validated, this work could position L. plantarum and related probiotic strains as novel microbiome-based adjuncts for managing SUDs and open broader therapeutic possibilities for neuropsychiatric and neurodegenerative conditions.},
}
RevDate: 2026-04-20
Metabolites and Polycystic Ovarian Syndrome: A Mendelian Randomization Study.
Current medicinal chemistry pii:CMC-EPUB-154921 [Epub ahead of print].
INTRODUCTION: Polycystic ovarian syndrome (PCOS) is a common reproductive disorder that affects a considerable number of women worldwide. Nevertheless, the causal relationship between metabolites and PCOS remains undetermined.
METHODS: We utilized a comprehensive two-sample Mendelian randomization (MR) analysis, a genetic epidemiological approach that uses genetic variants as instrumental variables to assess causal relationships between exposures and outcomes, to examine the causal link between 1352 metabolites and PCOS. We employed complementary MR methods, such as the inverse-variance weighted (IVW) method, and conducted sensitivity analyses to evaluate the reliability of the outcomes. Reverse MR analysis was performed to evaluate the possibility of reverse causation.
RESULTS: Five metabolites were identified to be significantly associated with PCOS risk: Methionine sulfoxide levels (IVW: OR [95%]: 1.549[1.274 to 1.883], p = 1.154E-5), Theophylline levels (IVW: OR [95%]: 0.725[0.589 to 0.890], p = 0.002), 4-hydroxycoumarin levels (IVW: OR [95%]: 0.786[0.658 to 0.940], p = 0.008), Tyramine O-sulfate levels (IVW: OR [95%]: 0.699[0.568 to 0.862], p = 0.0008), and Sulfate of piperine metabolite C16H19NO3 (3) levels (IVW: OR [95%]: 1.296[1.064 to 1.579], p = 0.009). We found PCOS was significantly associated with decreased Tyramine O-sulfate levels using the IVW method (OR [95%]: 0.953[0.917 to 0.991], p = 0.015) in the reverse MR analysis. The results of the sensitivity analyses were consistent with the main findings.
DISCUSSION: This study establishes causal relationships between specific metabolites and PCOS, highlighting the significant roles of oxidative stress (methionine sulfoxide), dietary components (theophylline, piperine metabolite), and gut microbiome-derived metabolites. These findings provide novel insights into PCOS pathogenesis and identify potential targets for prevention and treatment. However, the study's limitation to European populations necessitates further validation in diverse ethnic groups.
CONCLUSION: Our MR analysis provides strong evidence supporting a causal association between metabolites and the susceptibility of PCOS.
Additional Links: PMID-42003095
Publisher:
PubMed:
Citation:
show bibtex listing
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@article {pmid42003095,
year = {2026},
author = {Aru, N and Chen, Y and Li, T and Liu, J},
title = {Metabolites and Polycystic Ovarian Syndrome: A Mendelian Randomization Study.},
journal = {Current medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0109298673408216260414174125},
pmid = {42003095},
issn = {1875-533X},
abstract = {INTRODUCTION: Polycystic ovarian syndrome (PCOS) is a common reproductive disorder that affects a considerable number of women worldwide. Nevertheless, the causal relationship between metabolites and PCOS remains undetermined.
METHODS: We utilized a comprehensive two-sample Mendelian randomization (MR) analysis, a genetic epidemiological approach that uses genetic variants as instrumental variables to assess causal relationships between exposures and outcomes, to examine the causal link between 1352 metabolites and PCOS. We employed complementary MR methods, such as the inverse-variance weighted (IVW) method, and conducted sensitivity analyses to evaluate the reliability of the outcomes. Reverse MR analysis was performed to evaluate the possibility of reverse causation.
RESULTS: Five metabolites were identified to be significantly associated with PCOS risk: Methionine sulfoxide levels (IVW: OR [95%]: 1.549[1.274 to 1.883], p = 1.154E-5), Theophylline levels (IVW: OR [95%]: 0.725[0.589 to 0.890], p = 0.002), 4-hydroxycoumarin levels (IVW: OR [95%]: 0.786[0.658 to 0.940], p = 0.008), Tyramine O-sulfate levels (IVW: OR [95%]: 0.699[0.568 to 0.862], p = 0.0008), and Sulfate of piperine metabolite C16H19NO3 (3) levels (IVW: OR [95%]: 1.296[1.064 to 1.579], p = 0.009). We found PCOS was significantly associated with decreased Tyramine O-sulfate levels using the IVW method (OR [95%]: 0.953[0.917 to 0.991], p = 0.015) in the reverse MR analysis. The results of the sensitivity analyses were consistent with the main findings.
DISCUSSION: This study establishes causal relationships between specific metabolites and PCOS, highlighting the significant roles of oxidative stress (methionine sulfoxide), dietary components (theophylline, piperine metabolite), and gut microbiome-derived metabolites. These findings provide novel insights into PCOS pathogenesis and identify potential targets for prevention and treatment. However, the study's limitation to European populations necessitates further validation in diverse ethnic groups.
