MENU
The Electronic Scholarly Publishing Project: Providing world-wide, free access to classic scientific papers and other scholarly materials, since 1993.
More About: ESP | OUR CONTENT | THIS WEBSITE | WHAT'S NEW | WHAT'S HOT
ESP: PubMed Auto Bibliography 12 Mar 2026 at 01:57 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: 2026-03-10
CmpDate: 2026-03-11
Bacteroides-associated NAD[+] depletion correlates with exacerbated radiation-induced colorectal injury and impaired mucosal proliferative capacity.
Gut microbes, 18(1):2641260.
Radiation proctitis (RP) is a frequent complication of pelvic radiotherapy that compromises treatment delivery and patient quality of life, yet the factors shaping injury severity remain incompletely defined. We prospectively profiled pretreatment fecal microbiomes and metabolomes from 55 patients and stratified them by outcome into mild versus severe RP. Baseline microbial composition showed Bacteroidales enriched in severe RP and Firmicutes enriched in mild cases. Multi-omics integration highlighted nicotinate/nicotinamide pathways; severe RP was characterized by concomitant reductions in both fecal and tissue NAD[+] levels, along with an enrichment of microbial nicotinate/nicotinamide metabolism genes, primarily contributed by Bacteroides ovatus, B. xylanisolvens, and B. fragilis. In mice, fecal microbiota transplantation from severe-RP donors exacerbated radiation-induced colorectal injury and decreased colorectal NAD[+], supporting a causal role for the microbiota. Gavage with Bacteroides similarly worsened pathology and lowered NAD[+], whereas nicotinamide mononucleotide (NMN) supplementation attenuated the injury. Mechanistically, Bacteroides gavage reduced mitochondrial membrane potential, decreased the Lgr5[+] stem-cell proportion and proliferative indices, associated with Wnt pathway modulation. NMN reversed these effects in parallel with NAD[+] restoration. Together, these results identify a microbiota‒metabolite association wherein Bacteroidales enrichment is associated with NAD[+] depletion, reduced mucosal proliferative capacity, and exacerbated radiation-induced colorectal injury. The work deepens insight into RP pathogenesis and suggests a potential basis for microbiome- and metabolite-targeted approaches to attenuate severe RP.
Additional Links: PMID-41807298
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41807298,
year = {2026},
author = {Huang, J and Qin, Q and Li, X and Jiang, K and Xu, J and Mao, Y and Kang, W and Gao, R and Cheng, Y and Zhao, W and Ke, J and Mou, X},
title = {Bacteroides-associated NAD[+] depletion correlates with exacerbated radiation-induced colorectal injury and impaired mucosal proliferative capacity.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2641260},
doi = {10.1080/19490976.2026.2641260},
pmid = {41807298},
issn = {1949-0984},
mesh = {Animals ; Humans ; *NAD/metabolism/deficiency ; *Bacteroides/metabolism/genetics/isolation & purification ; Mice ; Male ; Female ; *Intestinal Mucosa/pathology/radiation effects ; *Radiation Injuries/microbiology/pathology ; Feces/microbiology/chemistry ; Mice, Inbred C57BL ; Middle Aged ; Gastrointestinal Microbiome ; Cell Proliferation ; Aged ; Nicotinamide Mononucleotide/metabolism/administration & dosage ; Fecal Microbiota Transplantation ; Colon/radiation effects/pathology ; },
abstract = {Radiation proctitis (RP) is a frequent complication of pelvic radiotherapy that compromises treatment delivery and patient quality of life, yet the factors shaping injury severity remain incompletely defined. We prospectively profiled pretreatment fecal microbiomes and metabolomes from 55 patients and stratified them by outcome into mild versus severe RP. Baseline microbial composition showed Bacteroidales enriched in severe RP and Firmicutes enriched in mild cases. Multi-omics integration highlighted nicotinate/nicotinamide pathways; severe RP was characterized by concomitant reductions in both fecal and tissue NAD[+] levels, along with an enrichment of microbial nicotinate/nicotinamide metabolism genes, primarily contributed by Bacteroides ovatus, B. xylanisolvens, and B. fragilis. In mice, fecal microbiota transplantation from severe-RP donors exacerbated radiation-induced colorectal injury and decreased colorectal NAD[+], supporting a causal role for the microbiota. Gavage with Bacteroides similarly worsened pathology and lowered NAD[+], whereas nicotinamide mononucleotide (NMN) supplementation attenuated the injury. Mechanistically, Bacteroides gavage reduced mitochondrial membrane potential, decreased the Lgr5[+] stem-cell proportion and proliferative indices, associated with Wnt pathway modulation. NMN reversed these effects in parallel with NAD[+] restoration. Together, these results identify a microbiota‒metabolite association wherein Bacteroidales enrichment is associated with NAD[+] depletion, reduced mucosal proliferative capacity, and exacerbated radiation-induced colorectal injury. The work deepens insight into RP pathogenesis and suggests a potential basis for microbiome- and metabolite-targeted approaches to attenuate severe RP.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
Humans
*NAD/metabolism/deficiency
*Bacteroides/metabolism/genetics/isolation & purification
Mice
Male
Female
*Intestinal Mucosa/pathology/radiation effects
*Radiation Injuries/microbiology/pathology
Feces/microbiology/chemistry
Mice, Inbred C57BL
Middle Aged
Gastrointestinal Microbiome
Cell Proliferation
Aged
Nicotinamide Mononucleotide/metabolism/administration & dosage
Fecal Microbiota Transplantation
Colon/radiation effects/pathology
RevDate: 2026-03-10
Early establishment of Bifidobacterium-dominant microbiome in planned cesarean-born infants via Bifidobacterium breve strain Yakult supplementation: A randomized, double-blind, placebo-controlled, parallel-group pilot study.
Pediatrics and neonatology pii:S1875-9572(26)00030-6 [Epub ahead of print].
OBJECTIVES: To investigate the effects of Bifidobacterium breve strain Yakult (BbrY) administration immediately after birth on the microbiome of cesarean-born full-term infants with an immature microbiota at birth.
METHODS: This single-center, placebo-controlled, randomized, double-blind, parallel-group intervention study included healthy, full-term Japanese infants born via planned cesarean section. Infants were administered either BbrY or placebo for the first month of life. The primary endpoint was the early establishment of a Bifidobacterium-dominant microbiome.
RESULTS: This study included 26 infants (14 in the BbrY group and 12 in the placebo group). Compared with the placebo group, the BbrY group showed significantly increased detection rates and counts of BbrY from day three to six months post-birth, with the level and proportion of Bifidobacterium and Bifidobacteriaceae remaining elevated until one month post-birth. Total bacterial counts and total organic acid concentrations, including acetic and lactic acids, were significantly higher in the BbrY group until the sixth day of life, concomitant with a decrease in fecal pH. At nine months, the BbrY group exhibited a significantly higher body weight than the placebo group, and the Kaup index remained within the normal range at six and nine months.
CONCLUSIONS: BbrY supplementation immediately after birth facilitated the early establishment of a Bifidobacterium-dominant microbiome and contributed to intestinal acidification in cesarean-born infants, indicating BbrY administration may support normal growth patterns during infancy.
Additional Links: PMID-41807185
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41807185,
year = {2026},
author = {Tsuji, H and Asahara, T and Sakai, T and Kado, Y and Moriyama-Ohara, K and Takahashi, A and Date, R and Atobe, S and Ishizuka, T and Takahashi, T and Ozaki, S and Shiono, Y and Fukada, Y and Kawashima, K and Yamashiro, K and Matsumoto, S and Yamashiro, Y},
title = {Early establishment of Bifidobacterium-dominant microbiome in planned cesarean-born infants via Bifidobacterium breve strain Yakult supplementation: A randomized, double-blind, placebo-controlled, parallel-group pilot study.},
journal = {Pediatrics and neonatology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.pedneo.2026.02.001},
pmid = {41807185},
issn = {2212-1692},
abstract = {OBJECTIVES: To investigate the effects of Bifidobacterium breve strain Yakult (BbrY) administration immediately after birth on the microbiome of cesarean-born full-term infants with an immature microbiota at birth.
METHODS: This single-center, placebo-controlled, randomized, double-blind, parallel-group intervention study included healthy, full-term Japanese infants born via planned cesarean section. Infants were administered either BbrY or placebo for the first month of life. The primary endpoint was the early establishment of a Bifidobacterium-dominant microbiome.
RESULTS: This study included 26 infants (14 in the BbrY group and 12 in the placebo group). Compared with the placebo group, the BbrY group showed significantly increased detection rates and counts of BbrY from day three to six months post-birth, with the level and proportion of Bifidobacterium and Bifidobacteriaceae remaining elevated until one month post-birth. Total bacterial counts and total organic acid concentrations, including acetic and lactic acids, were significantly higher in the BbrY group until the sixth day of life, concomitant with a decrease in fecal pH. At nine months, the BbrY group exhibited a significantly higher body weight than the placebo group, and the Kaup index remained within the normal range at six and nine months.
CONCLUSIONS: BbrY supplementation immediately after birth facilitated the early establishment of a Bifidobacterium-dominant microbiome and contributed to intestinal acidification in cesarean-born infants, indicating BbrY administration may support normal growth patterns during infancy.},
}
RevDate: 2026-03-10
Rifaximin in symptomatic uncomplicated diverticular disease: a stewardship perspective following the Fiesole Consensus.
Additional Links: PMID-41806989
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806989,
year = {2026},
author = {Marlicz, W and Krawczyk, M and Milkiewicz, P},
title = {Rifaximin in symptomatic uncomplicated diverticular disease: a stewardship perspective following the Fiesole Consensus.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2026-338607},
pmid = {41806989},
issn = {1468-3288},
}
RevDate: 2026-03-10
An integrative multi-omics approach identifies microbiome alterations linked to pathological and behavioral features in autism spectrum disorder.
Cell reports. Medicine pii:S2666-3791(26)00072-8 [Epub ahead of print].
This study employs a multi-omics approach to investigate the gut-brain axis in 326 children with autism spectrum disorder (ASD) and 169 typically developing (TD) controls, aged 0-10 years. By analyzing neuroimaging, gut microbiome, and plasma metabolome data, we find that microbial features could accurately distinguish ASD from TD children. A key finding is that gut microbial abundance, particularly an increase in Clostridioides difficile, serves as the strongest predictor of both ASD symptom severity and brain structural variations. Crucially, these gut and brain differences are age dependent, diminishing as children with ASD aged and converging toward TD patterns. A mediation model suggests a potential pathway where specific microbes influence brain structure and behavior via metabolites. The findings establish the gut microbiota as a robust predictor of brain and behavioral phenotypes in pediatric ASD, underscoring the necessity for early, age-stratified therapeutic strategies via modulating the composition of the gut microbiome.
Additional Links: PMID-41806837
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806837,
year = {2026},
author = {Mi, K and Cao, M and Zhang, L and Zhang, Q and Zhou, W and Deng, C and Zhang, Y and Zhao, Q and Wei, Y and Liu, X and Li, F},
title = {An integrative multi-omics approach identifies microbiome alterations linked to pathological and behavioral features in autism spectrum disorder.},
journal = {Cell reports. Medicine},
volume = {},
number = {},
pages = {102655},
doi = {10.1016/j.xcrm.2026.102655},
pmid = {41806837},
issn = {2666-3791},
abstract = {This study employs a multi-omics approach to investigate the gut-brain axis in 326 children with autism spectrum disorder (ASD) and 169 typically developing (TD) controls, aged 0-10 years. By analyzing neuroimaging, gut microbiome, and plasma metabolome data, we find that microbial features could accurately distinguish ASD from TD children. A key finding is that gut microbial abundance, particularly an increase in Clostridioides difficile, serves as the strongest predictor of both ASD symptom severity and brain structural variations. Crucially, these gut and brain differences are age dependent, diminishing as children with ASD aged and converging toward TD patterns. A mediation model suggests a potential pathway where specific microbes influence brain structure and behavior via metabolites. The findings establish the gut microbiota as a robust predictor of brain and behavioral phenotypes in pediatric ASD, underscoring the necessity for early, age-stratified therapeutic strategies via modulating the composition of the gut microbiome.},
}
RevDate: 2026-03-10
Immune-microbiome coordination defines interferon setpoints in healthy humans.
Cell pii:S0092-8674(26)00168-6 [Epub ahead of print].
Human immune systems are highly variable, with most variation attributable to non-genetic sources. The gut microbiome crucially shapes the immune system; however, its relationship with the baseline immune states of healthy humans remains incompletely understood. Therefore, we performed multi-omic profiling of 110 healthy participants through the ImmunoMicrobiome study. A factor-based integrative approach identified coordinated variation, revealing that the interferon response was amongst the most variable immune features in healthy participants. Microbiome composition, pathways, and stool metabolites varied concomitantly with interferon response pathways. Longitudinal data spanning more than a year indicated the significant stability of these parameters within individuals over time. Our study provides extensive data to examine the relationship between the immune states and microbiomes of healthy individuals at steady state, which paves the way for delineating inter-individual differences relevant for disease susceptibility and responses to therapy.
Additional Links: PMID-41806833
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806833,
year = {2026},
author = {Babdor, J and Patel, RK and Davidson, B and Koser, K and Noecker, C and Rahim, MK and Bisanz, JE and Tenvooren, I and Marquez, D and Calvo, M and Johri, V and McCarthy, EE and Shaheed, A and Ekstrand, C and Weakley, AM and Yu, FB and Krip, K and Shaikh, KA and Amatullah, H and Fiehn, O and Turnbaugh, PJ and Combes, AJ and Fragiadakis, GK and Spitzer, MH},
title = {Immune-microbiome coordination defines interferon setpoints in healthy humans.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2026.02.003},
pmid = {41806833},
issn = {1097-4172},
abstract = {Human immune systems are highly variable, with most variation attributable to non-genetic sources. The gut microbiome crucially shapes the immune system; however, its relationship with the baseline immune states of healthy humans remains incompletely understood. Therefore, we performed multi-omic profiling of 110 healthy participants through the ImmunoMicrobiome study. A factor-based integrative approach identified coordinated variation, revealing that the interferon response was amongst the most variable immune features in healthy participants. Microbiome composition, pathways, and stool metabolites varied concomitantly with interferon response pathways. Longitudinal data spanning more than a year indicated the significant stability of these parameters within individuals over time. Our study provides extensive data to examine the relationship between the immune states and microbiomes of healthy individuals at steady state, which paves the way for delineating inter-individual differences relevant for disease susceptibility and responses to therapy.},
}
RevDate: 2026-03-10
16S rRNA-based profiling of microbiota along the ground meat and sausage production lines in an Argentine meat processing facility.
International journal of food microbiology, 453:111716 pii:S0168-1605(26)00096-6 [Epub ahead of print].
Microbial contamination in food processing environments can compromise both product quality and safety. This study aimed to characterize the microbiota present along the ground meat and sausage production lines of an Argentine meat processing facility, with a focus on microbial dynamics in raw materials, environmental surfaces, and final products. Using next-generation sequencing (NGS), we identified a total of 57 unique bacterial genera across both production lines (37 in ground meat samples and 34 in sausage samples) showing ≥5% relative abundance in at least one sample. The core microbiota across both lines included Pseudomonas, Acinetobacter, and Psychrobacter, consistently detected in raw materials, pre- and post-operational environments, and final products. Notably, raw materials introduced variable microbial communities that influenced both environmental and product microbiomes. In the ground meat line, Carnobacterium became dominant in final products, likely masking the detection of other genera. In the sausage line, Brochothrix and Vibrio were prominent in final products. Staphylococcus and Clostridium sensu stricto were detected at low relative abundances and were mainly associated with raw materials; however, because the NGS analysis was conducted at the genus level, these findings do not imply the presence of pathogenic species. The persistence of specific genera in the environment, despite cleaning and disinfection, is consistent with the potential presence of biofilms, which may contribute to increased tolerance to Sanitation Standard Operating Procedures (SSOP). This study highlights the importance of raw material microbiota in shaping the production environment and product composition.
Additional Links: PMID-41806724
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806724,
year = {2026},
author = {Barril, PA and Brusa, V and Costa, M and Cap, M and Aguilera, P and Belforte, FS and Penas-Steinhardt, A and Leotta, G and Oteiza, JM},
title = {16S rRNA-based profiling of microbiota along the ground meat and sausage production lines in an Argentine meat processing facility.},
journal = {International journal of food microbiology},
volume = {453},
number = {},
pages = {111716},
doi = {10.1016/j.ijfoodmicro.2026.111716},
pmid = {41806724},
issn = {1879-3460},
abstract = {Microbial contamination in food processing environments can compromise both product quality and safety. This study aimed to characterize the microbiota present along the ground meat and sausage production lines of an Argentine meat processing facility, with a focus on microbial dynamics in raw materials, environmental surfaces, and final products. Using next-generation sequencing (NGS), we identified a total of 57 unique bacterial genera across both production lines (37 in ground meat samples and 34 in sausage samples) showing ≥5% relative abundance in at least one sample. The core microbiota across both lines included Pseudomonas, Acinetobacter, and Psychrobacter, consistently detected in raw materials, pre- and post-operational environments, and final products. Notably, raw materials introduced variable microbial communities that influenced both environmental and product microbiomes. In the ground meat line, Carnobacterium became dominant in final products, likely masking the detection of other genera. In the sausage line, Brochothrix and Vibrio were prominent in final products. Staphylococcus and Clostridium sensu stricto were detected at low relative abundances and were mainly associated with raw materials; however, because the NGS analysis was conducted at the genus level, these findings do not imply the presence of pathogenic species. The persistence of specific genera in the environment, despite cleaning and disinfection, is consistent with the potential presence of biofilms, which may contribute to increased tolerance to Sanitation Standard Operating Procedures (SSOP). This study highlights the importance of raw material microbiota in shaping the production environment and product composition.},
}
RevDate: 2026-03-10
Environmental factors outweigh seawater microbiomes in synergistically shaping epiphytic bacterial communities of Saccharina japonica.
Marine pollution bulletin, 227:119535 pii:S0025-326X(26)00322-X [Epub ahead of print].
Saccharina japonica is a commercially significant macroalgal species in coastal areas, where its growth and health are closely linked to epiphytic bacterial communities (EB). Previous studies have indicated that the structure of these EB communities is influenced by seawater microbiomes (SW) and various environmental factors. However, the mechanisms regulating these influences remain incompletely understood, particularly regarding their relative contributions throughout the life cycle, which are important for S. japonica production. To fill this gap, we investigated the diversity, composition, ecological networks, and functional predictions of EB and SW communities, as well as environmental factors from December 2022 to May 2023 in northern China. Mantel test results indicated that EB was significantly correlated with NO2[-], TN, NO3[-], and DIP, which was confirmed by Spearman's rank correlation coefficients and BIOENV analysis. Ecological network analysis revealed that the EB network was more simplified and clustered, with reduced robustness and increased vulnerability than SW. Only one keystone taxon identified in the EB network showed that the stability of the epiphytic microbiome may be highly dependent on the persistence of this key species. Environmental factors had a more substantial influence on EB communities compared to SW communities. Environmental factors uniquely explained 10.4% of the variation, while SW communities contributed only 2.4%. The combination effect accounted for 66.5% of the variation, indicating that their interplay is the key regulating driver of EB communities. Our findings provide a co-regulation framework between the environment and seawater microbiome for the sustainable development of kelp farming.
Additional Links: PMID-41806709
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806709,
year = {2026},
author = {Hu, Z and Liu, Q and Song, H and Liu, J},
title = {Environmental factors outweigh seawater microbiomes in synergistically shaping epiphytic bacterial communities of Saccharina japonica.},
journal = {Marine pollution bulletin},
volume = {227},
number = {},
pages = {119535},
doi = {10.1016/j.marpolbul.2026.119535},
pmid = {41806709},
issn = {1879-3363},
abstract = {Saccharina japonica is a commercially significant macroalgal species in coastal areas, where its growth and health are closely linked to epiphytic bacterial communities (EB). Previous studies have indicated that the structure of these EB communities is influenced by seawater microbiomes (SW) and various environmental factors. However, the mechanisms regulating these influences remain incompletely understood, particularly regarding their relative contributions throughout the life cycle, which are important for S. japonica production. To fill this gap, we investigated the diversity, composition, ecological networks, and functional predictions of EB and SW communities, as well as environmental factors from December 2022 to May 2023 in northern China. Mantel test results indicated that EB was significantly correlated with NO2[-], TN, NO3[-], and DIP, which was confirmed by Spearman's rank correlation coefficients and BIOENV analysis. Ecological network analysis revealed that the EB network was more simplified and clustered, with reduced robustness and increased vulnerability than SW. Only one keystone taxon identified in the EB network showed that the stability of the epiphytic microbiome may be highly dependent on the persistence of this key species. Environmental factors had a more substantial influence on EB communities compared to SW communities. Environmental factors uniquely explained 10.4% of the variation, while SW communities contributed only 2.4%. The combination effect accounted for 66.5% of the variation, indicating that their interplay is the key regulating driver of EB communities. Our findings provide a co-regulation framework between the environment and seawater microbiome for the sustainable development of kelp farming.},
}
RevDate: 2026-03-10
Revolutionizing hepatic fibrosis staging: A machine learning approach combining clinical, biochemical, and microbiome insights.
Computers in biology and medicine, 206:111584 pii:S0010-4825(26)00147-2 [Epub ahead of print].
Non-alcoholic Steatohepatitis (NASH) is a common disease that not only affects adults but has also been seen to affect all ages. This includes young adults, children and even babies. Non-alcoholic fatty liver disease (NAFLD), NASH and the progression of it to fibrosis have been the subject of extensive research, as there still remains a great deal we do not understand. There are multiple factors that will influence how quickly and aggressively the progression of the disease occurs and also the way the disease is diagnosed or assessed, such as medical history, blood results and ultrasound imaging. This study aims to look at the use of machine learning (ML) to integrate clinical, biochemical and microbiome data to create a model to allow for non-invasive staging of hepatic fibrosis for NASH patients. A total of 1834 patients with biopsy-confirmed NASH were included in the retrospective analysis. The cohort was comprised of patients from multiple healthcare systems with known biopsy-confirmed NASH and a stated fibrosis stage (F0, F1, F2, F3, F4). A range of clinical variables, including liver function tests, demographics and microbiome profiles (via 16S rRNA gene sequencing), were included to train the machine learning models (Random Forest & Extreme Gradient Boosting). The performance of these models were assessed using 10-fold cross-validation with the primary training cohort and external validation on an independent hospital database. The models demonstrated excellent classification accuracy, specifically a balanced accuracy of 99.1% for RF and an area under the curve (AUC) value of 1.0 for XGBoost. The addition of microbiome features (specifically, diversity indices and the relative abundance of certain taxa) enhanced the models' predictive capability, indicating that the gut-liver axis plays a significant role in the development of NASH. To interpret the machine learning models, we used SHapley Additive Explanations (SHAP) analysis to identify which of the clinical and microbiome features affected the models' predictions for the fibrosis stages. Advanced stages of fibrosis (F3 & F4) were found to have significant dysbiosis in the microbiome with increased relative abundance of pathogenic bacteria including Escherichia-Shigella and Enterococcus, as well as decreased Akkermansia and Ruminococcus. The study provides evidence for the accuracy of a non-invasive method of determining hepatic fibrosis stage in NASH and demonstrates its superiority compared to traditional scoring systems (i.e. APRI, FIB-4) for the purpose of guiding clinical decision making and risk assessment for patients in clinical practice.
Additional Links: PMID-41806697
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806697,
year = {2026},
author = {Faisal, S and Ullah, I and Kambey, PA and Malik, A and Shakeel, M},
title = {Revolutionizing hepatic fibrosis staging: A machine learning approach combining clinical, biochemical, and microbiome insights.},
journal = {Computers in biology and medicine},
volume = {206},
number = {},
pages = {111584},
doi = {10.1016/j.compbiomed.2026.111584},
pmid = {41806697},
issn = {1879-0534},
abstract = {Non-alcoholic Steatohepatitis (NASH) is a common disease that not only affects adults but has also been seen to affect all ages. This includes young adults, children and even babies. Non-alcoholic fatty liver disease (NAFLD), NASH and the progression of it to fibrosis have been the subject of extensive research, as there still remains a great deal we do not understand. There are multiple factors that will influence how quickly and aggressively the progression of the disease occurs and also the way the disease is diagnosed or assessed, such as medical history, blood results and ultrasound imaging. This study aims to look at the use of machine learning (ML) to integrate clinical, biochemical and microbiome data to create a model to allow for non-invasive staging of hepatic fibrosis for NASH patients. A total of 1834 patients with biopsy-confirmed NASH were included in the retrospective analysis. The cohort was comprised of patients from multiple healthcare systems with known biopsy-confirmed NASH and a stated fibrosis stage (F0, F1, F2, F3, F4). A range of clinical variables, including liver function tests, demographics and microbiome profiles (via 16S rRNA gene sequencing), were included to train the machine learning models (Random Forest & Extreme Gradient Boosting). The performance of these models were assessed using 10-fold cross-validation with the primary training cohort and external validation on an independent hospital database. The models demonstrated excellent classification accuracy, specifically a balanced accuracy of 99.1% for RF and an area under the curve (AUC) value of 1.0 for XGBoost. The addition of microbiome features (specifically, diversity indices and the relative abundance of certain taxa) enhanced the models' predictive capability, indicating that the gut-liver axis plays a significant role in the development of NASH. To interpret the machine learning models, we used SHapley Additive Explanations (SHAP) analysis to identify which of the clinical and microbiome features affected the models' predictions for the fibrosis stages. Advanced stages of fibrosis (F3 & F4) were found to have significant dysbiosis in the microbiome with increased relative abundance of pathogenic bacteria including Escherichia-Shigella and Enterococcus, as well as decreased Akkermansia and Ruminococcus. The study provides evidence for the accuracy of a non-invasive method of determining hepatic fibrosis stage in NASH and demonstrates its superiority compared to traditional scoring systems (i.e. APRI, FIB-4) for the purpose of guiding clinical decision making and risk assessment for patients in clinical practice.},
}
RevDate: 2026-03-10
Reshaping the lung microenvironment: MSCs attenuate Cr(VI)-induced pulmonary fibrosis associated with metabolic and microbial modulation.
Journal of hazardous materials, 507:141708 pii:S0304-3894(26)00686-2 [Epub ahead of print].
As a common environmental and occupational pollutant, hexavalent chromium [Cr(VI)] has been proved to induce pulmonary fibrosis. In recent years, mesenchymal stem cells (MSCs) have become a promising therapeutic strategy for pulmonary fibrosis. However, whether they can mitigate Cr(VI)-induced pulmonary fibrosis specifically through regulating the lung microenvironment and microbial homeostasis remains an open and critical question. This study aims to establish a Cr(VI)-induced lung fibrosis model in rats and investigate the protective mechanisms of MSCs through integrated metabolomic and microbiome analyses. MSCs attenuated lung structural destruction, reduced abnormal collagen fiber deposition, decreased the levels of TNF-α, IL6, MDA and 8-OHdG and increased T-AOC and T-SOD. In addition, Cr(VI) caused metabolic disorders in lung tissue, which was evidenced by the up-regulation or down-regulation of multiple phospholipid metabolites, down-regulation of immune-related pathways and up-regulation of arachidonic acid metabolism and glycerophospholipid metabolism pathways. Microbiome analysis revealed that Cr(VI) exposure significantly increased both the diversity and abundance of microbial communities in alveolar lavage fluid, promoting the enrichment of opportunistic pathogens and ultimately leading to microbial dysbiosis. After MSCs intervention, lipid metabolism disorder was alleviated, immune-related pathway was up-regulated, opportunistic bacteria was reduced, and dysbiosis was alleviated. Correlation analysis revealed that lung chromium and lipid-related metabolites were closely associated with microbial communities, suggesting that the pulmonary metabolism may interact with the lung microbiota to jointly maintain the homeostasis of the pulmonary microenvironment. Our study provides a new perspective on elucidating the role of MSCs in treating Cr(VI)-induced pulmonary fibrosis from the perspective of lung metabolism and microbiota.
Additional Links: PMID-41806586
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806586,
year = {2026},
author = {Ji, Z and Hong, S and Zhang, Y and Su, Z and Wang, X and Yu, X and Zhu, Z and Shi, K and Wu, D and Hu, G and Jia, G},
title = {Reshaping the lung microenvironment: MSCs attenuate Cr(VI)-induced pulmonary fibrosis associated with metabolic and microbial modulation.},
journal = {Journal of hazardous materials},
volume = {507},
number = {},
pages = {141708},
doi = {10.1016/j.jhazmat.2026.141708},
pmid = {41806586},
issn = {1873-3336},
abstract = {As a common environmental and occupational pollutant, hexavalent chromium [Cr(VI)] has been proved to induce pulmonary fibrosis. In recent years, mesenchymal stem cells (MSCs) have become a promising therapeutic strategy for pulmonary fibrosis. However, whether they can mitigate Cr(VI)-induced pulmonary fibrosis specifically through regulating the lung microenvironment and microbial homeostasis remains an open and critical question. This study aims to establish a Cr(VI)-induced lung fibrosis model in rats and investigate the protective mechanisms of MSCs through integrated metabolomic and microbiome analyses. MSCs attenuated lung structural destruction, reduced abnormal collagen fiber deposition, decreased the levels of TNF-α, IL6, MDA and 8-OHdG and increased T-AOC and T-SOD. In addition, Cr(VI) caused metabolic disorders in lung tissue, which was evidenced by the up-regulation or down-regulation of multiple phospholipid metabolites, down-regulation of immune-related pathways and up-regulation of arachidonic acid metabolism and glycerophospholipid metabolism pathways. Microbiome analysis revealed that Cr(VI) exposure significantly increased both the diversity and abundance of microbial communities in alveolar lavage fluid, promoting the enrichment of opportunistic pathogens and ultimately leading to microbial dysbiosis. After MSCs intervention, lipid metabolism disorder was alleviated, immune-related pathway was up-regulated, opportunistic bacteria was reduced, and dysbiosis was alleviated. Correlation analysis revealed that lung chromium and lipid-related metabolites were closely associated with microbial communities, suggesting that the pulmonary metabolism may interact with the lung microbiota to jointly maintain the homeostasis of the pulmonary microenvironment. Our study provides a new perspective on elucidating the role of MSCs in treating Cr(VI)-induced pulmonary fibrosis from the perspective of lung metabolism and microbiota.},
}
RevDate: 2026-03-10
Habitat-shaped microbial life-history strategies and host niche specialization govern soil ARG transfer potential.
Journal of hazardous materials, 507:141706 pii:S0304-3894(26)00684-9 [Epub ahead of print].
Antibiotic resistance genes (ARGs) have been extensively studied in terms of their environmental sources and anthropogenic drivers. However, the ecological mechanisms by which soil microbiomes mediate ARG persistence and transfer remain poorly understood, even though microorganisms are the primary hosts, vectors, and regulators of resistance traits. We compared alpine plateaus and lowland plains, two habitats with contrasting ecological and anthropogenic conditions, to investigate how habitat-driven microbiome processes affect ARG transmission. We found that plateau soils harbored lower ARG abundance (6.2%∼86.3%) and reduced horizontal transfer capacity (94.12%) compared to plain soils. This difference was primarily driven by distinct microbial traits shaped by habitat differences. Plateau microbiomes were dominated by k-strategist taxa characterized by slower growth rates and reduced connectivity in co-occurrence networks, thereby limiting opportunities for ARG exchange. In addition, ARG-carrying hosts in plateau soils exhibited broader ecological niches and a higher proportion of generalist taxa (48.2%), which exerted stronger negative interactions on specialists, thereby constraining the spread of resistance traits. These findings highlight how habitat-shaped microbial traits restrict ARG transmission and offer new insights into the ecological containment of antibiotic resistance in agroecosystems.
Additional Links: PMID-41806585
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806585,
year = {2026},
author = {Li, H and Yang, Q and Liu, T and Liu, W and Ding, Y and Xu, Y and Wei, Z},
title = {Habitat-shaped microbial life-history strategies and host niche specialization govern soil ARG transfer potential.},
journal = {Journal of hazardous materials},
volume = {507},
number = {},
pages = {141706},
doi = {10.1016/j.jhazmat.2026.141706},
pmid = {41806585},
issn = {1873-3336},
abstract = {Antibiotic resistance genes (ARGs) have been extensively studied in terms of their environmental sources and anthropogenic drivers. However, the ecological mechanisms by which soil microbiomes mediate ARG persistence and transfer remain poorly understood, even though microorganisms are the primary hosts, vectors, and regulators of resistance traits. We compared alpine plateaus and lowland plains, two habitats with contrasting ecological and anthropogenic conditions, to investigate how habitat-driven microbiome processes affect ARG transmission. We found that plateau soils harbored lower ARG abundance (6.2%∼86.3%) and reduced horizontal transfer capacity (94.12%) compared to plain soils. This difference was primarily driven by distinct microbial traits shaped by habitat differences. Plateau microbiomes were dominated by k-strategist taxa characterized by slower growth rates and reduced connectivity in co-occurrence networks, thereby limiting opportunities for ARG exchange. In addition, ARG-carrying hosts in plateau soils exhibited broader ecological niches and a higher proportion of generalist taxa (48.2%), which exerted stronger negative interactions on specialists, thereby constraining the spread of resistance traits. These findings highlight how habitat-shaped microbial traits restrict ARG transmission and offer new insights into the ecological containment of antibiotic resistance in agroecosystems.},
}
RevDate: 2026-03-10
Diversity and ecology of the prokaryotic microbiome associated with marine sponges across Antarctica.
The Science of the total environment, 1025:181655 pii:S0048-9697(26)00316-5 [Epub ahead of print].
Antarctic sponges host diverse and functionally relevant microbial communities that play central roles in the structure and resilience of polar benthic ecosystems. This review provides a focused analysis of the prokaryotic microbiomes associated with Antarctic sponges, with an emphasis on three ecologically significant species: Mycale (Oxymycale) acerata, Dendrilla antarctica, and Hymeniacidon torquata. Drawing from recent molecular studies, we examine the composition, predicted functional potential, and environmental responsiveness of these bacterial and archaeal communities. Comparative analyses with surrounding seawater and sediments reveal both overlaps and distinct host-specific microbial signatures, suggesting that sponge-associated microbiomes are shaped by selective pressures at the host and habitat levels. A conserved microbial core appears to coexist with more variable taxa influenced by host physiology and environmental gradients. We also discuss the impact of environmental stressors on microbiome structure and stability. Functional insights from metagenomic data highlight key microbial contributions to nutrient cycling, symbiotic lifestyles, secondary metabolite and vitamin production, quorum sensing, and the biodegradation of aromatic compounds. This review critically assesses current knowledge on Antarctic sponge-associated prokaryotic microbiomes, identifying recurrent taxonomic and functional patterns and evaluating evidence for core microbial functions across species and regions. We hypothesize that, despite taxonomic variability and geographical sampling bias, Antarctic sponge microbiomes share conserved functional traits shaped by host- and environment-driven selective pressures. Although foundational knowledge has expanded, particularly for shallow-water species, significant gaps persist-especially in underexplored habitats and in linking predicted functions to ecological dynamics. We conclude by outlining research priorities, including standardized protocols, broader spatial and temporal sampling, and multi-omics integration to better understand microbiome resilience under climate-driven change.
Additional Links: PMID-41806446
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806446,
year = {2026},
author = {Lo Giudice, A and Papale, M and Bertolino, M and Reboa, A and Rizzo, C},
title = {Diversity and ecology of the prokaryotic microbiome associated with marine sponges across Antarctica.},
journal = {The Science of the total environment},
volume = {1025},
number = {},
pages = {181655},
doi = {10.1016/j.scitotenv.2026.181655},
pmid = {41806446},
issn = {1879-1026},
abstract = {Antarctic sponges host diverse and functionally relevant microbial communities that play central roles in the structure and resilience of polar benthic ecosystems. This review provides a focused analysis of the prokaryotic microbiomes associated with Antarctic sponges, with an emphasis on three ecologically significant species: Mycale (Oxymycale) acerata, Dendrilla antarctica, and Hymeniacidon torquata. Drawing from recent molecular studies, we examine the composition, predicted functional potential, and environmental responsiveness of these bacterial and archaeal communities. Comparative analyses with surrounding seawater and sediments reveal both overlaps and distinct host-specific microbial signatures, suggesting that sponge-associated microbiomes are shaped by selective pressures at the host and habitat levels. A conserved microbial core appears to coexist with more variable taxa influenced by host physiology and environmental gradients. We also discuss the impact of environmental stressors on microbiome structure and stability. Functional insights from metagenomic data highlight key microbial contributions to nutrient cycling, symbiotic lifestyles, secondary metabolite and vitamin production, quorum sensing, and the biodegradation of aromatic compounds. This review critically assesses current knowledge on Antarctic sponge-associated prokaryotic microbiomes, identifying recurrent taxonomic and functional patterns and evaluating evidence for core microbial functions across species and regions. We hypothesize that, despite taxonomic variability and geographical sampling bias, Antarctic sponge microbiomes share conserved functional traits shaped by host- and environment-driven selective pressures. Although foundational knowledge has expanded, particularly for shallow-water species, significant gaps persist-especially in underexplored habitats and in linking predicted functions to ecological dynamics. We conclude by outlining research priorities, including standardized protocols, broader spatial and temporal sampling, and multi-omics integration to better understand microbiome resilience under climate-driven change.},
}
RevDate: 2026-03-10
Genome-Wide Association Study Reveals Insect Genetics and Microbial Symbiont Effects on Susceptibility of Diaphorina citri to the Citrus Greening Pathogen, Candidatus Liberibacter Asiaticus.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
Insect-vectored pathogens pose a significant threat to global agriculture. The colonization efficiency of pathogens in vectors plays a central role in these pathosystems, yet studies of the factors that affect this aspect are limited. This study investigates the genetic and microbial symbiont factors influencing the susceptibility of Diaphorina citri to Candidatus Liberibacter asiaticus (CLas), the pathogen causing citrus greening disease (huanglongbing). Through a microbiome Genome Wide Association Study (mGWAS) based on 16S amplicon sequencing and genomic resequencing of 120 D. citri individuals from six populations, we identified 79 SNPs significantly associated with the relative abundance of CLas within insects. Additionally, some of these SNPs were also associated with the relative abundance of Candidatus Profftella armature, a key endosymbiont of D. citri. SNPs in the regulatory region of gene Dcitr04g11610.1 led to its overexpression in CLas-susceptible D. citri, and CLas infection further elevated its expression. Conversely, RNAi knockdown of Dcitr04g11610.1 reduced CLas infection rates and abundance, accompanied by increased abundance of Profftella. Phylogenetic analysis revealed Dcitr04g11610.1's high homology to Major Facilitator Superfamily-type transporter SLC18B1 proteins, suggesting a role in CLas polyamine utilization. These findings highlight the importance and potential interplay of insect genetics and symbiotic microbiota in insect-vectored plant pathogen systems.
Additional Links: PMID-41806308
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806308,
year = {2026},
author = {Liu, K and He, Q and Lin, Z and Huang, S and Zhong, Z and Zhu, P and Gao, M and Zhao, L and Jin, H and Wu, G and Geoff, GM and Han, Q and Pang, R},
title = {Genome-Wide Association Study Reveals Insect Genetics and Microbial Symbiont Effects on Susceptibility of Diaphorina citri to the Citrus Greening Pathogen, Candidatus Liberibacter Asiaticus.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e17056},
doi = {10.1002/advs.202517056},
pmid = {41806308},
issn = {2198-3844},
support = {32001903//National Natural Science Foundation of China/ ; 2022ZDJS020//Guangdong Province Key Discipline Research Capacity Enhancement Project/ ; 2025A1515012591//Basic and Applied Basic Research Foundation of Guangdong Province/ ; 2023KTSCX046//Guangdong Provincial Universities Characteristic Innovation Project/ ; 2024A04J4995//Guangzhou Science and Technology Plan Project/ ; },
abstract = {Insect-vectored pathogens pose a significant threat to global agriculture. The colonization efficiency of pathogens in vectors plays a central role in these pathosystems, yet studies of the factors that affect this aspect are limited. This study investigates the genetic and microbial symbiont factors influencing the susceptibility of Diaphorina citri to Candidatus Liberibacter asiaticus (CLas), the pathogen causing citrus greening disease (huanglongbing). Through a microbiome Genome Wide Association Study (mGWAS) based on 16S amplicon sequencing and genomic resequencing of 120 D. citri individuals from six populations, we identified 79 SNPs significantly associated with the relative abundance of CLas within insects. Additionally, some of these SNPs were also associated with the relative abundance of Candidatus Profftella armature, a key endosymbiont of D. citri. SNPs in the regulatory region of gene Dcitr04g11610.1 led to its overexpression in CLas-susceptible D. citri, and CLas infection further elevated its expression. Conversely, RNAi knockdown of Dcitr04g11610.1 reduced CLas infection rates and abundance, accompanied by increased abundance of Profftella. Phylogenetic analysis revealed Dcitr04g11610.1's high homology to Major Facilitator Superfamily-type transporter SLC18B1 proteins, suggesting a role in CLas polyamine utilization. These findings highlight the importance and potential interplay of insect genetics and symbiotic microbiota in insect-vectored plant pathogen systems.},
}
RevDate: 2026-03-10
Prognostic prediction and immune microenvironment analysis in colorectal cancer using exosome-related lncRNA signatures.
Discover oncology pii:10.1007/s12672-026-04755-1 [Epub ahead of print].
BACKGROUND: Exosomes play a crucial role in tumor microenvironment (TME) by mediating cell-cell communication, but their role in colorectal cancer (CRC) remains unclear. This study aimed to investigate exosome-related lncRNAs (ER-lncRNAs) in CRC.
METHODS: mRNA profiles and clinical data from TCGA and GEO, microbiome data from TCMAand exosome-related genes from ExoCarta were analyzed. Consensus clustering, ER-lncRNA-related risk signature, and nomogram were developed.
RESULTS: A total of 797 differentially expressed lncRNAs (DE-lncRNAs)were identified, with 490 ER-lncRNAs selected based on their correlation with exosome-related mRNAs. Consensus clustering stratified CRC samples into four molecular subtypes, with Cluster 2 exhibiting the most favorable prognosis and Cluster 1 the poorest. These subtypes showed significant differences in survival outcomes, immune cell infiltration, and therapeutic responses. Nine ER-lncRNAs were identified as prognostic biomarkers and used to develop a risk score model. Furthermore, a nomogram incorporating the risk score and clinical parameters was constructed to predict individual prognosis.
CONCLUSION: These findings highlight the clinical relevance of ER-lncRNAs as in CRC and underscores their potential as novel diagnostic and therapeutic targets.
Additional Links: PMID-41806199
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806199,
year = {2026},
author = {Li, H and Huang, X and Luo, Z and Zhou, F and Deng, Y and Tan, C and Jin, Y and Yan, J and Xiao, G},
title = {Prognostic prediction and immune microenvironment analysis in colorectal cancer using exosome-related lncRNA signatures.},
journal = {Discover oncology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s12672-026-04755-1},
pmid = {41806199},
issn = {2730-6011},
abstract = {BACKGROUND: Exosomes play a crucial role in tumor microenvironment (TME) by mediating cell-cell communication, but their role in colorectal cancer (CRC) remains unclear. This study aimed to investigate exosome-related lncRNAs (ER-lncRNAs) in CRC.
METHODS: mRNA profiles and clinical data from TCGA and GEO, microbiome data from TCMAand exosome-related genes from ExoCarta were analyzed. Consensus clustering, ER-lncRNA-related risk signature, and nomogram were developed.