CONCLUSION: Our MR analysis provides strong evidence supporting a causal association between metabolites and the susceptibility of PCOS.},
}
RevDate: 2026-04-20
CmpDate: 2026-04-20
ChloroScan: Recovering Plastid Genome Bins From Metagenomic Data.
Molecular ecology resources, 26(3):e70143.
Genome-resolved metagenomics has contributed greatly to discovering prokaryotic genomes. When applied to microscopic eukaryotes (protists), challenges such as the high number of introns and repeat regions found in nuclear genomes have hampered the mining and discovery of novel protistan lineages. Organellar genomes are simpler, smaller, have higher abundance than their nuclear counterparts and contain valuable phylogenetic information, but are yet to be widely used to identify new protist lineages from metagenomes. Here we present "ChloroScan", a new bioinformatics pipeline to extract eukaryotic plastid genomes from metagenomes. It incorporates a deep learning contig classifier to identify putative plastid contigs and an automated binning module to recover bins with guidance from a curated marker gene database. Additionally, ChloroScan summarizes the results in different user-friendly formats, including annotated coding sequences and proteins for each bin. We show that ChloroScan recovers more high-quality plastid bins than MetaBAT2 for simulated metagenomes. The practical utility of ChloroScan is illustrated by recovering 16 medium to high-quality metagenome assembled genomes (MAGs) from four protist-size-fraction metagenomes, with several bins showing high taxonomic novelty. The ChloroScan code (v0.1.7) is available at https://github.com/Andyargueasae/chloroscan/tree/release_v0.1.7 under Apache-2.0 licence.
Additional Links: PMID-42003340
Publisher:
PubMed:
Citation:
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@article {pmid42003340,
year = {2026},
author = {Tong, Y and Marcelino, VR and Turnbull, R and Verbruggen, H},
title = {ChloroScan: Recovering Plastid Genome Bins From Metagenomic Data.},
journal = {Molecular ecology resources},
volume = {26},
number = {3},
pages = {e70143},
doi = {10.1111/1755-0998.70143},
pmid = {42003340},
issn = {1755-0998},
support = {2023.06155//Fundação para a Ciência e a Tecnologia/ ; DE220100965//Australian Research Council/ ; RYC2023-042907-I//Ministerio de Ciencia e Innovación/ ; //The University of Melbourne's Research Computing Services/ ; },
mesh = {*Metagenomics/methods ; *Computational Biology/methods ; *Genome, Plastid ; *Eukaryota/genetics/classification ; *Software ; Phylogeny ; Metagenome ; },
abstract = {Genome-resolved metagenomics has contributed greatly to discovering prokaryotic genomes. When applied to microscopic eukaryotes (protists), challenges such as the high number of introns and repeat regions found in nuclear genomes have hampered the mining and discovery of novel protistan lineages. Organellar genomes are simpler, smaller, have higher abundance than their nuclear counterparts and contain valuable phylogenetic information, but are yet to be widely used to identify new protist lineages from metagenomes. Here we present "ChloroScan", a new bioinformatics pipeline to extract eukaryotic plastid genomes from metagenomes. It incorporates a deep learning contig classifier to identify putative plastid contigs and an automated binning module to recover bins with guidance from a curated marker gene database. Additionally, ChloroScan summarizes the results in different user-friendly formats, including annotated coding sequences and proteins for each bin. We show that ChloroScan recovers more high-quality plastid bins than MetaBAT2 for simulated metagenomes. The practical utility of ChloroScan is illustrated by recovering 16 medium to high-quality metagenome assembled genomes (MAGs) from four protist-size-fraction metagenomes, with several bins showing high taxonomic novelty. The ChloroScan code (v0.1.7) is available at https://github.com/Andyargueasae/chloroscan/tree/release_v0.1.7 under Apache-2.0 licence.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Metagenomics/methods
*Computational Biology/methods
*Genome, Plastid
*Eukaryota/genetics/classification
*Software
Phylogeny
Metagenome
RevDate: 2026-04-20
Molecular strategies for heterocyclic frameworks in antidiabetic drug discovery: a vision from 2020-2024.
Future medicinal chemistry [Epub ahead of print].