RESULTS: A total of 797 differentially expressed lncRNAs (DE-lncRNAs)were identified, with 490 ER-lncRNAs selected based on their correlation with exosome-related mRNAs. Consensus clustering stratified CRC samples into four molecular subtypes, with Cluster 2 exhibiting the most favorable prognosis and Cluster 1 the poorest. These subtypes showed significant differences in survival outcomes, immune cell infiltration, and therapeutic responses. Nine ER-lncRNAs were identified as prognostic biomarkers and used to develop a risk score model. Furthermore, a nomogram incorporating the risk score and clinical parameters was constructed to predict individual prognosis.
CONCLUSION: These findings highlight the clinical relevance of ER-lncRNAs as in CRC and underscores their potential as novel diagnostic and therapeutic targets.},
}
RevDate: 2026-03-10
CmpDate: 2026-03-11
Dietary Protein Modulation, Gut Microbiota, and Metabolic Control in Methylmalonic Acidemia: A Prospective Longitudinal Study.
Journal of inherited metabolic disease, 49(2):e70172.
Methylmalonic acidemia (MMA) is a rare inherited metabolic disorder caused by defective conversion of methylmalonyl-CoA to succinyl-CoA. Emerging evidence suggests that both dietary protein composition and intestinal microbiota influence metabolic stability and clinical outcomes. This study aimed to evaluate the effects of stepwise dietary modification and short-term metronidazole therapy on systemic and gut-derived metabolic profiles in MMA. In this prospective, longitudinal, single-center study, eight genetically confirmed MMA patients underwent four sequential phases: baseline mixed-protein diet (50% intact protein/50% medical formula), protein restriction, intact protein enrichment (80% intact protein/20% medical formula), and adjunctive metronidazole therapy (20 mg/kg/day, 10 days/month for 3 months). Plasma amino acids, urinary metabolites, stool microbiota (16S rRNA long-read sequencing), and untargeted/tandem metabolomic profiles were analyzed at each phase. Transition to an intact protein-enriched diet significantly reduced plasma leucine levels (p = 0.008) without affecting isoleucine or valine. Urinary methylmalonic acid, 3-hydroxypropionate, lactate, and pyruvate decreased, indicating improved propionyl-CoA clearance. Microbiota diversity progressively declined, accompanied by reductions in butyrate-producing genera (Novisyntrophococcus, Lacrimispora, Hespellia). Metronidazole further lowered urinary methylmalonic acid and 3-hydroxypropionate (p = 0.017 and p = 0.028), with parallel decreases in fecal 3-indolelactic acid and phytosphingosine, suggesting suppression of gut-derived propionate and tryptophan metabolism. Despite antibiotic-induced dysbiosis with expansion of Trabulsiella (Proteobacteria), systemic propiogenic burden decreased. A phased dietary regimen emphasizing intact protein, combined with intermittent metronidazole therapy, favorably modulated biochemical and microbial parameters in MMA. These findings support microbiome-informed dietary strategies and selective gut-targeted interventions to optimize metabolic control in organic acidemias.
Additional Links: PMID-41806138
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41806138,
year = {2026},
author = {Köse, E and Ekren, BY and Doğulu, N and Yolcu, F and Eylem, CC and Nemutlu, E and Sezerman, U and Eminoğlu, FT},
title = {Dietary Protein Modulation, Gut Microbiota, and Metabolic Control in Methylmalonic Acidemia: A Prospective Longitudinal Study.},
journal = {Journal of inherited metabolic disease},
volume = {49},
number = {2},
pages = {e70172},
doi = {10.1002/jimd.70172},
pmid = {41806138},
issn = {1573-2665},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects/physiology ; *Amino Acid Metabolism, Inborn Errors/diet therapy/metabolism/microbiology ; Prospective Studies ; Male ; Female ; Longitudinal Studies ; *Dietary Proteins/administration & dosage/metabolism ; Child, Preschool ; Child ; Metronidazole/therapeutic use ; Adolescent ; Infant ; Adult ; Amino Acids/blood ; Young Adult ; },
abstract = {Methylmalonic acidemia (MMA) is a rare inherited metabolic disorder caused by defective conversion of methylmalonyl-CoA to succinyl-CoA. Emerging evidence suggests that both dietary protein composition and intestinal microbiota influence metabolic stability and clinical outcomes. This study aimed to evaluate the effects of stepwise dietary modification and short-term metronidazole therapy on systemic and gut-derived metabolic profiles in MMA. In this prospective, longitudinal, single-center study, eight genetically confirmed MMA patients underwent four sequential phases: baseline mixed-protein diet (50% intact protein/50% medical formula), protein restriction, intact protein enrichment (80% intact protein/20% medical formula), and adjunctive metronidazole therapy (20 mg/kg/day, 10 days/month for 3 months). Plasma amino acids, urinary metabolites, stool microbiota (16S rRNA long-read sequencing), and untargeted/tandem metabolomic profiles were analyzed at each phase. Transition to an intact protein-enriched diet significantly reduced plasma leucine levels (p = 0.008) without affecting isoleucine or valine. Urinary methylmalonic acid, 3-hydroxypropionate, lactate, and pyruvate decreased, indicating improved propionyl-CoA clearance. Microbiota diversity progressively declined, accompanied by reductions in butyrate-producing genera (Novisyntrophococcus, Lacrimispora, Hespellia). Metronidazole further lowered urinary methylmalonic acid and 3-hydroxypropionate (p = 0.017 and p = 0.028), with parallel decreases in fecal 3-indolelactic acid and phytosphingosine, suggesting suppression of gut-derived propionate and tryptophan metabolism. Despite antibiotic-induced dysbiosis with expansion of Trabulsiella (Proteobacteria), systemic propiogenic burden decreased. A phased dietary regimen emphasizing intact protein, combined with intermittent metronidazole therapy, favorably modulated biochemical and microbial parameters in MMA. These findings support microbiome-informed dietary strategies and selective gut-targeted interventions to optimize metabolic control in organic acidemias.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/drug effects/physiology
*Amino Acid Metabolism, Inborn Errors/diet therapy/metabolism/microbiology
Prospective Studies
Male
Female
Longitudinal Studies
*Dietary Proteins/administration & dosage/metabolism
Child, Preschool
Child
Metronidazole/therapeutic use
Adolescent
Infant
Adult
Amino Acids/blood
Young Adult
RevDate: 2026-03-11
CmpDate: 2026-03-11
Microbiome-assisted plant breeding: integrating host-microbiome interactions into crop improvement.
Archives of microbiology, 208(5):.
Conventional breeding and domestication have boosted crop productivity but have also narrowed plant genomic diversity and reduced the diversity of associated microbiota, contributing to domestication syndrome and limiting resilience under increasingly variable environments. Thus, genetic improvement remains essential for developing low-input, high-yielding, enhanced nutrient content and stress-tolerant crops. However, traditional breeding has largely focused on plant genomes, overlooking the microbial partners that influence plant performance. Plants function as holobionts where integrated units composed of the host and its microbiome. These microbial communities colonize all plant tissues and regulate nutrient acquisition, immunity, physiology, and yield, often generating novel phenotypes without altering the plant genome. Some beneficial microbial taxa can even restore plant traits lost during domestication, ascertaining their potential as heritable contributors to crop performance. Seeds play a major role in transmitting plant genes and vertically inherited microbiota, making them a strategic entry point for microbiome integration in breeding. Recent advances include seed microbiome inheritance, root-exudate-mediated microbial recruitment, microbiome-associated QTLs and synthetic microbial communities (SynComs) which can be harnessed to enhance crop traits. These insights provide the foundation for Microbiome-Assisted Plant Breeding (MAPB), a complementary breeding paradigm targeting both plant genomes and microbial partners. Hence, incorporating microbial inheritance, recruitment traits and holobiont performance into breeding pipelines positions MAPB as a promising path toward climate-resilient, resource-efficient, and sustainable crop varieties.
Additional Links: PMID-41805987
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805987,
year = {2026},
author = {Kumar, SM and Ragupathy, TV and Dananjeyan, B and Thiyagarajan, C and Loganathan, A and Natarajan, S},
title = {Microbiome-assisted plant breeding: integrating host-microbiome interactions into crop improvement.},
journal = {Archives of microbiology},
volume = {208},
number = {5},
pages = {},
pmid = {41805987},
issn = {1432-072X},
mesh = {*Plant Breeding/methods ; *Crops, Agricultural/microbiology/genetics/growth & development ; *Microbiota ; *Host Microbial Interactions ; Seeds/microbiology/genetics ; Quantitative Trait Loci ; Genome, Plant ; },
abstract = {Conventional breeding and domestication have boosted crop productivity but have also narrowed plant genomic diversity and reduced the diversity of associated microbiota, contributing to domestication syndrome and limiting resilience under increasingly variable environments. Thus, genetic improvement remains essential for developing low-input, high-yielding, enhanced nutrient content and stress-tolerant crops. However, traditional breeding has largely focused on plant genomes, overlooking the microbial partners that influence plant performance. Plants function as holobionts where integrated units composed of the host and its microbiome. These microbial communities colonize all plant tissues and regulate nutrient acquisition, immunity, physiology, and yield, often generating novel phenotypes without altering the plant genome. Some beneficial microbial taxa can even restore plant traits lost during domestication, ascertaining their potential as heritable contributors to crop performance. Seeds play a major role in transmitting plant genes and vertically inherited microbiota, making them a strategic entry point for microbiome integration in breeding. Recent advances include seed microbiome inheritance, root-exudate-mediated microbial recruitment, microbiome-associated QTLs and synthetic microbial communities (SynComs) which can be harnessed to enhance crop traits. These insights provide the foundation for Microbiome-Assisted Plant Breeding (MAPB), a complementary breeding paradigm targeting both plant genomes and microbial partners. Hence, incorporating microbial inheritance, recruitment traits and holobiont performance into breeding pipelines positions MAPB as a promising path toward climate-resilient, resource-efficient, and sustainable crop varieties.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Plant Breeding/methods
*Crops, Agricultural/microbiology/genetics/growth & development
*Microbiota
*Host Microbial Interactions
Seeds/microbiology/genetics
Quantitative Trait Loci
Genome, Plant
RevDate: 2026-03-10
Defensive symbionts of European beewolves face competition from brood cell microbiota during vertical transmission.
FEMS microbiology ecology pii:8512820 [Epub ahead of print].
Beewolf wasps rely on an ancient defensive symbiosis with Streptomyces bacteria that protect their larvae from fungal infection. Female beewolves apply the bacteria to the brood-cell ceiling, and larvae later transfer the symbionts onto the cocoon surface, where they produce antifungal metabolites. Here, we investigated the mechanism of symbiont transfer from the beewolf brood cell to the larval cocoon and characterized the microbial community dynamics across different beewolf life stages and during larval hibernation. Fluorescence in situ hybridization revealed that the symbionts are transiently taken up into the proximal midgut lumen and then regurgitated onto the cocoon during the spinning process. High-throughput sequencing showed that the bacterial community of beewolf feeding larvae resembles that of the honeybee prey, whereas that of adults and diapausing larvae is dominated by Wolbachia. Moreover, the cocoon bacterial community is initially dominated by the defensive Streptomyces philanthi symbiont, but when larvae excrete the gut content inside the cocoon, other bacterial taxa including Lactobacillus, Gilliamella and Bartonella shift the community composition toward dominance by Pseudomonadota. Our findings provide new insights into the transmission route of an ancient extracellular symbiont and its potential competition with other bacteria in this long-term defensive symbiosis.
Additional Links: PMID-41805839
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805839,
year = {2026},
author = {Matarrita-Carranza, B and Weiss, B and Sandoval-Calderón, M and Koehler, S and Engl, T and Kaltenpoth, M},
title = {Defensive symbionts of European beewolves face competition from brood cell microbiota during vertical transmission.},
journal = {FEMS microbiology ecology},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsec/fiag024},
pmid = {41805839},
issn = {1574-6941},
abstract = {Beewolf wasps rely on an ancient defensive symbiosis with Streptomyces bacteria that protect their larvae from fungal infection. Female beewolves apply the bacteria to the brood-cell ceiling, and larvae later transfer the symbionts onto the cocoon surface, where they produce antifungal metabolites. Here, we investigated the mechanism of symbiont transfer from the beewolf brood cell to the larval cocoon and characterized the microbial community dynamics across different beewolf life stages and during larval hibernation. Fluorescence in situ hybridization revealed that the symbionts are transiently taken up into the proximal midgut lumen and then regurgitated onto the cocoon during the spinning process. High-throughput sequencing showed that the bacterial community of beewolf feeding larvae resembles that of the honeybee prey, whereas that of adults and diapausing larvae is dominated by Wolbachia. Moreover, the cocoon bacterial community is initially dominated by the defensive Streptomyces philanthi symbiont, but when larvae excrete the gut content inside the cocoon, other bacterial taxa including Lactobacillus, Gilliamella and Bartonella shift the community composition toward dominance by Pseudomonadota. Our findings provide new insights into the transmission route of an ancient extracellular symbiont and its potential competition with other bacteria in this long-term defensive symbiosis.},
}
RevDate: 2026-03-10
CmpDate: 2026-03-10
Community-Acquired Pneumonia in Patients With Diabetes: Narrative Review.
JMIR diabetes, 11:e82215.
BACKGROUND: Patients with diabetes carry a 1.5- to 2-fold higher risk of community-acquired pneumonia (CAP) and experience more severe outcomes, yet the mechanisms that integrate metabolic dysregulation, pathogen shifts, and novel cell death pathways remain fragmented.
OBJECTIVE: This study aimed to synthesize current evidence on epidemiology, pathophysiology, causative pathogens, clinical outcomes, and management of CAP in adults with diabetes and to identify research gaps for future trials.
METHODS: A narrative review (1999 to August 2025) of PubMed, EMBASE, the Cochrane Library, and Web of Science was conducted. GRADE (Grading of Recommendations Assessment, Development, and Evaluation) was used to rate evidence from 81 selected English-language studies (randomized controlled trials, cohorts, and meta-analyses).
RESULTS: Diabetes increases CAP incidence (relative risk 1.73, 95% CI 1.46-2.04), hospitalization (+30%-50%), and 30-day mortality (odds ratio 1.67, 95 % CI 1.45-1.92). Key drivers include hyperglycemia-induced immune paralysis, pulmonary microangiopathy, ferroptosis, glycation and methylation changes, and gut-lung dysbiosis that collectively favor multidrug-resistant Gram-negative bacilli (Klebsiella and Pseudomonas) and severe viral and fungal coinfections. Host-targeted therapy with moderate glycemic control (5-10 mmol/L), continued metformin, and pathogen-directed antibiotics improves survival, whereas single-dose PCV20 and annual influenza vaccination prevents approximately 45% of CAP admissions. Emerging strategies (nanozymes, ferroptosis inhibitors, probiotics, and proteolysis-targeting chimeras) are still preclinical.
CONCLUSIONS: CAP in patients with diabetes is a distinct, more severe entity mediated by metabolic-immune crosstalk. Multicenter randomized controlled trials integrating tight glucose monitoring, novel host-directed agents, and microbiome modulation are warranted to translate mechanistic insights into better outcomes.
Additional Links: PMID-41805689
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805689,
year = {2026},
author = {Xie, Y and Zhang, A and Wang, Y and Wang, R},
title = {Community-Acquired Pneumonia in Patients With Diabetes: Narrative Review.},
journal = {JMIR diabetes},
volume = {11},
number = {},
pages = {e82215},
pmid = {41805689},
issn = {2371-4379},
abstract = {BACKGROUND: Patients with diabetes carry a 1.5- to 2-fold higher risk of community-acquired pneumonia (CAP) and experience more severe outcomes, yet the mechanisms that integrate metabolic dysregulation, pathogen shifts, and novel cell death pathways remain fragmented.
OBJECTIVE: This study aimed to synthesize current evidence on epidemiology, pathophysiology, causative pathogens, clinical outcomes, and management of CAP in adults with diabetes and to identify research gaps for future trials.
METHODS: A narrative review (1999 to August 2025) of PubMed, EMBASE, the Cochrane Library, and Web of Science was conducted. GRADE (Grading of Recommendations Assessment, Development, and Evaluation) was used to rate evidence from 81 selected English-language studies (randomized controlled trials, cohorts, and meta-analyses).
RESULTS: Diabetes increases CAP incidence (relative risk 1.73, 95% CI 1.46-2.04), hospitalization (+30%-50%), and 30-day mortality (odds ratio 1.67, 95 % CI 1.45-1.92). Key drivers include hyperglycemia-induced immune paralysis, pulmonary microangiopathy, ferroptosis, glycation and methylation changes, and gut-lung dysbiosis that collectively favor multidrug-resistant Gram-negative bacilli (Klebsiella and Pseudomonas) and severe viral and fungal coinfections. Host-targeted therapy with moderate glycemic control (5-10 mmol/L), continued metformin, and pathogen-directed antibiotics improves survival, whereas single-dose PCV20 and annual influenza vaccination prevents approximately 45% of CAP admissions. Emerging strategies (nanozymes, ferroptosis inhibitors, probiotics, and proteolysis-targeting chimeras) are still preclinical.
CONCLUSIONS: CAP in patients with diabetes is a distinct, more severe entity mediated by metabolic-immune crosstalk. Multicenter randomized controlled trials integrating tight glucose monitoring, novel host-directed agents, and microbiome modulation are warranted to translate mechanistic insights into better outcomes.},
}
RevDate: 2026-03-10
CmpDate: 2026-03-11
Coexpression among eastern oyster host and microbiome genes suggests coordinated regulation of calcifying fluid chemistry.
Proceedings of the National Academy of Sciences of the United States of America, 123(11):e2521539123.
Marine animals that build shells, such as oysters, carefully regulate the chemistry of their internal calcifying fluids, but the molecular mechanisms behind this control, as well as whether microbes play a role in calcification, are poorly understood. To better understand oysters' molecular mechanisms and the role of their calcifying-fluid microbes, we conducted experiments that simulated a tidal cycle, measured calcifying fluid pH and total dissolved inorganic carbon, and characterized host and microbial gene expression via transcriptomics. These experiments showed that calcifying fluid pH remained relatively stable throughout tidal pH fluctuations, with corresponding increases in oyster transcripts for ion transport and acid-base regulation. These data provide direct evidence that tidal fluctuations drive rapid changes in oyster calcifying fluid chemistry. Most surprisingly, increases in microbial transcripts related to nitrogen and sulfur cycling correlated to higher calcifying fluid DIC, and coexpression network analysis revealed patterns of gene expression that linked oyster immune and neural pathways to microbial redox processes, providing molecular evidence of potential host modulation of microbial metabolism. Together, these results reveal that oysters actively regulate their calcifying fluid pH over short timescales, and the endemic microbiome metabolic responses can yield metabolites that influence calcifying fluid pH, alkalinity, and ultimately calcification. These data offer a perspective on oyster physiological capacity and, most importantly, the potential role of microbes in oyster calcification. In light of ongoing changes in ocean pH and temperature, oysters provide a model for studying animal-microbial responses to environmental acidification and how their interactions may shape biomineralization.
Additional Links: PMID-41805583
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805583,
year = {2026},
author = {Unzueta-MartÃnez, A and Delaney, JA and Morkeski, K and Ross, A and Wang, ZA and Girguis, PR},
title = {Coexpression among eastern oyster host and microbiome genes suggests coordinated regulation of calcifying fluid chemistry.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {11},
pages = {e2521539123},
doi = {10.1073/pnas.2521539123},
pmid = {41805583},
issn = {1091-6490},
support = {2109473//National Science Foundation (NSF)/ ; 9208//Gordon and Betty Moore Foundation (GBMF)/ ; },
mesh = {Animals ; *Microbiota/genetics ; *Calcification, Physiologic/genetics ; Hydrogen-Ion Concentration ; *Ostreidae/genetics/microbiology/metabolism ; Transcriptome ; Seawater/chemistry ; },
abstract = {Marine animals that build shells, such as oysters, carefully regulate the chemistry of their internal calcifying fluids, but the molecular mechanisms behind this control, as well as whether microbes play a role in calcification, are poorly understood. To better understand oysters' molecular mechanisms and the role of their calcifying-fluid microbes, we conducted experiments that simulated a tidal cycle, measured calcifying fluid pH and total dissolved inorganic carbon, and characterized host and microbial gene expression via transcriptomics. These experiments showed that calcifying fluid pH remained relatively stable throughout tidal pH fluctuations, with corresponding increases in oyster transcripts for ion transport and acid-base regulation. These data provide direct evidence that tidal fluctuations drive rapid changes in oyster calcifying fluid chemistry. Most surprisingly, increases in microbial transcripts related to nitrogen and sulfur cycling correlated to higher calcifying fluid DIC, and coexpression network analysis revealed patterns of gene expression that linked oyster immune and neural pathways to microbial redox processes, providing molecular evidence of potential host modulation of microbial metabolism. Together, these results reveal that oysters actively regulate their calcifying fluid pH over short timescales, and the endemic microbiome metabolic responses can yield metabolites that influence calcifying fluid pH, alkalinity, and ultimately calcification. These data offer a perspective on oyster physiological capacity and, most importantly, the potential role of microbes in oyster calcification. In light of ongoing changes in ocean pH and temperature, oysters provide a model for studying animal-microbial responses to environmental acidification and how their interactions may shape biomineralization.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Microbiota/genetics
*Calcification, Physiologic/genetics
Hydrogen-Ion Concentration
*Ostreidae/genetics/microbiology/metabolism
Transcriptome
Seawater/chemistry
RevDate: 2026-03-10
Metacycloprodigiosin from Rhizosphere Streptomyces aurantiacus as a Natural Antifungal Agent against Fusarium oxysporum.
Journal of agricultural and food chemistry [Epub ahead of print].
Microbiome-guided crop protection increasingly emphasizes the chemical basis of disease suppression. Here, we identify Streptomyces aurantiacus YS-4, a rhizosphere-enriched actinobacterium selectively recruited by resistant cultivars of Salvia miltiorrhiza, as a producer of metacycloprodigiosin, a previously reported secondary metabolite that is reported for the first time in this strain and further investigated for its role in suppressing Fusarium oxysporum-induced root rot in S. miltiorrhiza. Metacycloprodigiosin inhibited Fusarium oxysporum growth by 81.66% at 200 μg mL[-1] and induced extensive cellular and transcriptional changes related to membrane function and virulence-associated pathways. Transmission electron microscopy confirmed severe hyphal damage, while transcriptomic profiling revealed broad downregulation of virulence-associated genes. Pot experiments demonstrated that YS-4 application alleviated root rot symptoms and enhanced plant biomass. Collectively, these findings establish a direct link between metabolite chemistry and pathogen suppression, advancing molecular understanding of plant-fungal interactions and highlighting metacycloprodigiosin as a promising biocontrol agent for sustainable management of crops.
Additional Links: PMID-41805347
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805347,
year = {2026},
author = {Song, L and Zhang, H and Wang, M and Li, S and Wang, F and Zhang, M and Qu, Y and Ma, Y and Ma, Q and Wen, C and Zhao, Y and Liu, M and Wang, F},
title = {Metacycloprodigiosin from Rhizosphere Streptomyces aurantiacus as a Natural Antifungal Agent against Fusarium oxysporum.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c15856},
pmid = {41805347},
issn = {1520-5118},
abstract = {Microbiome-guided crop protection increasingly emphasizes the chemical basis of disease suppression. Here, we identify Streptomyces aurantiacus YS-4, a rhizosphere-enriched actinobacterium selectively recruited by resistant cultivars of Salvia miltiorrhiza, as a producer of metacycloprodigiosin, a previously reported secondary metabolite that is reported for the first time in this strain and further investigated for its role in suppressing Fusarium oxysporum-induced root rot in S. miltiorrhiza. Metacycloprodigiosin inhibited Fusarium oxysporum growth by 81.66% at 200 μg mL[-1] and induced extensive cellular and transcriptional changes related to membrane function and virulence-associated pathways. Transmission electron microscopy confirmed severe hyphal damage, while transcriptomic profiling revealed broad downregulation of virulence-associated genes. Pot experiments demonstrated that YS-4 application alleviated root rot symptoms and enhanced plant biomass. Collectively, these findings establish a direct link between metabolite chemistry and pathogen suppression, advancing molecular understanding of plant-fungal interactions and highlighting metacycloprodigiosin as a promising biocontrol agent for sustainable management of crops.},
}
RevDate: 2026-03-10
Nicotinamide mononucleotide supplementation modulates gut microbiota and metabolites to mitigate Alzheimer's disease pathology in APP/PS1 mice.
Journal of Alzheimer's disease : JAD [Epub ahead of print].
BackgroundEmerging evidence indicates that gut microbiome dysbiosis may be linked to Nicotinamide adenine dinucleotide (NAD[+]) deficiency during Alzheimer's disease (AD) progression, a condition potentially alleviated by nicotinamide mononucleotide (NMN) supplementation.ObjectiveTo explore the therapeutic potential of NMN supplementation in regulating AD pathology as well as gut microbiome dynamics, APP/PS1 transgenic mouse models were employed in the research.MethodsMetagenomic and metabolomics analysis were conducted to assess modifications in the intestinal microbiota and metabolites of AD mice post-NMN treatment. Moreover, immunohistochemistry, immunofluorescence, western blot, and Morris water maze were applied to evaluate NMN's ameliorative effects on AD.ResultsNMN administration significantly altered gut microbial composition and fecal metabolite profiles, leading to improvements in colon damage and AD-related neuropathology. Key findings include the restoration of gut microbial balance, particularly increasing Bacteroides abundance, and the modulation of metabolites involved in lipid metabolism. Furthermore, NMN was found to regulate ferroptosis, improving gut barrier function in AD mice, which were mediated through gut-brain communication pathways. NMN supplementation also enhanced ATP production, mitochondrial function, and synaptic density in the hippocampus while reducing oxidative stress and Aβ accumulation in the brain. Ultimately, these multi-faceted improvements collectively alleviated cognitive deficits in AD mice.ConclusionsIn summary, NMN supplementation effectively modulated gut microbiota and metabolites, thus mitigating AD pathology in APP/PS1 mice. Our study offers novel perspectives on the mechanisms underlying NMN's therapeutic effects in AD and underlines its potential as a promising intervention strategy.
Additional Links: PMID-41805251
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805251,
year = {2026},
author = {Zhou, H and Zhao, X and Li, Y and Wang, Y and Zhang, S and Xu, H and Sui, S and Wang, Q and He, Y and Gu, J},
title = {Nicotinamide mononucleotide supplementation modulates gut microbiota and metabolites to mitigate Alzheimer's disease pathology in APP/PS1 mice.},
journal = {Journal of Alzheimer's disease : JAD},
volume = {},
number = {},
pages = {13872877261422502},
doi = {10.1177/13872877261422502},
pmid = {41805251},
issn = {1875-8908},
abstract = {BackgroundEmerging evidence indicates that gut microbiome dysbiosis may be linked to Nicotinamide adenine dinucleotide (NAD[+]) deficiency during Alzheimer's disease (AD) progression, a condition potentially alleviated by nicotinamide mononucleotide (NMN) supplementation.ObjectiveTo explore the therapeutic potential of NMN supplementation in regulating AD pathology as well as gut microbiome dynamics, APP/PS1 transgenic mouse models were employed in the research.MethodsMetagenomic and metabolomics analysis were conducted to assess modifications in the intestinal microbiota and metabolites of AD mice post-NMN treatment. Moreover, immunohistochemistry, immunofluorescence, western blot, and Morris water maze were applied to evaluate NMN's ameliorative effects on AD.ResultsNMN administration significantly altered gut microbial composition and fecal metabolite profiles, leading to improvements in colon damage and AD-related neuropathology. Key findings include the restoration of gut microbial balance, particularly increasing Bacteroides abundance, and the modulation of metabolites involved in lipid metabolism. Furthermore, NMN was found to regulate ferroptosis, improving gut barrier function in AD mice, which were mediated through gut-brain communication pathways. NMN supplementation also enhanced ATP production, mitochondrial function, and synaptic density in the hippocampus while reducing oxidative stress and Aβ accumulation in the brain. Ultimately, these multi-faceted improvements collectively alleviated cognitive deficits in AD mice.ConclusionsIn summary, NMN supplementation effectively modulated gut microbiota and metabolites, thus mitigating AD pathology in APP/PS1 mice. Our study offers novel perspectives on the mechanisms underlying NMN's therapeutic effects in AD and underlines its potential as a promising intervention strategy.},
}
RevDate: 2026-03-10
Draft genome sequence of a family Acutalibacteraceae isolate, a human gut-derived cholesterol metabolizer.
Microbiology resource announcements [Epub ahead of print].
We report the draft genome sequence of a family Acutalibacteraceae isolate, which is an obligate anaerobe that converts cholesterol to coprostanol. The organism was isolated from a healthy adult's fecal sample, plated on cholesterol brain agar, and incubated anaerobically, yielding distinctive star-shaped colonies. This isolate is from an unclassified genus within the Acutalibacteraceae, highlighting the unexplored diversity within the gut microbiome.
Additional Links: PMID-41805178
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805178,
year = {2026},
author = {Skolnick, S and Hall, B},
title = {Draft genome sequence of a family Acutalibacteraceae isolate, a human gut-derived cholesterol metabolizer.},
journal = {Microbiology resource announcements},
volume = {},
number = {},
pages = {e0113725},
doi = {10.1128/mra.01137-25},
pmid = {41805178},
issn = {2576-098X},
abstract = {We report the draft genome sequence of a family Acutalibacteraceae isolate, which is an obligate anaerobe that converts cholesterol to coprostanol. The organism was isolated from a healthy adult's fecal sample, plated on cholesterol brain agar, and incubated anaerobically, yielding distinctive star-shaped colonies. This isolate is from an unclassified genus within the Acutalibacteraceae, highlighting the unexplored diversity within the gut microbiome.},
}
RevDate: 2026-03-10
Emerging strategies in drug repurposing for decreasing the risk of age-related macular degeneration.
Expert opinion on drug discovery [Epub ahead of print].
INTRODUCTION: Vision loss in older adults is largely driven by age-related macular degeneration (AMD), characterized by progressive damage central visual field damage and functional decline. While current options for wet and dry AMD are limited and expensive, drug repurposing represents a promising strategy to accelerate the discovery of effective, accessible treatment by leveraging medications with established safety profiles. Notably, anti-diabetic agents including metformin, sulfonylureas, glucagon-like peptide-1 receptor agonists (GLP-1RAs), and insulin have emerged as modulators of the retinal pigment epithelium (RPE) function, photoreceptors, and retinal vascular integrity.
AREAS COVERED: This review highlights the roles of oxidative stress, inflammation, and complement-mediated immune dysregulation in AMD pathogenesis, alongside preclinical data demonstrating metformin's protective effects via AMP-activated protein kinase (AMPK) activation. Population-based studies and meta-analyses further suggest a modest reduction in AMD risk associated with metformin use in both diabetic and non-diabetic cohorts. Additional pharmacological agents include statins, glyburide, L-DOPA, fluoxetine, dimethyl fumarate, and nutraceuticals such as curcumin, melatonin, and N-acetylcysteine.
EXPERT OPINION: Early AMD prevention through repurposed therapeutics, guided by AI-driven design and systems biology, may enable personalized care via multimodal risk stratification incorporating genetic, metabolomic, and microbiome data. Rigorous, stratified clinical trials integrating bioinformatics and precision medicine are essential to validate the most effective candidates.
Additional Links: PMID-41805144
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805144,
year = {2026},
author = {Zhou, B and Mokhashi, N and Skondra, D},
title = {Emerging strategies in drug repurposing for decreasing the risk of age-related macular degeneration.},
journal = {Expert opinion on drug discovery},
volume = {},
number = {},
pages = {1-16},
doi = {10.1080/17460441.2026.2635492},
pmid = {41805144},
issn = {1746-045X},
abstract = {INTRODUCTION: Vision loss in older adults is largely driven by age-related macular degeneration (AMD), characterized by progressive damage central visual field damage and functional decline. While current options for wet and dry AMD are limited and expensive, drug repurposing represents a promising strategy to accelerate the discovery of effective, accessible treatment by leveraging medications with established safety profiles. Notably, anti-diabetic agents including metformin, sulfonylureas, glucagon-like peptide-1 receptor agonists (GLP-1RAs), and insulin have emerged as modulators of the retinal pigment epithelium (RPE) function, photoreceptors, and retinal vascular integrity.
AREAS COVERED: This review highlights the roles of oxidative stress, inflammation, and complement-mediated immune dysregulation in AMD pathogenesis, alongside preclinical data demonstrating metformin's protective effects via AMP-activated protein kinase (AMPK) activation. Population-based studies and meta-analyses further suggest a modest reduction in AMD risk associated with metformin use in both diabetic and non-diabetic cohorts. Additional pharmacological agents include statins, glyburide, L-DOPA, fluoxetine, dimethyl fumarate, and nutraceuticals such as curcumin, melatonin, and N-acetylcysteine.
EXPERT OPINION: Early AMD prevention through repurposed therapeutics, guided by AI-driven design and systems biology, may enable personalized care via multimodal risk stratification incorporating genetic, metabolomic, and microbiome data. Rigorous, stratified clinical trials integrating bioinformatics and precision medicine are essential to validate the most effective candidates.},
}
RevDate: 2026-03-10
Specific Metabolites Modulate Core Microbes and Microbial Interactions to Drive Fomesafen Dissipation in the Soybean Rhizosphere.
Journal of agricultural and food chemistry [Epub ahead of print].
Rhizosphere metabolites regulate organic pollutant dissipation through microbiome modulation, yet dynamic interrelationships among metabolite shifts, microbial assembly, and pollutant removal remain unclear. Using multiomics (16S rRNA sequencing, metabolomics, and metagenomics), this study deciphered the temporal dynamics of rhizosphere metabolites and microbiome during the dissipation of fomesafen in soybean pots. Fomesafen dissipation exhibited biphasic kinetics during soybean growth, with an initial rapid phase followed by prolonged stabilization, which was synchronized with time-dependent microbiome perturbations of initial enrichment and subsequent attenuation. Metabolomics revealed fomesafen-induced shifts in rhizosphere metabolites, with 2-naphthalenesulfonic acid (↓20.84%) and 2-hydroxyoctadecanoic acid (↑13.30%) exhibiting opposing effects on microbial assembly, which ultimately affect fomesafen dissipation, as outlined in our conceptual model. Microcosm experiments further demonstrated 2-naphthalenesulfonic acid enhanced while 2-hydroxyoctadecanoic acid inhibited fomesafen dissipation. Our findings highlight the significance of rhizosphere metabolite-mediated interactions between core microbes and potential fomesafen-degraders in governing fomesafen dissipation.
Additional Links: PMID-41805117
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41805117,
year = {2026},
author = {Chen, S and Li, C and Wang, Z and Teng, Y and Ren, W and Wang, H and Ma, J and Ma, W and Luo, Y and Kuramae, EE},
title = {Specific Metabolites Modulate Core Microbes and Microbial Interactions to Drive Fomesafen Dissipation in the Soybean Rhizosphere.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c15254},
pmid = {41805117},
issn = {1520-5118},
abstract = {Rhizosphere metabolites regulate organic pollutant dissipation through microbiome modulation, yet dynamic interrelationships among metabolite shifts, microbial assembly, and pollutant removal remain unclear. Using multiomics (16S rRNA sequencing, metabolomics, and metagenomics), this study deciphered the temporal dynamics of rhizosphere metabolites and microbiome during the dissipation of fomesafen in soybean pots. Fomesafen dissipation exhibited biphasic kinetics during soybean growth, with an initial rapid phase followed by prolonged stabilization, which was synchronized with time-dependent microbiome perturbations of initial enrichment and subsequent attenuation. Metabolomics revealed fomesafen-induced shifts in rhizosphere metabolites, with 2-naphthalenesulfonic acid (↓20.84%) and 2-hydroxyoctadecanoic acid (↑13.30%) exhibiting opposing effects on microbial assembly, which ultimately affect fomesafen dissipation, as outlined in our conceptual model. Microcosm experiments further demonstrated 2-naphthalenesulfonic acid enhanced while 2-hydroxyoctadecanoic acid inhibited fomesafen dissipation. Our findings highlight the significance of rhizosphere metabolite-mediated interactions between core microbes and potential fomesafen-degraders in governing fomesafen dissipation.},
}
RevDate: 2026-03-10
Gut microbiome and aging-A dynamic interplay of microbes, metabolites, and the immune system.
FEBS letters [Epub ahead of print].
Aging is accompanied by profound changes in both the gut microbiome and the immune system, which engage in continuous, bidirectional communication. Alterations in microbial diversity and metabolism, particularly reductions in short-chain fatty acid (SCFA) producers as well as shifts in bile acid and tryptophan-metabolizing species, can incite and worsen inflammation, damage barrier integrity, and accelerate immunosenescence. Concomitantly, immune aging and reduced mucosal IgA promote microbial dysbiosis, forming a self-reinforcing cycle that fuels chronic inflammation ("inflammaging"). Microbial metabolites such as SCFAs, secondary bile acids, and indole derivatives play central roles in this gut-immune dialog, influencing regulatory T-cell balance, epithelial repair, and neurological health through the gut-brain axis. Emerging evidence suggests that diet, probiotics, postbiotics, and microbiome transplantations can restore beneficial microbial and, consequently, immune functions, offering opportunities to promote healthy aging and potentially reverse adverse symptoms. Understanding and targeting the gut microbiome-immune feedback loops may reveal new strategies to modulate inflammaging and extend health span.
Additional Links: PMID-41804973
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804973,
year = {2026},
author = {Mehl, A and Blacher, E},
title = {Gut microbiome and aging-A dynamic interplay of microbes, metabolites, and the immune system.},
journal = {FEBS letters},
volume = {},
number = {},
pages = {},
doi = {10.1002/1873-3468.70324},
pmid = {41804973},
issn = {1873-3468},
support = {03-23-24//The National Institute for Psychobiology in Israel/ ; 2023061//The United States-Israel Binational Science Foundation/ ; //Uncle Kory Foundation/ ; //Keren Shemesh: HUJI-STMC collaborative grant/ ; //The Abisch Frenkel Foundation for the Promotion of Life Sciences/ ; //ERA-Net NEURON MOODYGUT/ ; //The Azrieli Foundation Faculty Fellowship/ ; 888494//HORIZON EUROPE Marie Sklodowska-Curie Actions/ ; },
abstract = {Aging is accompanied by profound changes in both the gut microbiome and the immune system, which engage in continuous, bidirectional communication. Alterations in microbial diversity and metabolism, particularly reductions in short-chain fatty acid (SCFA) producers as well as shifts in bile acid and tryptophan-metabolizing species, can incite and worsen inflammation, damage barrier integrity, and accelerate immunosenescence. Concomitantly, immune aging and reduced mucosal IgA promote microbial dysbiosis, forming a self-reinforcing cycle that fuels chronic inflammation ("inflammaging"). Microbial metabolites such as SCFAs, secondary bile acids, and indole derivatives play central roles in this gut-immune dialog, influencing regulatory T-cell balance, epithelial repair, and neurological health through the gut-brain axis. Emerging evidence suggests that diet, probiotics, postbiotics, and microbiome transplantations can restore beneficial microbial and, consequently, immune functions, offering opportunities to promote healthy aging and potentially reverse adverse symptoms. Understanding and targeting the gut microbiome-immune feedback loops may reveal new strategies to modulate inflammaging and extend health span.},
}
RevDate: 2026-03-10
Integrated Multiomics Analysis Indicates Seasonal and Geographical Drivers of Rhizosphere Microbiome-Metabolome Interactions and Dihydrochalcone Accumulation in Lithocarpus litseifolius (Hance) Chun.
Journal of agricultural and food chemistry [Epub ahead of print].
Lithocarpus litseifolius (L. litseifolius) is a valuable economic crop rich in dihydrochalcones (DHCs), with wide applications in medicines, tea, and sweeteners. By integrating multiomics approaches, the relationship between rhizosphere microecology and quality formation in L. litseifolius was systematically elucidated. Key bacterial groups, such as Burkholderia-Caballeronia-Paraburkholderia, Conexibacter, and Bradyrhizobium, were driven by soil physicochemical properties (available copper, exchangeable manganese, alkali-hydrolyzable nitrogen, and organic matter) and rhizosphere metabolome and were strongly associated with the up-regulation of key genes in phenylpropanoid biosynthesis (phenylalanine ammonia lyase, cinnamate 4 hydroxylase, chalcone synthase, phloretin 4'-O-glucosyltransferase), thereby promoting DHC accumulation. A pot experiment confirmed the functional contribution of Burkholderia in promoting the growth of L. litseifolius and the accumulation of its secondary metabolites. The mechanisms by which soil characteristics and microbial communities regulate DHC biosynthesis in L. litseifolius were elucidated, providing insights into the coupling mechanism of "soil-microbiome-metabolome-plant secondary metabolism".
Additional Links: PMID-41804971
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804971,
year = {2026},
author = {Wang, Y and Cao, B and Liu, C and Ling, Q and Qiu, Z and Yan, W},
title = {Integrated Multiomics Analysis Indicates Seasonal and Geographical Drivers of Rhizosphere Microbiome-Metabolome Interactions and Dihydrochalcone Accumulation in Lithocarpus litseifolius (Hance) Chun.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c11982},
pmid = {41804971},
issn = {1520-5118},
abstract = {Lithocarpus litseifolius (L. litseifolius) is a valuable economic crop rich in dihydrochalcones (DHCs), with wide applications in medicines, tea, and sweeteners. By integrating multiomics approaches, the relationship between rhizosphere microecology and quality formation in L. litseifolius was systematically elucidated. Key bacterial groups, such as Burkholderia-Caballeronia-Paraburkholderia, Conexibacter, and Bradyrhizobium, were driven by soil physicochemical properties (available copper, exchangeable manganese, alkali-hydrolyzable nitrogen, and organic matter) and rhizosphere metabolome and were strongly associated with the up-regulation of key genes in phenylpropanoid biosynthesis (phenylalanine ammonia lyase, cinnamate 4 hydroxylase, chalcone synthase, phloretin 4'-O-glucosyltransferase), thereby promoting DHC accumulation. A pot experiment confirmed the functional contribution of Burkholderia in promoting the growth of L. litseifolius and the accumulation of its secondary metabolites. The mechanisms by which soil characteristics and microbial communities regulate DHC biosynthesis in L. litseifolius were elucidated, providing insights into the coupling mechanism of "soil-microbiome-metabolome-plant secondary metabolism".},
}
RevDate: 2026-03-10
CmpDate: 2026-03-10
Inference for microbe-metabolite association networks using a latent graph model.
Biometrics, 82(1):.
Correlation networks are commonly used to infer associations between microbes and metabolites. The resulting $p$-values are then corrected for multiple comparisons using existing methods such as the Benjamini & Hochberg (BH) procedure to control the false discovery rate (FDR). However, most existing methods for FDR control assume the $p$-values are weakly dependent. Consequently, they can have low power in recovering microbe-metabolite association networks that exhibit important topological features, such as the presence of densely associated modules. We propose a novel inference procedure that is both powerful for detecting significant associations in the microbe-metabolite network and capable of controlling the FDR. Power enhancement is achieved by modeling latent structures in the form of a bipartite stochastic block model. We develop a variational expectation-maximization (EM) algorithm to estimate the model parameters and incorporate the learned graph in the testing procedure. In addition to FDR control, this procedure provides a clustering of microbes and metabolites into modules, which is useful for interpretation. We demonstrate the merit of the proposed method in simulations and an application to bacterial vaginosis.