Diabetes mellitus represents a global health crisis requiring innovative therapeutic strategies beyond traditional treatments. This comprehensive review analyzes heterocyclic frameworks developed between 2020-2024 for antidiabetic drug discovery, highlighting structure-activity relationships (SAR), molecular docking insights, and therapeutic mechanisms. Key scaffold classes emerged as potent antidiabetic agents, with benzimidazoles and triazoles demonstrating dual α-amylase/α-glucosidase inhibition (IC50 values 1.20-22.46 µg/mL), thiazolidinediones and quinazolines showing PPAR-γ agonism with improved insulin sensitivity and reduced cardiovascular risks, DPP-4 inhibitory scaffolds (pyrrolidines, pyrimidines) achieving IC50 values as low as 0.021 µM, and SGLT2-targeting heterocycles exhibiting glucose-lowering effects with cardio-renal protection. Major findings revealed that electron-donating groups (methoxy, hydroxyl) consistently enhanced binding affinity across multiple targets, halogen substitutions (fluoro, chloro, bromo) improved metabolic stability and selectivity, hybrid molecules combining multiple pharmacophores achieved superior multi-target effects, and natural product-derived heterocycles (flavonoids, coumarins, alkaloids) showed IC50values 10-100× better than acarbose. Emerging frontiers include multi-agonist therapies (GLP-1/GIP, dual SGLT1/SGLT2 inhibitors), glucokinase activators for insulin-independent glucose control, microbiome-targeting agents, and AI-driven rational drug design integrating SAR, docking, and ADMET prediction. This review provides a strategic framework for developing safer, more selective antidiabetic agents through systematic exploitation of heterocyclic chemistry, advancing toward personalized diabetes management.
Additional Links: PMID-42003351
Publisher:
PubMed:
Citation:
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@article {pmid42003351,
year = {2026},
author = {Tahlan, S and Singh, S and Dey, H and Kaira, M and Pandey, KC},
title = {Molecular strategies for heterocyclic frameworks in antidiabetic drug discovery: a vision from 2020-2024.},
journal = {Future medicinal chemistry},
volume = {},
number = {},
pages = {1-24},
doi = {10.1080/17568919.2026.2658007},
pmid = {42003351},
issn = {1756-8927},
abstract = {Diabetes mellitus represents a global health crisis requiring innovative therapeutic strategies beyond traditional treatments. This comprehensive review analyzes heterocyclic frameworks developed between 2020-2024 for antidiabetic drug discovery, highlighting structure-activity relationships (SAR), molecular docking insights, and therapeutic mechanisms. Key scaffold classes emerged as potent antidiabetic agents, with benzimidazoles and triazoles demonstrating dual α-amylase/α-glucosidase inhibition (IC50 values 1.20-22.46 µg/mL), thiazolidinediones and quinazolines showing PPAR-γ agonism with improved insulin sensitivity and reduced cardiovascular risks, DPP-4 inhibitory scaffolds (pyrrolidines, pyrimidines) achieving IC50 values as low as 0.021 µM, and SGLT2-targeting heterocycles exhibiting glucose-lowering effects with cardio-renal protection. Major findings revealed that electron-donating groups (methoxy, hydroxyl) consistently enhanced binding affinity across multiple targets, halogen substitutions (fluoro, chloro, bromo) improved metabolic stability and selectivity, hybrid molecules combining multiple pharmacophores achieved superior multi-target effects, and natural product-derived heterocycles (flavonoids, coumarins, alkaloids) showed IC50values 10-100× better than acarbose. Emerging frontiers include multi-agonist therapies (GLP-1/GIP, dual SGLT1/SGLT2 inhibitors), glucokinase activators for insulin-independent glucose control, microbiome-targeting agents, and AI-driven rational drug design integrating SAR, docking, and ADMET prediction. This review provides a strategic framework for developing safer, more selective antidiabetic agents through systematic exploitation of heterocyclic chemistry, advancing toward personalized diabetes management.},
}
RevDate: 2026-04-20
Bacterial alteration of redox stressors impacts environmental stability of influenza A virus.
mSphere [Epub ahead of print].
Influenza A virus (IAV) causes annual morbidity and mortality and remains a constant pandemic threat due to the emergence of novel strains. Therefore, understanding the factors important in host-to-host transmission of IAV is a key control point for protecting individual and public health. Transmission is highly heterogeneous with viral factors and host inflammatory and immune factors being implicated. Also implicated is the upper respiratory microbiome. While typically thought to act indirectly on viral pathogenesis, in an immunomodulatory capacity to enhance or reduce susceptibility to viral infection, recent studies on the pathogenesis of IAV have identified direct interactions between the virus and upper respiratory pathobiont bacteria. We hypothesize that the bacterial cells and their metabolites co-shed into respiratory droplets with IAV particles alter the viability of the IAV particles in the environment, therefore altering the capacity for host-to-host transmission. In this investigation, we utilize a simplified model of fomite transmission in the absence of confounding host factors and demonstrate how oxidative stress from both the environment and the metabolic activity of Streptococcus pneumoniae contributes to the killing of IAV, while catalase or the metabolic activity of Staphylococcus aureus can protect IAV from environmental or pneumococcally produced reactive oxygen species. These findings support a mechanism for bacterial modulation of viral transmission where bacterial metabolic products present in the respiratory droplet are capable of stabilizing and destabilizing viral particles during environmental transit and therefore modulating viral transmissibility.IMPORTANCEInfluenza A virus is a major cause of illness and death every year. A key knowledge gap exists in understanding what factors modulate viral transmission. One potential mediator of viral transmission is the bacteria that are found in the human nasopharynx. However, the mechanisms responsible for bacterial modulation of viral transmission are unclear. Here, we utilize a simplified model of environmental survival where we expose viral particles to indoor environmental conditions in the presence of bacterial cells. We demonstrate that hydrogen peroxide produced by Streptococcus pneumoniae reduces viral environmental survival, while incubation with catalase or viable Staphylococcus aureus cells can protect viral particles from S. pneumoniae-mediated viability loss. This supports a model of trans-kingdom bacterial-viral interactions where bacterial metabolites produced in the respiratory droplet are capable of modulating viral environmental survival and therefore transmission.