Additional Links: PMID-41804865
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804865,
year = {2026},
author = {Ma, J},
title = {Inference for microbe-metabolite association networks using a latent graph model.},
journal = {Biometrics},
volume = {82},
number = {1},
pages = {},
doi = {10.1093/biomtc/ujag042},
pmid = {41804865},
issn = {1541-0420},
support = {R01 GM145772/GF/NIH HHS/United States ; },
mesh = {Algorithms ; Computer Simulation ; Humans ; *Models, Statistical ; Female ; *Microbiota ; *Metabolic Networks and Pathways ; Stochastic Processes ; },
abstract = {Correlation networks are commonly used to infer associations between microbes and metabolites. The resulting $p$-values are then corrected for multiple comparisons using existing methods such as the Benjamini & Hochberg (BH) procedure to control the false discovery rate (FDR). However, most existing methods for FDR control assume the $p$-values are weakly dependent. Consequently, they can have low power in recovering microbe-metabolite association networks that exhibit important topological features, such as the presence of densely associated modules. We propose a novel inference procedure that is both powerful for detecting significant associations in the microbe-metabolite network and capable of controlling the FDR. Power enhancement is achieved by modeling latent structures in the form of a bipartite stochastic block model. We develop a variational expectation-maximization (EM) algorithm to estimate the model parameters and incorporate the learned graph in the testing procedure. In addition to FDR control, this procedure provides a clustering of microbes and metabolites into modules, which is useful for interpretation. We demonstrate the merit of the proposed method in simulations and an application to bacterial vaginosis.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Algorithms
Computer Simulation
Humans
*Models, Statistical
Female
*Microbiota
*Metabolic Networks and Pathways
Stochastic Processes
RevDate: 2026-03-10
CmpDate: 2026-03-10
The Polymer-Plastisphere-Function Nexus Links to Divergent Biodegradation of Microplastics During Composting.
Environmental microbiology, 28(3):e70278.
Microplastic (MP) biodegradation is critical for mitigating plastic pollution, yet the ecological mechanisms linking polymer properties to plastisphere microbiome assembly and catalytic function remain unclear. Using thermophilic composting as an accelerated model, we reveal a fundamental dichotomy in which biodegradable MPs (BMPs: polylactic acid [PLA] > polybutylene succinate [PBS] > poly (butylene adipate-co-terephthalate) [PBAT]) undergo rapid thermophilic degradation shaped by stronger environmental filtering of diverse degraders, whereas conventional MPs (CMPs: low-density polyethylene [LDPE]) exhibit delayed degradation with greater stochastic influence. Metagenomics uncovered 489 degradative genes predominantly distributed across uncultured taxa, enabling reconstruction of polymer-specific multi-enzyme pathways, supported by isolating 32 potential degraders (31 candidate novel). PLA/PBS degradation primarily relied on thermophilic-phase PLA depolymerase and cutinase, PBAT on late-stage polyesterase and PETase, and LDPE on alkane monooxygenase and laccase. Statistical modelling showed BMP degradation strongly associated with plastisphere-physicochemical interactions (> 90% variance), whereas CMP appeared primarily constrained by material properties (e.g., degrader succession in PLA, enrichment in PBS/PBAT, and high molecular weight in LDPE). Functionally dominant degraders (1.9% of total microbes) were estimated to contribute 52.4%-80.6% of biodegradation efficiency. This work elucidates the core polymer-plastisphere-functional nexus underlying MP biodegradation during composting, providing a predictive framework and microbial resource for targeted remediation.
Additional Links: PMID-41804664
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804664,
year = {2026},
author = {Bai, Y and Xu, Y and Wu, D and Su, Y and Zhan, M and Xie, B},
title = {The Polymer-Plastisphere-Function Nexus Links to Divergent Biodegradation of Microplastics During Composting.},
journal = {Environmental microbiology},
volume = {28},
number = {3},
pages = {e70278},
doi = {10.1111/1462-2920.70278},
pmid = {41804664},
issn = {1462-2920},
support = {22276059//National Natural Science Foundation of China/ ; 2018YFC1901000//National Key Research and Development Program of China/ ; },
mesh = {Biodegradation, Environmental ; *Composting ; *Microplastics/metabolism ; *Bacteria/metabolism/genetics/classification/isolation & purification ; *Polymers/metabolism/chemistry ; *Soil Microbiology ; Microbiota ; Polyesters/metabolism ; *Soil Pollutants/metabolism ; Soil/chemistry ; },
abstract = {Microplastic (MP) biodegradation is critical for mitigating plastic pollution, yet the ecological mechanisms linking polymer properties to plastisphere microbiome assembly and catalytic function remain unclear. Using thermophilic composting as an accelerated model, we reveal a fundamental dichotomy in which biodegradable MPs (BMPs: polylactic acid [PLA] > polybutylene succinate [PBS] > poly (butylene adipate-co-terephthalate) [PBAT]) undergo rapid thermophilic degradation shaped by stronger environmental filtering of diverse degraders, whereas conventional MPs (CMPs: low-density polyethylene [LDPE]) exhibit delayed degradation with greater stochastic influence. Metagenomics uncovered 489 degradative genes predominantly distributed across uncultured taxa, enabling reconstruction of polymer-specific multi-enzyme pathways, supported by isolating 32 potential degraders (31 candidate novel). PLA/PBS degradation primarily relied on thermophilic-phase PLA depolymerase and cutinase, PBAT on late-stage polyesterase and PETase, and LDPE on alkane monooxygenase and laccase. Statistical modelling showed BMP degradation strongly associated with plastisphere-physicochemical interactions (> 90% variance), whereas CMP appeared primarily constrained by material properties (e.g., degrader succession in PLA, enrichment in PBS/PBAT, and high molecular weight in LDPE). Functionally dominant degraders (1.9% of total microbes) were estimated to contribute 52.4%-80.6% of biodegradation efficiency. This work elucidates the core polymer-plastisphere-functional nexus underlying MP biodegradation during composting, providing a predictive framework and microbial resource for targeted remediation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Biodegradation, Environmental
*Composting
*Microplastics/metabolism
*Bacteria/metabolism/genetics/classification/isolation & purification
*Polymers/metabolism/chemistry
*Soil Microbiology
Microbiota
Polyesters/metabolism
*Soil Pollutants/metabolism
Soil/chemistry
RevDate: 2026-03-10
Synthetic Antibody Mimetics with ROS-Gated Saccharide Release for Targeted Colitis Therapy.
Advanced healthcare materials [Epub ahead of print].
Conventional targeted therapies for inflammatory bowel disease (IBD) often rely on unstable biological recognition elements. While molecularly imprinted polymers (MIP) offer robust synthetic alternatives, their utility is limited by an "always-on" binding state: even weak non-specific adsorption can significantly compromise their target-binding capacity. We convert static MIP into reactive oxygen species (ROS)-activated therapeutic actuators by conjugating mannose to transferrin-imprinted MIP via a ROS-cleavable linker. The saccharide acts dually as a therapeutic agent and a protective cloak. It sterically blocks non-specific binding during intestinal transit. At inflammatory sites, elevated ROS levels (higher than in healthy tissue) trigger simultaneous mannose release and activation of high-affinity targeting. This enables precise MIP anchoring to the inflamed epithelium for physical barrier formation and localized microbiome modulation. In murine colitis models, this achieved mucosal healing, mitigated inflammation, and microbiota rebalancing using a mannose equivalent dose of 27.2 mg/kg/d, benchmarking against free mannose and non-responsive MIP controls. This work establishes a generalizable paradigm for targeted recognition and drug delivery in complex physiological environments, paving the way for intelligent, disease-responsive nanomedicines.
Additional Links: PMID-41804655
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804655,
year = {2026},
author = {Zhang, Y and Li, S and Li, Q and Wang, R and Sun, Y and Wang, Y and Yan, X and Wang, X and Wang, Y and Xue, Y and Ding, C and Gong, J and Ding, L and Ju, H},
title = {Synthetic Antibody Mimetics with ROS-Gated Saccharide Release for Targeted Colitis Therapy.},
journal = {Advanced healthcare materials},
volume = {},
number = {},
pages = {e05869},
doi = {10.1002/adhm.202505869},
pmid = {41804655},
issn = {2192-2659},
support = {22574077//National Natural Science Foundation of China/ ; 22274073//National Natural Science Foundation of China/ ; 5431ZZXM2504//State Key Laboratory of Analytical Chemistry for Life Science/ ; },
abstract = {Conventional targeted therapies for inflammatory bowel disease (IBD) often rely on unstable biological recognition elements. While molecularly imprinted polymers (MIP) offer robust synthetic alternatives, their utility is limited by an "always-on" binding state: even weak non-specific adsorption can significantly compromise their target-binding capacity. We convert static MIP into reactive oxygen species (ROS)-activated therapeutic actuators by conjugating mannose to transferrin-imprinted MIP via a ROS-cleavable linker. The saccharide acts dually as a therapeutic agent and a protective cloak. It sterically blocks non-specific binding during intestinal transit. At inflammatory sites, elevated ROS levels (higher than in healthy tissue) trigger simultaneous mannose release and activation of high-affinity targeting. This enables precise MIP anchoring to the inflamed epithelium for physical barrier formation and localized microbiome modulation. In murine colitis models, this achieved mucosal healing, mitigated inflammation, and microbiota rebalancing using a mannose equivalent dose of 27.2 mg/kg/d, benchmarking against free mannose and non-responsive MIP controls. This work establishes a generalizable paradigm for targeted recognition and drug delivery in complex physiological environments, paving the way for intelligent, disease-responsive nanomedicines.},
}
RevDate: 2026-03-10
CmpDate: 2026-03-10
Unravelling the role of the gut microbiome in antipsychotic-induced weight gain and metabolic dysfunction in humans and rodents: A systematic review.
Dialogues in clinical neuroscience, 28(1):131-144.
Second-generation antipsychotics are frequently linked to weight gain and metabolic dysfunction, yet the mechanisms driving these effects remain elusive. The gut microbiome has been proposed as a potential mediator of these adverse outcomes. This study aimed to investigate the role of the gut microbiota in antipsychotic-induced weight gain. A systematic search of PubMed and Embase was conducted. In total, 24 publications were included in this review, including clinical and preclinical observational and intervention studies. Collectively, there is strong evidence that atypical antipsychotic-induced weight gain and metabolic dysfunction is accompanied by microbiota alterations. However, there is a lack of consensus with regards to the exact mechanisms and involvement of the microbiome in antipsychotic-induced weight gain. Nevertheless, a few patterns and common observations were found across studies, such as reduced diversity, increased Firmicutes/Bacteroidetes ratio and a reduction in Akkermansia species. While microbiota-targeted interventions had generally weak effects on weight gain and metabolic dysfunction in clinical cohorts, the use of specific probiotic strains and microbiota metabolites showed promise in preclinical studies. Thus, while the relationship between antipsychotic-induced weight gain, metabolic dysfunction, and changes in the gut microbiome are evident, further research is warranted to establish definitive causal relationships and to aid in the development of precision microbiota-targeted interventions to counteract these adverse effects.
Additional Links: PMID-41804549
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804549,
year = {2026},
author = {Tufvesson-Alm, M and Walsh, L and Pierce, S and Keohane, F and Clarke, G and O'Connor, K and Cryan, JF and Schellekens, H},
title = {Unravelling the role of the gut microbiome in antipsychotic-induced weight gain and metabolic dysfunction in humans and rodents: A systematic review.},
journal = {Dialogues in clinical neuroscience},
volume = {28},
number = {1},
pages = {131-144},
doi = {10.1080/19585969.2026.2637716},
pmid = {41804549},
issn = {1958-5969},
mesh = {*Gastrointestinal Microbiome/drug effects/physiology ; Humans ; *Antipsychotic Agents/adverse effects ; *Weight Gain/drug effects/physiology ; Animals ; *Metabolic Diseases/chemically induced/microbiology ; },
abstract = {Second-generation antipsychotics are frequently linked to weight gain and metabolic dysfunction, yet the mechanisms driving these effects remain elusive. The gut microbiome has been proposed as a potential mediator of these adverse outcomes. This study aimed to investigate the role of the gut microbiota in antipsychotic-induced weight gain. A systematic search of PubMed and Embase was conducted. In total, 24 publications were included in this review, including clinical and preclinical observational and intervention studies. Collectively, there is strong evidence that atypical antipsychotic-induced weight gain and metabolic dysfunction is accompanied by microbiota alterations. However, there is a lack of consensus with regards to the exact mechanisms and involvement of the microbiome in antipsychotic-induced weight gain. Nevertheless, a few patterns and common observations were found across studies, such as reduced diversity, increased Firmicutes/Bacteroidetes ratio and a reduction in Akkermansia species. While microbiota-targeted interventions had generally weak effects on weight gain and metabolic dysfunction in clinical cohorts, the use of specific probiotic strains and microbiota metabolites showed promise in preclinical studies. Thus, while the relationship between antipsychotic-induced weight gain, metabolic dysfunction, and changes in the gut microbiome are evident, further research is warranted to establish definitive causal relationships and to aid in the development of precision microbiota-targeted interventions to counteract these adverse effects.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Gastrointestinal Microbiome/drug effects/physiology
Humans
*Antipsychotic Agents/adverse effects
*Weight Gain/drug effects/physiology
Animals
*Metabolic Diseases/chemically induced/microbiology
RevDate: 2026-03-10
CmpDate: 2026-03-10
Seasonality shapes gut microbiota composition in two sympatric sea urchins.
PeerJ, 14:e20918.
BACKGROUND: The gut microbiota plays critical roles in digestion, immunity, and environmental adaptation in marine invertebrates. Its composition is shaped by both host traits and abiotic factors such as temperature and seasonality. In Caribbean reefs, sea urchins like Diadema antillarum and Echinometra lucunter are important grazers that regulate algal biomass and influence benthic community dynamics. This study used 16S rRNA gene sequencing to compare, for the first time, the gut microbiota of these two sympatric species across contrasting seasons.
METHODS: Adults of D. antillarum and E. lucunter were collected during summer and winter from three fringing reefs in Puerto Rico. Gut contents were extracted under sterile conditions, and bacterial DNA was extracted amplified for their 16S rRNA genes and sequenced. Microbial diversity and structure were assessed standard microbiota pipelines.
RESULTS: Microbial communities in both echinoids were dominated by Bacillota, Bacteroidota, Desulfobacterota, and Pseudomonadota. Core microbiota analysis revealed stable taxa across hosts and seasons, most notably Propionigenium, supporting host-driven selection mechanisms that maintain functional stability despite seasonal turnover. Core microbiome analyses revealed Bacillota, Bacteroidota, Desulfobacterota_G_459543, and Pseudomonadota as persistent phyla across seasons, and genera such as Desulfotalea, Photobacterium, and Propionigenium consistently present in both species. Alpha diversity was significantly higher in winter for both D. antillarum and E. lucunter, while species-level differences were not significant. Beta diversity analyses showed significant seasonal clustering, with no consistent segregation between species within seasons. Our findings demonstrate that shared environmental conditions, particularly seasonality, are the primary modulators of gut microbiota in sympatric sea urchins, while host selection preserves a conserved core community. This dual influence of environment and host highlights the ecological plasticity and resilience of sea urchin microbiotas under fluctuating reef conditions.
Additional Links: PMID-41804484
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804484,
year = {2026},
author = {RodrÃguez-Barreras, R and Suárez-Pérez, J and Godoy-Vitorino, F},
title = {Seasonality shapes gut microbiota composition in two sympatric sea urchins.},
journal = {PeerJ},
volume = {14},
number = {},
pages = {e20918},
pmid = {41804484},
issn = {2167-8359},
mesh = {Animals ; *Seasons ; *Sea Urchins/microbiology ; *Gastrointestinal Microbiome/genetics ; RNA, Ribosomal, 16S/genetics ; Puerto Rico ; Sympatry ; *Bacteria/genetics/classification ; },
abstract = {BACKGROUND: The gut microbiota plays critical roles in digestion, immunity, and environmental adaptation in marine invertebrates. Its composition is shaped by both host traits and abiotic factors such as temperature and seasonality. In Caribbean reefs, sea urchins like Diadema antillarum and Echinometra lucunter are important grazers that regulate algal biomass and influence benthic community dynamics. This study used 16S rRNA gene sequencing to compare, for the first time, the gut microbiota of these two sympatric species across contrasting seasons.
METHODS: Adults of D. antillarum and E. lucunter were collected during summer and winter from three fringing reefs in Puerto Rico. Gut contents were extracted under sterile conditions, and bacterial DNA was extracted amplified for their 16S rRNA genes and sequenced. Microbial diversity and structure were assessed standard microbiota pipelines.
RESULTS: Microbial communities in both echinoids were dominated by Bacillota, Bacteroidota, Desulfobacterota, and Pseudomonadota. Core microbiota analysis revealed stable taxa across hosts and seasons, most notably Propionigenium, supporting host-driven selection mechanisms that maintain functional stability despite seasonal turnover. Core microbiome analyses revealed Bacillota, Bacteroidota, Desulfobacterota_G_459543, and Pseudomonadota as persistent phyla across seasons, and genera such as Desulfotalea, Photobacterium, and Propionigenium consistently present in both species. Alpha diversity was significantly higher in winter for both D. antillarum and E. lucunter, while species-level differences were not significant. Beta diversity analyses showed significant seasonal clustering, with no consistent segregation between species within seasons. Our findings demonstrate that shared environmental conditions, particularly seasonality, are the primary modulators of gut microbiota in sympatric sea urchins, while host selection preserves a conserved core community. This dual influence of environment and host highlights the ecological plasticity and resilience of sea urchin microbiotas under fluctuating reef conditions.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Seasons
*Sea Urchins/microbiology
*Gastrointestinal Microbiome/genetics
RNA, Ribosomal, 16S/genetics
Puerto Rico
Sympatry
*Bacteria/genetics/classification
RevDate: 2026-03-10
CmpDate: 2026-03-10
Portal Vein Tryptophan Pathway Analysis Reveals Gut-Mediated Inflammatory Pathway Predominance in HCV Infection.
Liver international : official journal of the International Association for the Study of the Liver, 46(4):e70584.
BACKGROUND AND AIMS: The tryptophan pathway is an integral component of the gut-liver axis; however, the role in hepatitis C virus infection (HCV) and liver disease progression remains poorly understood. This study investigated tryptophan metabolites in portal and peripheral serum during and after HCV, and their relationship to inflammatory and clinical markers.
METHODS: HCV infected patients were evaluated during infection (HCVi, n = 24) and 6 months after sofosbuvir/velpatasvir mediated sustained virologic response (SVR, n = 19) (NCT02400216). Liver biopsies, portal and peripheral blood collection, and stool sampling were performed at both time points. Statistical analyses assessed metabolite abundance during infection and recovery, and their associations with cytokines, clinical parameters, and the microbiome.
RESULTS: During infection, peripheral tryptophan and kynurenine were elevated while indolelactate and xanthurenate were reduced (p < 0.05). In the portal blood, kynurenine/tryptophan ratio and kynurenine were increased, whereas indoleacetate and xanthurenate were decreased (p < 0.05). Tryptophan metabolites positively correlated with hepatic activity index, gamma-glutamyl transferase, total bilirubin, spleen volume/height ratio, and pro-inflammatory cytokines including CXCL9, CXCL10, TNFα, IL6, and IL-12p40. Negatively, correlations were observed with gut microbes Dorea longicatena and Qiania dongpingenesis.
CONCLUSIONS: Elevated kynurenine in portal blood suggests upregulation of gut-mediated pro-inflammatory pathways during HCV infection. Integration of multi-omics data from the gut-liver axis highlights the contribution of the tryptophan pathway to inflammatory responses in HCV. However, small sample size, absence of quantitative values for all pathway metabolites, and reliance on correlative rather than causative associations limit mechanistic interpretation. Future studies with larger cohorts and functional analyses are needed to clarify causal mechanisms and evaluate therapeutic potential of targeting the tryptophan pathway.
TRIAL REGISTRATION: NCT02400216.
Additional Links: PMID-41804293
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41804293,
year = {2026},
author = {Oringher, JL and Afruza, R and Chakraborty, M and Akiva, KL and Zhang, GY and Townsend, EC and Quinn, GM and Scheuing, L and Menkart, MG and Rai, A and Kleiner, DE and Levy, EB and Koh, C and Ali, RO and Etzion, O and Heller, T},
title = {Portal Vein Tryptophan Pathway Analysis Reveals Gut-Mediated Inflammatory Pathway Predominance in HCV Infection.},
journal = {Liver international : official journal of the International Association for the Study of the Liver},
volume = {46},
number = {4},
pages = {e70584},
doi = {10.1111/liv.70584},
pmid = {41804293},
issn = {1478-3231},
support = {DK054514/DK/NIDDK NIH HHS/United States ; },
mesh = {Humans ; *Tryptophan/blood/metabolism ; Male ; Female ; Middle Aged ; Kynurenine/blood ; *Gastrointestinal Microbiome ; *Portal Vein/metabolism ; Adult ; Antiviral Agents/therapeutic use ; Cytokines/blood ; Sofosbuvir/therapeutic use ; Sustained Virologic Response ; Liver/pathology ; *Hepatitis C, Chronic/drug therapy/blood ; Xanthurenates/blood ; Inflammation ; *Hepatitis C/drug therapy ; Biomarkers/blood ; Aged ; Heterocyclic Compounds, 4 or More Rings/therapeutic use ; },
abstract = {BACKGROUND AND AIMS: The tryptophan pathway is an integral component of the gut-liver axis; however, the role in hepatitis C virus infection (HCV) and liver disease progression remains poorly understood. This study investigated tryptophan metabolites in portal and peripheral serum during and after HCV, and their relationship to inflammatory and clinical markers.
METHODS: HCV infected patients were evaluated during infection (HCVi, n = 24) and 6 months after sofosbuvir/velpatasvir mediated sustained virologic response (SVR, n = 19) (NCT02400216). Liver biopsies, portal and peripheral blood collection, and stool sampling were performed at both time points. Statistical analyses assessed metabolite abundance during infection and recovery, and their associations with cytokines, clinical parameters, and the microbiome.
RESULTS: During infection, peripheral tryptophan and kynurenine were elevated while indolelactate and xanthurenate were reduced (p < 0.05). In the portal blood, kynurenine/tryptophan ratio and kynurenine were increased, whereas indoleacetate and xanthurenate were decreased (p < 0.05). Tryptophan metabolites positively correlated with hepatic activity index, gamma-glutamyl transferase, total bilirubin, spleen volume/height ratio, and pro-inflammatory cytokines including CXCL9, CXCL10, TNFα, IL6, and IL-12p40. Negatively, correlations were observed with gut microbes Dorea longicatena and Qiania dongpingenesis.
CONCLUSIONS: Elevated kynurenine in portal blood suggests upregulation of gut-mediated pro-inflammatory pathways during HCV infection. Integration of multi-omics data from the gut-liver axis highlights the contribution of the tryptophan pathway to inflammatory responses in HCV. However, small sample size, absence of quantitative values for all pathway metabolites, and reliance on correlative rather than causative associations limit mechanistic interpretation. Future studies with larger cohorts and functional analyses are needed to clarify causal mechanisms and evaluate therapeutic potential of targeting the tryptophan pathway.
TRIAL REGISTRATION: NCT02400216.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Tryptophan/blood/metabolism
Male
Female
Middle Aged
Kynurenine/blood
*Gastrointestinal Microbiome
*Portal Vein/metabolism
Adult
Antiviral Agents/therapeutic use
Cytokines/blood
Sofosbuvir/therapeutic use
Sustained Virologic Response
Liver/pathology
*Hepatitis C, Chronic/drug therapy/blood
Xanthurenates/blood
Inflammation
*Hepatitis C/drug therapy
Biomarkers/blood
Aged
Heterocyclic Compounds, 4 or More Rings/therapeutic use
RevDate: 2026-03-10
Integrated cross-sectional study and functional validation indicate the association of lactobacillus crispatus-derived D-lactic acid with cervical gene expression and precancerous cervical lesions.
Journal of translational medicine pii:10.1186/s12967-026-07982-w [Epub ahead of print].
Additional Links: PMID-41803943
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803943,
year = {2026},
author = {Dai, W and Jiang, X and Liu, Y and Yu, Y and Hou, J and Xia, J and Li, SC and Li, C and Du, H and Wu, R},
title = {Integrated cross-sectional study and functional validation indicate the association of lactobacillus crispatus-derived D-lactic acid with cervical gene expression and precancerous cervical lesions.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07982-w},
pmid = {41803943},
issn = {1479-5876},
}
RevDate: 2026-03-10
Longitudinal source-sink dynamics of fecal litter and farm indoor environmental resistomes in broiler chicken and Cherry Valley ducks.
Animal microbiome pii:10.1186/s42523-026-00544-x [Epub ahead of print].
Additional Links: PMID-41803939
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803939,
year = {2026},
author = {Fauszt, P and Mikolas, M and David, P and Szoke, Z and Gashi, N and Szilagyi-Tolnai, E and Szilágyi, E and Szarvas, MM and Fazekas, ME and Kun-Nemes, A and Stagel, A and Gal, F and Czegledi, L and Biro, S and Stundl, L and Remenyik, J and Paholcsek, M},
title = {Longitudinal source-sink dynamics of fecal litter and farm indoor environmental resistomes in broiler chicken and Cherry Valley ducks.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00544-x},
pmid = {41803939},
issn = {2524-4671},
}
RevDate: 2026-03-10
Towards standardization in pig microbiome research based on a comprehensive twenty-year review.
Animal microbiome pii:10.1186/s42523-026-00541-0 [Epub ahead of print].
Additional Links: PMID-41803924
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803924,
year = {2026},
author = {Enokela, SO and Yergaliyev, T and Flisikowski, K and Hornburg, SC and Reyer, H and Tetens, J and Wimmers, K and Zentek, J and Camarinha-Silva, A},
title = {Towards standardization in pig microbiome research based on a comprehensive twenty-year review.},
journal = {Animal microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s42523-026-00541-0},
pmid = {41803924},
issn = {2524-4671},
support = {28N-2-051-01//German Federal Ministry of Food and Agriculture/ ; 28N-2-051-01//German Federal Ministry of Food and Agriculture/ ; },
}
RevDate: 2026-03-10
The antimicrobial gut resistome of the Wayampi reveals a shared background of antibiotic and metal resistance genes with industrialized populations, underscoring the "robust-yet-fragile" architecture of human gut microbiomes.
Microbiome pii:10.1186/s40168-026-02345-5 [Epub ahead of print].
BACKGROUND: Metagenomics enables detailed profiling of genes encoding antimicrobial resistance. However, most studies focus exclusively on antibiotic resistance genes (ARGs), excluding those associated with non-antibiotic antimicrobials (metals, biocides), and often rely on methods with low-sensitivity and low-specificity. Furthermore, they rarely examine populations exposed to minimal anthropogenic pollution. We analyzed fecal resistomes of 95 Wayampi individuals, an Indigenous community in remote French Guiana, using a targeted metagenomic capture platform covering 8667 genes, including ARGs, metal resistance genes (MRGs) and biocide resistance genes (BRGs) (PMID: 29335005). Resistome profiles were compared with those of Europeans to assess population-level differences.
RESULTS: ARG richness was similar between groups (259 in Wayampi vs. 264 in Europeans, 159 shared), but MRGs + BRGs gene richness was significantly higher in Wayampi (11,930 vs. 7419). Most genes appeared in a minority of individuals (mean 5% for ARGs, 2% for MRGs + BRGs), but several ARGs for tetracyclines [tet(32), tet(40), tet(O), tet(Q), tet(W), tet(X), tetAB(P)], aminoglycosides (ant6'-I, aph3-III), macrolides (ermB, ermF, mefA), and sulfonamides (sul2) were present in all individuals. Tetracycline resistance genes predominated overall, while beta-lactam resistance genes were more common in Wayampi, and genes conferring resistance to aminoglycosides, amphenicols, and folate inhibitors were more frequent in Europeans. Among MRGs, copper and arsenic resistance genes prevailed in both groups, followed by those for zinc, iron, cobalt, and nickel. Up to 76% of Wayampiis carried acquired MRGs for copper (pcoABCDRS and tcrB), silver (silACFPRS), arsenic (ars), and mercury (mer) detoxification. Shannon diversity indices were similar for ARGs, MRGs, and BRGs, but composition and evenness differed significantly. UMAP and ADONIS analyses distinguished cohorts based on ARG profiles (p < 0.001), but not on MRGs or BRGs. Correlation analysis revealed conserved gene-sharing networks and introgression of acquired ARGs and MRGs within both gut microbiomes.
CONCLUSIONS: The diverse and balanced Wayampi resistome reflects a less perturbed microbiome compared to industrialized populations, and reveals a background of "core" and "shell" acquired ARGs and MRGs, consistent with the "robust-yet-fragile" architecture of scale-free networks. The patchy yet resilient gene distribution suggests varying levels of conserved gene sharing highways among populations, likely shaped by long-term microbial-human evolution, and supports a broader view on acquired antimicrobial resistance. Video Abstract.
Additional Links: PMID-41803907
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803907,
year = {2026},
author = {Fernández-de-Bobadilla, MD and Pérez-Cobas, AE and Andremont, A and MartÃnez, JL and Baquero, F and Lanza, VF and Coque, TM},
title = {The antimicrobial gut resistome of the Wayampi reveals a shared background of antibiotic and metal resistance genes with industrialized populations, underscoring the "robust-yet-fragile" architecture of human gut microbiomes.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02345-5},
pmid = {41803907},
issn = {2049-2618},
support = {pFIS F19/00366//Instituto de Salud Carlos III/ ; CB21/13/00084//Instituto de Salud Carlos III/ ; CC23140547//Fundación Francisco Soria Melguizo/ ; MISTAR AC21_2/00041//Joint Programming Initiative on Antimicrobial Resistance/ ; "Ayudas de atracción de talento investigador César Nombela" 2023-T1/SAL-GL28953//Comunidad de Madrid/ ; FP7#282004//European Union/ ; },
abstract = {BACKGROUND: Metagenomics enables detailed profiling of genes encoding antimicrobial resistance. However, most studies focus exclusively on antibiotic resistance genes (ARGs), excluding those associated with non-antibiotic antimicrobials (metals, biocides), and often rely on methods with low-sensitivity and low-specificity. Furthermore, they rarely examine populations exposed to minimal anthropogenic pollution. We analyzed fecal resistomes of 95 Wayampi individuals, an Indigenous community in remote French Guiana, using a targeted metagenomic capture platform covering 8667 genes, including ARGs, metal resistance genes (MRGs) and biocide resistance genes (BRGs) (PMID: 29335005). Resistome profiles were compared with those of Europeans to assess population-level differences.
RESULTS: ARG richness was similar between groups (259 in Wayampi vs. 264 in Europeans, 159 shared), but MRGs + BRGs gene richness was significantly higher in Wayampi (11,930 vs. 7419). Most genes appeared in a minority of individuals (mean 5% for ARGs, 2% for MRGs + BRGs), but several ARGs for tetracyclines [tet(32), tet(40), tet(O), tet(Q), tet(W), tet(X), tetAB(P)], aminoglycosides (ant6'-I, aph3-III), macrolides (ermB, ermF, mefA), and sulfonamides (sul2) were present in all individuals. Tetracycline resistance genes predominated overall, while beta-lactam resistance genes were more common in Wayampi, and genes conferring resistance to aminoglycosides, amphenicols, and folate inhibitors were more frequent in Europeans. Among MRGs, copper and arsenic resistance genes prevailed in both groups, followed by those for zinc, iron, cobalt, and nickel. Up to 76% of Wayampiis carried acquired MRGs for copper (pcoABCDRS and tcrB), silver (silACFPRS), arsenic (ars), and mercury (mer) detoxification. Shannon diversity indices were similar for ARGs, MRGs, and BRGs, but composition and evenness differed significantly. UMAP and ADONIS analyses distinguished cohorts based on ARG profiles (p < 0.001), but not on MRGs or BRGs. Correlation analysis revealed conserved gene-sharing networks and introgression of acquired ARGs and MRGs within both gut microbiomes.
CONCLUSIONS: The diverse and balanced Wayampi resistome reflects a less perturbed microbiome compared to industrialized populations, and reveals a background of "core" and "shell" acquired ARGs and MRGs, consistent with the "robust-yet-fragile" architecture of scale-free networks. The patchy yet resilient gene distribution suggests varying levels of conserved gene sharing highways among populations, likely shaped by long-term microbial-human evolution, and supports a broader view on acquired antimicrobial resistance. Video Abstract.},
}
RevDate: 2026-03-10
Integrated multiomics profiling predicts anti-tuberculosis drug-induced liver injury.
Respiratory research pii:10.1186/s12931-026-03608-3 [Epub ahead of print].
Additional Links: PMID-41803902
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803902,
year = {2026},
author = {Liu, Q and Wang, C and Si, G and He, J},
title = {Integrated multiomics profiling predicts anti-tuberculosis drug-induced liver injury.},
journal = {Respiratory research},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12931-026-03608-3},
pmid = {41803902},
issn = {1465-993X},
support = {2023YFS0236//Sichuan Science and Technology Program Key R&D Project/ ; },
}
RevDate: 2026-03-10
Regulatory effects of winter Morchella esculenta cultivation on the summer maize phyllosphere microbiome and plant health-related traits.
BMC plant biology pii:10.1186/s12870-026-08489-8 [Epub ahead of print].
Additional Links: PMID-41803738
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803738,
year = {2026},
author = {Liu, G and Zhou, K and An, Q and Yang, C and Yang, S and Xu, L},
title = {Regulatory effects of winter Morchella esculenta cultivation on the summer maize phyllosphere microbiome and plant health-related traits.},
journal = {BMC plant biology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12870-026-08489-8},
pmid = {41803738},
issn = {1471-2229},
support = {202305AC160057//Project for Reserve Talents of Young and Middle-aged Academic and Technical Leaders/ ; 2023//Xingzhao Talent Support Program/ ; 2025//Yunnan Colorful Clouds Postdoctoral Program Innovation Project/ ; },
}
RevDate: 2026-03-10
Global genomic diversity of temperate P2-like viruses.
Communications biology pii:10.1038/s42003-026-09823-4 [Epub ahead of print].
P2-like viruses (P2Vs), temperate phages of the Peduoviridae family, possess a lysogenic lifestyle that renders traditional isolation unsuitable, hindering our understanding of their diversity and ecological roles. Utilizing profile-hidden Markov models to analyze public databases, this study achieved four major advances: (1) Identified 5945 P2V genomes and built the P2V Genome Dataset (P2VGD), expanding known genomes 48-fold; (2) Phylogenetic classification into 13 superclades and 4671 genus-level clusters, a 106-fold diversity increase; (3) Identification of 757 auxiliary metabolic genes with biome-specific metatranscriptomic activities: human gut P2Vs encode antibiotic efflux and cell-wall remodeling enzymes, while oligotrophic marine P2Vs express glycan-scavenging enzymes; (4) Uncovering their widespread distribution across diverse biomes, dominated by host-associated environments but extending to under-sampled natural ecosystems. These findings greatly expand the genomic and functional understanding of P2Vs, highlighting their biological strategies in host adaptation, virus-host co-evolution, and microbiome dynamics.
Additional Links: PMID-41803419
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803419,
year = {2026},
author = {Liu, Y and Liu, R and Zheng, K and Wang, Z and Shao, H and McMinn, A and Wang, M and Liang, Y},
title = {Global genomic diversity of temperate P2-like viruses.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-09823-4},
pmid = {41803419},
issn = {2399-3642},
support = {42176111//National Natural Science Foundation of China (National Science Foundation of China)/ ; 42120104006//National Natural Science Foundation of China (National Science Foundation of China)/ ; 2025M770867//China Postdoctoral Science Foundation/ ; },
abstract = {P2-like viruses (P2Vs), temperate phages of the Peduoviridae family, possess a lysogenic lifestyle that renders traditional isolation unsuitable, hindering our understanding of their diversity and ecological roles. Utilizing profile-hidden Markov models to analyze public databases, this study achieved four major advances: (1) Identified 5945 P2V genomes and built the P2V Genome Dataset (P2VGD), expanding known genomes 48-fold; (2) Phylogenetic classification into 13 superclades and 4671 genus-level clusters, a 106-fold diversity increase; (3) Identification of 757 auxiliary metabolic genes with biome-specific metatranscriptomic activities: human gut P2Vs encode antibiotic efflux and cell-wall remodeling enzymes, while oligotrophic marine P2Vs express glycan-scavenging enzymes; (4) Uncovering their widespread distribution across diverse biomes, dominated by host-associated environments but extending to under-sampled natural ecosystems. These findings greatly expand the genomic and functional understanding of P2Vs, highlighting their biological strategies in host adaptation, virus-host co-evolution, and microbiome dynamics.},
}
RevDate: 2026-03-10
Microbiome modulation in cancer immunotherapy.
Nature medicine [Epub ahead of print].
Additional Links: PMID-41803343
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803343,
year = {2026},
author = {Pal, SK and Davar, D},
title = {Microbiome modulation in cancer immunotherapy.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {41803343},
issn = {1546-170X},
}
RevDate: 2026-03-10
Soil Microbiome for Climate Smart Agriculture in Legumes: A Review.
Current microbiology, 83(4):.
Climate-smart agriculture is a multidisciplinary farm model approach that helps reduce the impact of climate change not only on soil but on entire agricultural systems. One of the critical approaches of climate-smart agriculture is using the soil microbiome to help the crop adapt to the changing climate and increase crop production. The microorganisms that are present in the soil play a crucial role in ecosystem services, crop protection and performance, and productivity. Legumes are essential for their nutritional value and interaction with soil microbes, particularly in fixing atmospheric nitrogen and improving soil health through plant-microbe association. Beyond Rhizobium, a wide range of microorganisms and fungi assist legumes in adapting to climate stresses such as drought stress and salinity, which ultimately enhances biomass and legume yield. However, the molecular mechanisms behind the interactions between microbiomes and plant growth, ecosystem services, and carbon sequestration remain unclear in legumes. This review aims to explain the key roles of the soil microbiome, legume rhizobiome, and the microbial genes associated with functional plant traits that help plants adapt to a changing climate. Understanding how microbial populations shift due to climate variations and how these changes affect legume yields is crucial, given the ever-changing nature of ecosystems due to climatic shifts. Therefore, more research is warranted to explore plant microbial interactions, understand the dynamics of climatic shifts, and develop microbiome engineering tools for the improved health of crop and rhizobiome ecosystems. Furthermore, a parallel study is required to examine the harmful microbiome that causes crop destruction and antagonizes important bacteria.
Additional Links: PMID-41803338
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803338,
year = {2026},
author = {Tamang, KR and Mahdi, S and Koirala, P and Asiamah, JY and Sharma, S and Padyana, S and Carson, CB and Valliyodan, B},
title = {Soil Microbiome for Climate Smart Agriculture in Legumes: A Review.},
journal = {Current microbiology},
volume = {83},
number = {4},
pages = {},
pmid = {41803338},
issn = {1432-0991},
support = {U.S. Department of Agriculture//U.S. Department of Agriculture/ ; },
abstract = {Climate-smart agriculture is a multidisciplinary farm model approach that helps reduce the impact of climate change not only on soil but on entire agricultural systems. One of the critical approaches of climate-smart agriculture is using the soil microbiome to help the crop adapt to the changing climate and increase crop production. The microorganisms that are present in the soil play a crucial role in ecosystem services, crop protection and performance, and productivity. Legumes are essential for their nutritional value and interaction with soil microbes, particularly in fixing atmospheric nitrogen and improving soil health through plant-microbe association. Beyond Rhizobium, a wide range of microorganisms and fungi assist legumes in adapting to climate stresses such as drought stress and salinity, which ultimately enhances biomass and legume yield. However, the molecular mechanisms behind the interactions between microbiomes and plant growth, ecosystem services, and carbon sequestration remain unclear in legumes. This review aims to explain the key roles of the soil microbiome, legume rhizobiome, and the microbial genes associated with functional plant traits that help plants adapt to a changing climate. Understanding how microbial populations shift due to climate variations and how these changes affect legume yields is crucial, given the ever-changing nature of ecosystems due to climatic shifts. Therefore, more research is warranted to explore plant microbial interactions, understand the dynamics of climatic shifts, and develop microbiome engineering tools for the improved health of crop and rhizobiome ecosystems. Furthermore, a parallel study is required to examine the harmful microbiome that causes crop destruction and antagonizes important bacteria.},
}
RevDate: 2026-03-10
Symbiotic in Alzheimer's disease: modulating the gut-brain axis for neuroimmune homeostasis and cognitive protection.
Inflammopharmacology [Epub ahead of print].
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder defined by progressive cognitive impairment, neuroinflammation, oxidative stress, amyloid-β (Aβ) accumulation, synaptic dysfunction, mitochondrial impairment, and tau hyperphosphorylation. The gut-brain axis (GBA) is a crucial regulatory signaling cascade that links intestinal microbiome composition with both neural health and disease through the vagus nerve. Gut dysbiosis has increasingly been implicated in AD pathogenesis by exacerbating systemic and neuroinflammatory signaling, disrupting intestinal and blood-brain barrier (BBB) structural stability, and promoting microglial activation, thereby facilitating Aβ aggregation and neurodegeneration. Preclinical studies indicate that symbiotic interventions restore microbial balance and improve gut-brain communication, contributing to neuroprotective effects. Additionally, it has been demonstrated that symbiotics can restore synaptic plasticity and cognitive resilience by suppressing pro-inflammatory cytokines, as exemplified by interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α), and by upregulating neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF). These effects are associated with normalised glial reactivity, attenuation of oxidative stress, and improved mitochondrial bioenergetics, together contributing to enhanced synaptic function, reduced neuroinflammation, and preservation of cognitive performance. This review highlights a critical assessment of the treatment potential of symbiotic interventions in modulating the GBA in AD, emphasising mechanistic insights into neurodegenerative pathways and evaluating their capacity to mitigate symptoms and delay disease progression, as supported by current preclinical evidence.
Additional Links: PMID-41803336
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803336,
year = {2026},
author = {Mandal, S and Aran, KR},
title = {Symbiotic in Alzheimer's disease: modulating the gut-brain axis for neuroimmune homeostasis and cognitive protection.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {41803336},
issn = {1568-5608},
abstract = {Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder defined by progressive cognitive impairment, neuroinflammation, oxidative stress, amyloid-β (Aβ) accumulation, synaptic dysfunction, mitochondrial impairment, and tau hyperphosphorylation. The gut-brain axis (GBA) is a crucial regulatory signaling cascade that links intestinal microbiome composition with both neural health and disease through the vagus nerve. Gut dysbiosis has increasingly been implicated in AD pathogenesis by exacerbating systemic and neuroinflammatory signaling, disrupting intestinal and blood-brain barrier (BBB) structural stability, and promoting microglial activation, thereby facilitating Aβ aggregation and neurodegeneration. Preclinical studies indicate that symbiotic interventions restore microbial balance and improve gut-brain communication, contributing to neuroprotective effects. Additionally, it has been demonstrated that symbiotics can restore synaptic plasticity and cognitive resilience by suppressing pro-inflammatory cytokines, as exemplified by interleukin-1β (IL-1β) and tumour necrosis factor-α (TNF-α), and by upregulating neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF). These effects are associated with normalised glial reactivity, attenuation of oxidative stress, and improved mitochondrial bioenergetics, together contributing to enhanced synaptic function, reduced neuroinflammation, and preservation of cognitive performance. This review highlights a critical assessment of the treatment potential of symbiotic interventions in modulating the GBA in AD, emphasising mechanistic insights into neurodegenerative pathways and evaluating their capacity to mitigate symptoms and delay disease progression, as supported by current preclinical evidence.},
}
RevDate: 2026-03-10
Morpho-biochemical and molecular identification of Bacillus licheniformis and Bacillus cereus isolates from sorghum (Sorghum bicolor L.) rhizosphere.