Additional Links: PMID-42003595
Publisher:
PubMed:
Citation:
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@article {pmid42003595,
year = {2026},
author = {Williams, MR and Rowe, HM},
title = {Bacterial alteration of redox stressors impacts environmental stability of influenza A virus.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0012526},
doi = {10.1128/msphere.00125-26},
pmid = {42003595},
issn = {2379-5042},
abstract = {Influenza A virus (IAV) causes annual morbidity and mortality and remains a constant pandemic threat due to the emergence of novel strains. Therefore, understanding the factors important in host-to-host transmission of IAV is a key control point for protecting individual and public health. Transmission is highly heterogeneous with viral factors and host inflammatory and immune factors being implicated. Also implicated is the upper respiratory microbiome. While typically thought to act indirectly on viral pathogenesis, in an immunomodulatory capacity to enhance or reduce susceptibility to viral infection, recent studies on the pathogenesis of IAV have identified direct interactions between the virus and upper respiratory pathobiont bacteria. We hypothesize that the bacterial cells and their metabolites co-shed into respiratory droplets with IAV particles alter the viability of the IAV particles in the environment, therefore altering the capacity for host-to-host transmission. In this investigation, we utilize a simplified model of fomite transmission in the absence of confounding host factors and demonstrate how oxidative stress from both the environment and the metabolic activity of Streptococcus pneumoniae contributes to the killing of IAV, while catalase or the metabolic activity of Staphylococcus aureus can protect IAV from environmental or pneumococcally produced reactive oxygen species. These findings support a mechanism for bacterial modulation of viral transmission where bacterial metabolic products present in the respiratory droplet are capable of stabilizing and destabilizing viral particles during environmental transit and therefore modulating viral transmissibility.IMPORTANCEInfluenza A virus is a major cause of illness and death every year. A key knowledge gap exists in understanding what factors modulate viral transmission. One potential mediator of viral transmission is the bacteria that are found in the human nasopharynx. However, the mechanisms responsible for bacterial modulation of viral transmission are unclear. Here, we utilize a simplified model of environmental survival where we expose viral particles to indoor environmental conditions in the presence of bacterial cells. We demonstrate that hydrogen peroxide produced by Streptococcus pneumoniae reduces viral environmental survival, while incubation with catalase or viable Staphylococcus aureus cells can protect viral particles from S. pneumoniae-mediated viability loss. This supports a model of trans-kingdom bacterial-viral interactions where bacterial metabolites produced in the respiratory droplet are capable of modulating viral environmental survival and therefore transmission.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
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In reading the early works of classical genetics, one is drawn, almost inexorably, into ever more complex models, until molecular explanations begin to seem both necessary and natural. At that point, the tools for understanding genome research are at hand. Assisting readers reach this point was the original goal of The Electronic Scholarly Publishing Project.
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Usage of the site grew rapidly and has remained high. Faculty began to use the site for their assigned readings. Other on-line publishers, ranging from The New York Times to Nature referenced ESP materials in their own publications. Nobel laureates (e.g., Joshua Lederberg) regularly used the site and even wrote to suggest changes and improvements.
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When the site began, no journals were making their early content available in digital format. As a result, ESP was obliged to digitize classic literature before it could be made available. For many important papers — such as Mendel's original paper or the first genetic map — ESP had to produce entirely new typeset versions of the works, if they were to be available in a high-quality format.
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Early support from the DOE component of the Human Genome Project was critically important for getting the ESP project on a firm foundation. Since that funding ended (nearly 20 years ago), the project has been operated as a purely volunteer effort. Anyone wishing to assist in these efforts should send an email to Robbins.
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With the development of methods for adding typeset side notes to PDF files, the ESP project now plans to add annotated versions of some classical papers to its holdings. We also plan to add new reference and pedagogical material. We have already started providing regularly updated, comprehensive bibliographies to the ESP.ORG site.
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Big Data: Buzzword or Big Deal?
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