Scientific reports pii:10.1038/s41598-026-42932-y [Epub ahead of print].
This study isolated, characterized, and identified rhizosphere-associated soil bacteria from sorghum-cultivated soils in Bhubaneswar, India, using serial dilution and spread plate techniques on Nutrient Agar. Morphological and biochemical analyses (Gram staining, catalase, oxidase, MR, and indole tests) identified 13 bacterial isolates, predominantly Gram-positive rods (Bacillus, Paenibacillus) and cocci (Staphylococcus, Micrococcus), with one Gram-negative isolate. Molecular characterization involved 16S rRNA gene amplification (~ 1500 bp), sanger sequencing, and phylogenetic analysis. BLASTN confirmed AG3 as Bacillus licheniformis (99.37% identity) (GenBank: PV590072), and AG11 as Bacillus cereus (100% identity) (GenBank: PV590099). The phylogenetic tress analysis of bacterial isolates AG3 and AG11 revealed distinct evolutionary rate variations. For AG3, site-specific rates ranged from 0.07 to 3.64 substitutions/site (nucleotide frequencies: A = 24.50%, T/U = 19.99%, C = 24.70%, G = 30.81%), while AG11 exhibited more uniform rates ranged from 0.90 to 1.10 substitutions/site (nucleotide frequencies: A = 25.79%, T/U = 20.86%, C = 22.71%, G = 30.64%). Maximum likelihood trees (log-likelihood: - 4077.853 for AG3, - 1928.562 for AG11) with 1,531 (AG3) and 1,402 (AG11) aligned positions resolved their phylogenetic relationships. This study provides valuable insights into the diversity and evolutionary dynamics of rhizosphere-associated Bacillus spp. in sorghum-cultivated soils, contributing to a better understanding of their ecological significance and potential application in sustainable agriculture and plant growth promotion.
Additional Links: PMID-41803252
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803252,
year = {2026},
author = {Jurry, AG and Sahoo, JP and Sharma, SS and Praveena, J and Hossain, SN and Sahu, N and Pradhan, S and Nayak, P and Tripathy, S and Vijayakumar, D and Dash, SS and Jena, B and Pradhan, P and Pradhan, SS},
title = {Morpho-biochemical and molecular identification of Bacillus licheniformis and Bacillus cereus isolates from sorghum (Sorghum bicolor L.) rhizosphere.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-42932-y},
pmid = {41803252},
issn = {2045-2322},
abstract = {This study isolated, characterized, and identified rhizosphere-associated soil bacteria from sorghum-cultivated soils in Bhubaneswar, India, using serial dilution and spread plate techniques on Nutrient Agar. Morphological and biochemical analyses (Gram staining, catalase, oxidase, MR, and indole tests) identified 13 bacterial isolates, predominantly Gram-positive rods (Bacillus, Paenibacillus) and cocci (Staphylococcus, Micrococcus), with one Gram-negative isolate. Molecular characterization involved 16S rRNA gene amplification (~ 1500 bp), sanger sequencing, and phylogenetic analysis. BLASTN confirmed AG3 as Bacillus licheniformis (99.37% identity) (GenBank: PV590072), and AG11 as Bacillus cereus (100% identity) (GenBank: PV590099). The phylogenetic tress analysis of bacterial isolates AG3 and AG11 revealed distinct evolutionary rate variations. For AG3, site-specific rates ranged from 0.07 to 3.64 substitutions/site (nucleotide frequencies: A = 24.50%, T/U = 19.99%, C = 24.70%, G = 30.81%), while AG11 exhibited more uniform rates ranged from 0.90 to 1.10 substitutions/site (nucleotide frequencies: A = 25.79%, T/U = 20.86%, C = 22.71%, G = 30.64%). Maximum likelihood trees (log-likelihood: - 4077.853 for AG3, - 1928.562 for AG11) with 1,531 (AG3) and 1,402 (AG11) aligned positions resolved their phylogenetic relationships. This study provides valuable insights into the diversity and evolutionary dynamics of rhizosphere-associated Bacillus spp. in sorghum-cultivated soils, contributing to a better understanding of their ecological significance and potential application in sustainable agriculture and plant growth promotion.},
}
RevDate: 2026-03-10
Diversity of culturable gut bacteria associated with brown planthopper, Nilaparvata lugens (Stål) and their role in imidacloprid degradation.
Scientific reports pii:10.1038/s41598-026-41348-y [Epub ahead of print].
The brown planthopper, Nilaparvata lugens (Stål), is a major pest of rice across Asia and has developed significant metabolic resistance to multiple insecticides. Microbiome-mediated insecticide resistance is of emerging interest in various insect pests, including N. lugens. In this study, we assessed the diversity of culturable gut bacteria in imidacloprid-susceptible (IMI-S) and imidacloprid-resistant (IMI-R) populations of N. lugens and their potential to degrade imidacloprid. Molecular characterization and phylogenetic analysis identified 13 bacterial isolates, representing ten families from three phyla: Proteobacteria, Actinobacteria and Firmicutes. The IMI-R population has contributed to nine of the 13 isolates. Screening for imidacloprid degradation identified four bacterial strains viz., Paenibacillus amylolyticus, Serratia marcescens, Acinetobacter soli and Brucella sp. associated with the IMI-R population were capable of growing in minimal salt medium supplemented with imidacloprid. Notably, S. marcescens and P. amylolyticus could utilize imidacloprid as a sole source of carbon and nitrogen, respectively. LC-MS/MS analysis revealed that P. amylolyticus and S. marcescens after 14 days of inoculation degraded 73.07 and 66.92% of imidacloprid (100 mg/L), respectively. These findings underscore a strong association between gut-microbial composition and insecticide resistance in N. lugens and highlight the potential of specific bacterial strains for microbiome-based pest and resistance management strategies.
Additional Links: PMID-41803235
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803235,
year = {2026},
author = {Chowdary, DD and Sridhar, Y and Rao, GR and Madhav, MS and Latha, PC and Malathi, VM and Padmakumari, AP and Sundaram, RM},
title = {Diversity of culturable gut bacteria associated with brown planthopper, Nilaparvata lugens (Stål) and their role in imidacloprid degradation.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-41348-y},
pmid = {41803235},
issn = {2045-2322},
abstract = {The brown planthopper, Nilaparvata lugens (Stål), is a major pest of rice across Asia and has developed significant metabolic resistance to multiple insecticides. Microbiome-mediated insecticide resistance is of emerging interest in various insect pests, including N. lugens. In this study, we assessed the diversity of culturable gut bacteria in imidacloprid-susceptible (IMI-S) and imidacloprid-resistant (IMI-R) populations of N. lugens and their potential to degrade imidacloprid. Molecular characterization and phylogenetic analysis identified 13 bacterial isolates, representing ten families from three phyla: Proteobacteria, Actinobacteria and Firmicutes. The IMI-R population has contributed to nine of the 13 isolates. Screening for imidacloprid degradation identified four bacterial strains viz., Paenibacillus amylolyticus, Serratia marcescens, Acinetobacter soli and Brucella sp. associated with the IMI-R population were capable of growing in minimal salt medium supplemented with imidacloprid. Notably, S. marcescens and P. amylolyticus could utilize imidacloprid as a sole source of carbon and nitrogen, respectively. LC-MS/MS analysis revealed that P. amylolyticus and S. marcescens after 14 days of inoculation degraded 73.07 and 66.92% of imidacloprid (100 mg/L), respectively. These findings underscore a strong association between gut-microbial composition and insecticide resistance in N. lugens and highlight the potential of specific bacterial strains for microbiome-based pest and resistance management strategies.},
}
RevDate: 2026-03-10
Large-scale distribution of cestode infections in wild gentoo penguins and their impact on the host microbiome.
Scientific reports pii:10.1038/s41598-026-39642-w [Epub ahead of print].
Additional Links: PMID-41803202
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803202,
year = {2026},
author = {Kaczvinsky, C and Levy, H and Preston, S and Youngflesh, C and Clucas, G and Lynch, HJ and Christodoulou, MD and Hart, T and Smith, AL},
title = {Large-scale distribution of cestode infections in wild gentoo penguins and their impact on the host microbiome.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-39642-w},
pmid = {41803202},
issn = {2045-2322},
}
RevDate: 2026-03-10
Chicken vaccination reduces colonization and dissemination of Salmonella serovar Enteritidis with decreased susceptibility to ciprofloxacin.
NPJ vaccines pii:10.1038/s41541-026-01414-y [Epub ahead of print].
Salmonella enterica serovar Enteritidis (S. Enteritidis) is one of most common Salmonella serovars associated with human illness in the U.S. and worldwide. Surveillance from the U.S. National Antimicrobial Resistance Monitoring System indicates an increase in both chicken and human isolates of S. Enteritidis with decreased susceptibility to ciprofloxacin (DSC), a critical antibiotic prescribed for complicated human salmonellosis infections. S. Enteritidis reduction in chickens is a priority of poultry producers and public health agencies to improve food safety. In the current study, efficacy assessment of a live Salmonella vaccine (BBS 1134) revealed significant reduction of cecal and splenic colonization, and prevention of dissemination to the bone marrow by DSC S. Enteritidis in broiler chickens. Microbiome analysis indicated the cecal microbiota of vaccinated chickens is distinct compared to mock-vaccinated birds. The IDEXX SE Ab X2 Test did not detect antibodies to S. Enteritidis in vaccinated chicken serum, thereby permitting differentiation of infected from vaccinated animals (DIVA). Altogether, the Salmonella vaccine is a DIVA vaccine, afforded cross-protection, and significantly reduced intestinal colonization and dissemination to the spleen and bone marrow by DSC S. Enteritidis in chickens, thereby offering a prospective intervention for animal production to reduce food product contamination and improve food safety.
Additional Links: PMID-41803165
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803165,
year = {2026},
author = {Bearson, BL and Whelan, SJ and Encinosa, MPN and Neupane, DP and Bradshaw, DJ and Monson, MS and Anderson, CL and Bearson, SMD},
title = {Chicken vaccination reduces colonization and dissemination of Salmonella serovar Enteritidis with decreased susceptibility to ciprofloxacin.},
journal = {NPJ vaccines},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41541-026-01414-y},
pmid = {41803165},
issn = {2059-0105},
support = {CRIS project 5030-31000-007-000-D//United States Department of Agriculture (USDA), Agricultural Research Service (ARS) appropriated funds/ ; CRIS project 5030-32000-227-000D//United States Department of Agriculture (USDA), Agricultural Research Service (ARS) appropriated funds/ ; },
abstract = {Salmonella enterica serovar Enteritidis (S. Enteritidis) is one of most common Salmonella serovars associated with human illness in the U.S. and worldwide. Surveillance from the U.S. National Antimicrobial Resistance Monitoring System indicates an increase in both chicken and human isolates of S. Enteritidis with decreased susceptibility to ciprofloxacin (DSC), a critical antibiotic prescribed for complicated human salmonellosis infections. S. Enteritidis reduction in chickens is a priority of poultry producers and public health agencies to improve food safety. In the current study, efficacy assessment of a live Salmonella vaccine (BBS 1134) revealed significant reduction of cecal and splenic colonization, and prevention of dissemination to the bone marrow by DSC S. Enteritidis in broiler chickens. Microbiome analysis indicated the cecal microbiota of vaccinated chickens is distinct compared to mock-vaccinated birds. The IDEXX SE Ab X2 Test did not detect antibodies to S. Enteritidis in vaccinated chicken serum, thereby permitting differentiation of infected from vaccinated animals (DIVA). Altogether, the Salmonella vaccine is a DIVA vaccine, afforded cross-protection, and significantly reduced intestinal colonization and dissemination to the spleen and bone marrow by DSC S. Enteritidis in chickens, thereby offering a prospective intervention for animal production to reduce food product contamination and improve food safety.},
}
RevDate: 2026-03-10
CmpDate: 2026-03-10
Impact of the defined Oligo-MM[12] microbiota on intestinal colonisation and dissemination of Listeria monocytogenes.
Scientific reports, 16(1):.
Listeria monocytogenes is a foodborne pathogen of global concern, particularly for immunocompromised individuals at risk of severe disease. In mice, infection outcomes are strongly influenced by host immunity and gut microbiome composition. The Oligo-MM[12] defined microbiota mouse model, containing a simplified community of 12 bacterial strains, offers a controlled system to study L. monocytogenes pathogenesis and microbiome interactions. Defined or reduced-complexity microbiota models are increasingly used to investigate colonisation resistance and identify protective taxa. In this study, we compared Oligo-MM[12] mice with conventionally raised Specific Pathogen Free (SPF) mice to assess how microbiome complexity shapes infection. This allowed us to explore how microbiome complexity affects resistance to L. monocytogenes. We performed an in vivo infection study to assess host responses and pathogen-related outcomes, alongside an ex vivo fermentation assay that simulated the murine distal colon, to monitor microbial dynamics. Building on our earlier work, we now demonstrate that in vivo, Oligo-MM[12] mice showed significantly higher L. monocytogenes shedding in faeces during infection, whereas SPF mice progressively reduced L. monocytogenes levels. Despite this, L. monocytogenes dissemination to internal organs after three days of infection was similar in both models. Alterations to gut Prevotella, Akkermansia and Blautia species following L. monocytogenes infection were noteworthy. Ex vivo fermentation mirrored in vivo patterns, validating the Oligo-MM[12] system for mechanistic studies. Together, these results highlight the importance of microbiome complexity in modulating infection outcomes and establish a foundation for identifying protective taxa and mechanisms of colonization resistance.
Additional Links: PMID-41803145
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803145,
year = {2026},
author = {Cazzaniga, M and Bra, KK and Herzog, MKM and Hardt, WD and Claesson, MJ and Mathur, H and Gahan, CGM},
title = {Impact of the defined Oligo-MM[12] microbiota on intestinal colonisation and dissemination of Listeria monocytogenes.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41803145},
issn = {2045-2322},
support = {NCCR Microbiomes//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung/ ; Marie Skłodowska-Curie grant agreement No 956279//H2020 European Institute of Innovation and Technology/ ; centres grant number SFI/12/RC/2273_P2/SFI_/Science Foundation Ireland/Ireland ; },
mesh = {Animals ; *Listeria monocytogenes/pathogenicity/physiology ; *Gastrointestinal Microbiome ; *Listeriosis/microbiology/immunology ; Mice ; Disease Models, Animal ; Feces/microbiology ; Specific Pathogen-Free Organisms ; Mice, Inbred C57BL ; Female ; },
abstract = {Listeria monocytogenes is a foodborne pathogen of global concern, particularly for immunocompromised individuals at risk of severe disease. In mice, infection outcomes are strongly influenced by host immunity and gut microbiome composition. The Oligo-MM[12] defined microbiota mouse model, containing a simplified community of 12 bacterial strains, offers a controlled system to study L. monocytogenes pathogenesis and microbiome interactions. Defined or reduced-complexity microbiota models are increasingly used to investigate colonisation resistance and identify protective taxa. In this study, we compared Oligo-MM[12] mice with conventionally raised Specific Pathogen Free (SPF) mice to assess how microbiome complexity shapes infection. This allowed us to explore how microbiome complexity affects resistance to L. monocytogenes. We performed an in vivo infection study to assess host responses and pathogen-related outcomes, alongside an ex vivo fermentation assay that simulated the murine distal colon, to monitor microbial dynamics. Building on our earlier work, we now demonstrate that in vivo, Oligo-MM[12] mice showed significantly higher L. monocytogenes shedding in faeces during infection, whereas SPF mice progressively reduced L. monocytogenes levels. Despite this, L. monocytogenes dissemination to internal organs after three days of infection was similar in both models. Alterations to gut Prevotella, Akkermansia and Blautia species following L. monocytogenes infection were noteworthy. Ex vivo fermentation mirrored in vivo patterns, validating the Oligo-MM[12] system for mechanistic studies. Together, these results highlight the importance of microbiome complexity in modulating infection outcomes and establish a foundation for identifying protective taxa and mechanisms of colonization resistance.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Listeria monocytogenes/pathogenicity/physiology
*Gastrointestinal Microbiome
*Listeriosis/microbiology/immunology
Mice
Disease Models, Animal
Feces/microbiology
Specific Pathogen-Free Organisms
Mice, Inbred C57BL
Female
RevDate: 2026-03-10
CmpDate: 2026-03-10
Water mass specific genes dominate the Southern Ocean microbiome.
Nature communications, 17(1):.
The Southern Ocean (SO) plays a key role in regulating global biogeochemical cycles and climate, yet microbial genes sustaining its biological activity remain poorly characterized. We introduce a microbial genes collection from 218 metagenomes sampled during the Antarctic Circumnavigation Expedition, the majority of which are missing from functional databases. 38% even lack homologs in current reference marine gene catalogs, defining a singular genetic seascape. We show that SO gene assemblages exhibit a common polar signature with the Arctic Ocean while being structured by water masses at the SO-scale. We analyze genomic markers of diverse SO biomes, focusing on dimethylsulphoniopropionate (DMSP) cleavage by polar-adapted bacteria, organic matter consumption in the blooming Mertz polynya and adaptation to polar conditions in the ubiquitous bacteria Pelagibacter. Our work takes a step towards a comprehensive understanding of SO's plankton ecology and evolution, capturing the current state of the unique microbial diversity in this rapidly changing Ocean.
Additional Links: PMID-41803086
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41803086,
year = {2026},
author = {Faure, E and Pommellec, J and Noel, C and Cormier, A and Delpech, LM and Eren, AM and Fernandez-Guerra, A and Vanni, C and Fourquez, M and Houssais, MN and Guyet, U and Da Silva, C and Gavory, F and Perdereau, A and Labadie, K and Wincker, P and Poulain, J and Hassler, C and Lin, Y and Cassar, N and Maignien, L},
title = {Water mass specific genes dominate the Southern Ocean microbiome.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {},
pmid = {41803086},
issn = {2041-1723},
support = {18-CE02-0024//Agence Nationale de la Recherche (French National Research Agency)/ ; ANR-10-INBS-09-08//Agence Nationale de la Recherche (French National Research Agency)/ ; },
mesh = {*Microbiota/genetics ; *Seawater/microbiology ; Oceans and Seas ; Metagenome/genetics ; Antarctic Regions ; *Bacteria/genetics/classification ; Sulfonium Compounds/metabolism ; Arctic Regions ; Plankton/genetics ; Phylogeny ; },
abstract = {The Southern Ocean (SO) plays a key role in regulating global biogeochemical cycles and climate, yet microbial genes sustaining its biological activity remain poorly characterized. We introduce a microbial genes collection from 218 metagenomes sampled during the Antarctic Circumnavigation Expedition, the majority of which are missing from functional databases. 38% even lack homologs in current reference marine gene catalogs, defining a singular genetic seascape. We show that SO gene assemblages exhibit a common polar signature with the Arctic Ocean while being structured by water masses at the SO-scale. We analyze genomic markers of diverse SO biomes, focusing on dimethylsulphoniopropionate (DMSP) cleavage by polar-adapted bacteria, organic matter consumption in the blooming Mertz polynya and adaptation to polar conditions in the ubiquitous bacteria Pelagibacter. Our work takes a step towards a comprehensive understanding of SO's plankton ecology and evolution, capturing the current state of the unique microbial diversity in this rapidly changing Ocean.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Microbiota/genetics
*Seawater/microbiology
Oceans and Seas
Metagenome/genetics
Antarctic Regions
*Bacteria/genetics/classification
Sulfonium Compounds/metabolism
Arctic Regions
Plankton/genetics
Phylogeny
RevDate: 2026-03-09
CmpDate: 2026-03-09
Lacticaseibacillus paracasei KBL382 contributes to the immunomodulation in THP-1 cells.
Journal of microbiology (Seoul, Korea), 64(2):e2509016.
Gut microbiome imbalance can induce inflammatory responses via Toll-like receptor 2 (TLR2) signaling pathways. Lactobacillus spp., popularly applied as probiotics in both humans and animals, have come into the spotlight for their strong immunomodulatory effects. We aimed to evaluate the immunomodulatory potential of live or pasteurized Lacticaseibacillus paracasei (L. paracasei) KBL382, isolated from healthy Korean individuals, in an in vitro monocytic THP-1 cell model. Live L. paracasei KBL382 significantly increased TLR2 and MyD88 expressions and induced IRAK1 expression, irrespective of lipopolysaccharide (LPS) stimulation (p < 0.05). Under LPS stimulation, THP-1 cells treated with live L. paracasei KBL382 showed significantly increased interleukin (IL)-6 and IL-10 levels (p < 0.05). Pasteurized L. paracasei exhibited a decrease in IL-12 levels (p < 0.05). Moreover, live L. paracasei KBL382 also markedly elevated A20 and SOCS1 expressions, the critical negative regulators of inflammation, regardless of LPS stimulation (p < 0.05). The expression of IRAK3, another negative regulator of inflammation, was increased in THP-1 cells with live L. paracasei KBL382 under LPS stimulation (p < 0.05). Our findings demonstrate that L. paracasei KBL382 contributes to the immunomodulation in THP-1 cells by coordinating both positive and negative regulatory signaling. L. paracasei KBL382 could be used as a promising probiotic strain for attenuating chronic inflammation through the gut-immune axis mechanisms.
Additional Links: PMID-41802805
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802805,
year = {2026},
author = {Kim, M and Jo, MJ and Park, S and Lee, SB and Jang, SJ and Lee, C and Kim, WK and Ko, G},
title = {Lacticaseibacillus paracasei KBL382 contributes to the immunomodulation in THP-1 cells.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {64},
number = {2},
pages = {e2509016},
doi = {10.71150/jm.2509016},
pmid = {41802805},
issn = {1976-3794},
support = {2021R1I1A1A01048923//National Research Foundation of Korea/ ; //Ministry of Education/ ; RS-2022-NR067344//Ministry of Science and ICT/ ; },
mesh = {Humans ; THP-1 Cells/immunology ; *Immunomodulation ; *Probiotics/pharmacology ; Interleukin-1 Receptor-Associated Kinases/metabolism/genetics ; Lipopolysaccharides/immunology/pharmacology ; *Lacticaseibacillus paracasei/immunology/physiology/isolation & purification ; Toll-Like Receptor 2/metabolism/genetics/immunology ; Monocytes/immunology/microbiology ; Interleukin-10/metabolism/immunology ; Interleukin-6/metabolism/immunology ; Suppressor of Cytokine Signaling 1 Protein/genetics/metabolism ; Signal Transduction ; Cytokines/metabolism ; Interleukin-12/metabolism ; Myeloid Differentiation Factor 88 ; },
abstract = {Gut microbiome imbalance can induce inflammatory responses via Toll-like receptor 2 (TLR2) signaling pathways. Lactobacillus spp., popularly applied as probiotics in both humans and animals, have come into the spotlight for their strong immunomodulatory effects. We aimed to evaluate the immunomodulatory potential of live or pasteurized Lacticaseibacillus paracasei (L. paracasei) KBL382, isolated from healthy Korean individuals, in an in vitro monocytic THP-1 cell model. Live L. paracasei KBL382 significantly increased TLR2 and MyD88 expressions and induced IRAK1 expression, irrespective of lipopolysaccharide (LPS) stimulation (p < 0.05). Under LPS stimulation, THP-1 cells treated with live L. paracasei KBL382 showed significantly increased interleukin (IL)-6 and IL-10 levels (p < 0.05). Pasteurized L. paracasei exhibited a decrease in IL-12 levels (p < 0.05). Moreover, live L. paracasei KBL382 also markedly elevated A20 and SOCS1 expressions, the critical negative regulators of inflammation, regardless of LPS stimulation (p < 0.05). The expression of IRAK3, another negative regulator of inflammation, was increased in THP-1 cells with live L. paracasei KBL382 under LPS stimulation (p < 0.05). Our findings demonstrate that L. paracasei KBL382 contributes to the immunomodulation in THP-1 cells by coordinating both positive and negative regulatory signaling. L. paracasei KBL382 could be used as a promising probiotic strain for attenuating chronic inflammation through the gut-immune axis mechanisms.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
THP-1 Cells/immunology
*Immunomodulation
*Probiotics/pharmacology
Interleukin-1 Receptor-Associated Kinases/metabolism/genetics
Lipopolysaccharides/immunology/pharmacology
*Lacticaseibacillus paracasei/immunology/physiology/isolation & purification
Toll-Like Receptor 2/metabolism/genetics/immunology
Monocytes/immunology/microbiology
Interleukin-10/metabolism/immunology
Interleukin-6/metabolism/immunology
Suppressor of Cytokine Signaling 1 Protein/genetics/metabolism
Signal Transduction
Cytokines/metabolism
Interleukin-12/metabolism
Myeloid Differentiation Factor 88
RevDate: 2026-03-09
Diet, Gut Microbiota, and Intestinal Permeability: Emerging Mechanisms in Hypertension Pathogenesis.
The Canadian journal of cardiology pii:S0828-282X(26)00246-1 [Epub ahead of print].
Hypertension is a leading contributor to global morbidity and mortality, arising from the interplay of genetic and environmental risk factors together with the dysregulation of multiple physiological systems involved in blood pressure control. Recent advances have established the gut as a central regulator, implicating the intestinal microbiota and barrier integrity in the modulation of blood pressure. Alterations in the gut microbial consortium, along with changes in levels of metabolites produced by the microbiota, have been associated with blood pressure regulation in both animal models and human studies. Key microbial metabolites, including short-chain fatty acids (SCFA), trimethylamine-N-oxide, and bile acids, influence endothelial function, immune activation, and renal signalling pathways. Concurrently, intestinal permeability facilitates the translocation of microbial products, such as lipopolysaccharides, triggering systemic inflammation, leading to renal and vascular dysfunction. Diet plays a pivotal role in shaping both microbiome composition and barrier integrity. Western-style diets rich in saturated fats, sugars, and processed additives promote gut dysbiosis and increased permeability, whereas fibre-rich, plant-based diets support microbial diversity, SCFA production, and tight-junction integrity. This review synthesises the current evidence linking diet, microbiota, and gut permeability to hypertension, integrating mechanistic insights from preclinical models with emerging human data. We propose a conceptual framework in which the gut serves as a modifiable target for the prevention and treatment of hypertension. By exploring dietary strategies that restore microbial balance and barrier function, this review underscores the potential of integrative, gut-targeted approaches to address a major global health burden.
Additional Links: PMID-41802666
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802666,
year = {2026},
author = {Vashisht, E and Nguyen, H and Marques, FZ and Snelson, M},
title = {Diet, Gut Microbiota, and Intestinal Permeability: Emerging Mechanisms in Hypertension Pathogenesis.},
journal = {The Canadian journal of cardiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cjca.2026.03.005},
pmid = {41802666},
issn = {1916-7075},
abstract = {Hypertension is a leading contributor to global morbidity and mortality, arising from the interplay of genetic and environmental risk factors together with the dysregulation of multiple physiological systems involved in blood pressure control. Recent advances have established the gut as a central regulator, implicating the intestinal microbiota and barrier integrity in the modulation of blood pressure. Alterations in the gut microbial consortium, along with changes in levels of metabolites produced by the microbiota, have been associated with blood pressure regulation in both animal models and human studies. Key microbial metabolites, including short-chain fatty acids (SCFA), trimethylamine-N-oxide, and bile acids, influence endothelial function, immune activation, and renal signalling pathways. Concurrently, intestinal permeability facilitates the translocation of microbial products, such as lipopolysaccharides, triggering systemic inflammation, leading to renal and vascular dysfunction. Diet plays a pivotal role in shaping both microbiome composition and barrier integrity. Western-style diets rich in saturated fats, sugars, and processed additives promote gut dysbiosis and increased permeability, whereas fibre-rich, plant-based diets support microbial diversity, SCFA production, and tight-junction integrity. This review synthesises the current evidence linking diet, microbiota, and gut permeability to hypertension, integrating mechanistic insights from preclinical models with emerging human data. We propose a conceptual framework in which the gut serves as a modifiable target for the prevention and treatment of hypertension. By exploring dietary strategies that restore microbial balance and barrier function, this review underscores the potential of integrative, gut-targeted approaches to address a major global health burden.},
}
RevDate: 2026-03-11
Differential effects of sulfide-induced transformation of biodegradable and conventional microplastics on sedimentary CO2 and CH4 emissions: Underlying microbiome-mediated mechanisms.
Environmental research, 298:124216 pii:S0013-9351(26)00546-3 [Epub ahead of print].
The accumulation of microplastics (MPs) in sediments presents serious ecological risks. Although sulfidation is a key aging process in anoxic environments, its impact on sedimentary CO2 and CH4 emissions and underlying microbiome-mediated mechanisms remains unclear, particularly for biodegradable versus conventional MPs. Sediment incubation experiments with pristine and sulfidation-aged polyethylene (PE) and polylactic acid (PLA) revealed distinct carbon-related greenhouse gases patterns driven by material-specific microbial responses. Compared to controls, pristine PLA significantly enhanced cumulative CO2 and CH4 emissions by 4.47- and 2.59-fold, respectively, accelerating the CH4 emission peak due to its rapid carbon release. Conversely, sulfidation-aged PLA (PLA-S) reversed this trend, reducing CO2 emissions by 61.5%. This suppression was linked to an enriched microbiome (e.g., Acidobacteriota, ester-hydrolyzing Myxococcota) adapted to acidic stress, nitrogen fixation, and pathogenicity, likely diverted carbon flows. In contrast, sulfidation-aged PE (PE-S) exhibited surface oxidation, which led to a 36.7% increase in CH4 emissions, along with higher dissolved organic carbon (DOC) and microbial metabolic quotient (qCO2). This shift correlated with the enrichment of alkane-degrading Methylomirabilota and Bacillota, potentially converting plastic-derived carbon into methane. These findings emphasize the necessity of considering MPs' natural aging (e.g., sulfidation) and material types (degradable vs. conventional) when assessing their ecological risks and roles in CO2 and CH4 emissions, revealing key microbiome mechanisms linking MPs to the global carbon cycle.
Additional Links: PMID-41802661
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802661,
year = {2026},
author = {Hu, J and He, W and Liu, Z and Qiao, Q and Zhao, L and Li, Y and Ma, M and Yu, H and Shi, L and Huang, J},
title = {Differential effects of sulfide-induced transformation of biodegradable and conventional microplastics on sedimentary CO2 and CH4 emissions: Underlying microbiome-mediated mechanisms.},
journal = {Environmental research},
volume = {298},
number = {},
pages = {124216},
doi = {10.1016/j.envres.2026.124216},
pmid = {41802661},
issn = {1096-0953},
abstract = {The accumulation of microplastics (MPs) in sediments presents serious ecological risks. Although sulfidation is a key aging process in anoxic environments, its impact on sedimentary CO2 and CH4 emissions and underlying microbiome-mediated mechanisms remains unclear, particularly for biodegradable versus conventional MPs. Sediment incubation experiments with pristine and sulfidation-aged polyethylene (PE) and polylactic acid (PLA) revealed distinct carbon-related greenhouse gases patterns driven by material-specific microbial responses. Compared to controls, pristine PLA significantly enhanced cumulative CO2 and CH4 emissions by 4.47- and 2.59-fold, respectively, accelerating the CH4 emission peak due to its rapid carbon release. Conversely, sulfidation-aged PLA (PLA-S) reversed this trend, reducing CO2 emissions by 61.5%. This suppression was linked to an enriched microbiome (e.g., Acidobacteriota, ester-hydrolyzing Myxococcota) adapted to acidic stress, nitrogen fixation, and pathogenicity, likely diverted carbon flows. In contrast, sulfidation-aged PE (PE-S) exhibited surface oxidation, which led to a 36.7% increase in CH4 emissions, along with higher dissolved organic carbon (DOC) and microbial metabolic quotient (qCO2). This shift correlated with the enrichment of alkane-degrading Methylomirabilota and Bacillota, potentially converting plastic-derived carbon into methane. These findings emphasize the necessity of considering MPs' natural aging (e.g., sulfidation) and material types (degradable vs. conventional) when assessing their ecological risks and roles in CO2 and CH4 emissions, revealing key microbiome mechanisms linking MPs to the global carbon cycle.},
}
RevDate: 2026-03-09
Microbiota metabolite lithocholic acid in cancer: Mechanisms and therapeutic potential.
Experimental cell research pii:S0014-4827(26)00098-4 [Epub ahead of print].
The human gut microbiome is centrally implicated in host disease and health control via the production of a range of bioactive metabolites. Of these, lithocholic acid (LCA), a derivative of microbial metabolism secondary bile acid, has received attention owing to its multifaceted functions in cancer. LCA, a hydrophobic microbiota-derived bile acid, was implicated in carcinogenicity and hepatotoxicity even in the ancient era. In this sense, studies have found a contrasting role of LCA as a tumor promoter or tumor suppressor based on the molecular environment and type of tumor. Antitumor effects of LCA have also been observed in various cancers such as breast, prostate, colon, and neuroblastoma. Interestingly, LCA induces selective apoptosis of cancer cells through intrinsic and extrinsic pathways but without damaging normal cells, and the process is partly caspase-dependent. Mechanistically, LCA induces endoplasmic reticulum (ER) stress response, induces autophagy in certain cancer cell lines, and inhibits mitochondrial function, all contributing to its cytotoxic effect. It also causes oxidative and nitrosative stress through downregulation of nuclear factor erythroid 2-related factor 2 (NRF2)/Kelch-like ECH-associated protein 1(Keap1) pathway and induction of inducible nitric oxide synthase (iNOS) mediated through TGR5 and Chimeric antigen receptor (CAR) receptor activation. Besides its cytostatic action on itself, LCA was determined to have the capability to modulate the tumor microenvironment through immunomodulation and anti-inflammation, which are behind its therapeutic actions. Via its action on nuclear receptors like the vitamin D receptor (VDR), LCA has been shown to inhibit proteasome activity, create pores in membranes, and alter calcium uptake and epithelial integrity under conditions of oxidative stress. Because of its selective anticancer action, receptor-mediated signal activity, and microbiota origin, LCA is a good cancer drug candidate. This review discusses primarily the molecular processes through which LCA regulates cancer pathogenesis and determines its therapeutic potential based on preclinical and clinical data.
Additional Links: PMID-41802534
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802534,
year = {2026},
author = {Darmadi, D and Muhame, AJ and Gerasimov, SG and Mirzaei, R and Karampoor, S},
title = {Microbiota metabolite lithocholic acid in cancer: Mechanisms and therapeutic potential.},
journal = {Experimental cell research},
volume = {},
number = {},
pages = {114981},
doi = {10.1016/j.yexcr.2026.114981},
pmid = {41802534},
issn = {1090-2422},
abstract = {The human gut microbiome is centrally implicated in host disease and health control via the production of a range of bioactive metabolites. Of these, lithocholic acid (LCA), a derivative of microbial metabolism secondary bile acid, has received attention owing to its multifaceted functions in cancer. LCA, a hydrophobic microbiota-derived bile acid, was implicated in carcinogenicity and hepatotoxicity even in the ancient era. In this sense, studies have found a contrasting role of LCA as a tumor promoter or tumor suppressor based on the molecular environment and type of tumor. Antitumor effects of LCA have also been observed in various cancers such as breast, prostate, colon, and neuroblastoma. Interestingly, LCA induces selective apoptosis of cancer cells through intrinsic and extrinsic pathways but without damaging normal cells, and the process is partly caspase-dependent. Mechanistically, LCA induces endoplasmic reticulum (ER) stress response, induces autophagy in certain cancer cell lines, and inhibits mitochondrial function, all contributing to its cytotoxic effect. It also causes oxidative and nitrosative stress through downregulation of nuclear factor erythroid 2-related factor 2 (NRF2)/Kelch-like ECH-associated protein 1(Keap1) pathway and induction of inducible nitric oxide synthase (iNOS) mediated through TGR5 and Chimeric antigen receptor (CAR) receptor activation. Besides its cytostatic action on itself, LCA was determined to have the capability to modulate the tumor microenvironment through immunomodulation and anti-inflammation, which are behind its therapeutic actions. Via its action on nuclear receptors like the vitamin D receptor (VDR), LCA has been shown to inhibit proteasome activity, create pores in membranes, and alter calcium uptake and epithelial integrity under conditions of oxidative stress. Because of its selective anticancer action, receptor-mediated signal activity, and microbiota origin, LCA is a good cancer drug candidate. This review discusses primarily the molecular processes through which LCA regulates cancer pathogenesis and determines its therapeutic potential based on preclinical and clinical data.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiome in colorectal cancer: recent advances and clinical implications.
Annals of coloproctology, 42(1):72-85.
The gut microbiome is not just a bystander of colorectal carcinogenesis but is an active driver of colorectal cancer (CRC). CRC-associated microbiome contributes in the tumorigenesis through chronic inflammation, formation of toxic metabolite and genotoxins, oncogenic signal activation, immune evasion, and barrier disruption-all reinforcing a tumor microenvironment. In contrast, beneficial microbiome supports the barrier-immune-metabolic axis by maintaining mucosal integrity and balanced immune tone. Despite extensive studies of microbiome-based CRC biomarkers, microbiome-based CRC biomarkers have not been yet ready for routine clinical use due to variation across populations and lack of standardization of key steps such as sampling, analysis, cutoffs, and interpretation. Microbiome-based therapies aim to change the overall intestinal ecosystem rather than simply adding or removing single strains. At present, dietary modulation and prebiotics are considered supportive measures, while probiotics or synbiotics are in preclinical stage. Fecal microbiota transplantation (FMT) still faces important challenges in effectiveness, standardization and safety. By its role in reshaping the tumor-host immune environment, FMT is viewed as a potential option for cancer therapy after further development through well-controlled clinical trials with careful safety monitoring.
Additional Links: PMID-41802308
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802308,
year = {2026},
author = {Han, JY and Kim, MJ and Park, JW and Jeong, SY},
title = {Gut microbiome in colorectal cancer: recent advances and clinical implications.},
journal = {Annals of coloproctology},
volume = {42},
number = {1},
pages = {72-85},
pmid = {41802308},
issn = {2287-9714},
abstract = {The gut microbiome is not just a bystander of colorectal carcinogenesis but is an active driver of colorectal cancer (CRC). CRC-associated microbiome contributes in the tumorigenesis through chronic inflammation, formation of toxic metabolite and genotoxins, oncogenic signal activation, immune evasion, and barrier disruption-all reinforcing a tumor microenvironment. In contrast, beneficial microbiome supports the barrier-immune-metabolic axis by maintaining mucosal integrity and balanced immune tone. Despite extensive studies of microbiome-based CRC biomarkers, microbiome-based CRC biomarkers have not been yet ready for routine clinical use due to variation across populations and lack of standardization of key steps such as sampling, analysis, cutoffs, and interpretation. Microbiome-based therapies aim to change the overall intestinal ecosystem rather than simply adding or removing single strains. At present, dietary modulation and prebiotics are considered supportive measures, while probiotics or synbiotics are in preclinical stage. Fecal microbiota transplantation (FMT) still faces important challenges in effectiveness, standardization and safety. By its role in reshaping the tumor-host immune environment, FMT is viewed as a potential option for cancer therapy after further development through well-controlled clinical trials with careful safety monitoring.},
}
RevDate: 2026-03-09
Off to a good start: Current gaps and priorities in early-life microbiome research.
FEMS microbiology reviews pii:8512260 [Epub ahead of print].
Early-life microbial exposures are essential for optimal development of human physiology. Yet, understanding of the human microbiome during pregnancy and childhood is still far from being complete. To identify knowledge gaps and establish research priorities, a multidisciplinary expert panel used the Delphi method for consensus development and conducted a literature search on early-life microbiome determinants. Responses from 55 researchers from an online survey were analyzed alongside keyword frequency from 20 501 publications. This approach enabled us to categorize existing evidence and highlight areas requiring investigation. While the main routes for mother-to-child bacterial transmission and their contributions to the newborn microbiome have been studied, many gaps remain. Priority areas include non-bacterial microbes, ecological principles of colonization, environmental and social influences, body sites beyond the gut, and factors affecting the maternal microbiome and its effects on the child's microbiome. Significance of factors such as hygiene habits, non-antibiotic medications, and pollution remains to be uncovered. Knowledge is also limited on postnatal microbial sharing via household contacts and shared environments (e.g. family members, peers) and the contribution of these pathways to microbiome assembly. We hope this report will guide and inspire future research into the early-life microbiome as a modifiable factor in reducing disease risk.
Additional Links: PMID-41802201
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802201,
year = {2026},
author = {Pettersen, VK and Ponsero, AJ and Jian, C and Riumin, A and Kurilshikov, A and Moyo, SJ and Justine, M and Klingenberg, C and Debelius, J and Valles-Colomer, M and Noordzij, HT and Zhernakova, A and Korpela, K and Esteban-Torres, M and Brusselaers, N},
title = {Off to a good start: Current gaps and priorities in early-life microbiome research.},
journal = {FEMS microbiology reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsre/fuag010},
pmid = {41802201},
issn = {1574-6976},
abstract = {Early-life microbial exposures are essential for optimal development of human physiology. Yet, understanding of the human microbiome during pregnancy and childhood is still far from being complete. To identify knowledge gaps and establish research priorities, a multidisciplinary expert panel used the Delphi method for consensus development and conducted a literature search on early-life microbiome determinants. Responses from 55 researchers from an online survey were analyzed alongside keyword frequency from 20 501 publications. This approach enabled us to categorize existing evidence and highlight areas requiring investigation. While the main routes for mother-to-child bacterial transmission and their contributions to the newborn microbiome have been studied, many gaps remain. Priority areas include non-bacterial microbes, ecological principles of colonization, environmental and social influences, body sites beyond the gut, and factors affecting the maternal microbiome and its effects on the child's microbiome. Significance of factors such as hygiene habits, non-antibiotic medications, and pollution remains to be uncovered. Knowledge is also limited on postnatal microbial sharing via household contacts and shared environments (e.g. family members, peers) and the contribution of these pathways to microbiome assembly. We hope this report will guide and inspire future research into the early-life microbiome as a modifiable factor in reducing disease risk.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Microalgal delivery of recombinant fish interferon modulates gut microbiota and enhances antiviral immunity in fish.
Journal of immunology (Baltimore, Md. : 1950), 215(2):.
Viral infections remain a challenge to aquaculture, resulting in severe economic losses and threatening fish health worldwide. As a key immunomodulatory and antiviral factor, interferon (IFN) plays a crucial role in regulating immune responses. We constructed a high-level expression strain of recombinant interferon (Rec-IFN) using Synechococcus sp. PCC 7002, which also served as a delivery system, and evaluated its efficacy as a dietary immunostimulant in gibel carp (Carassius gibelio) and zebrafish (Danio rerio). Analysis of the intestinal microbiome indicated that the Rec-IFN diet promoted beneficial bacteria such as Cetobacterium while reducing opportunistic pathogens including Aeromonas and Vibrio in gibel carp. Notably, after Cyprinid herpesvirus-2 (CyHV-2) infection, the Rec-IFN diet enhanced microbial connectivity, helping to preserve gut microbiota function. In zebrafish, the Rec-IFN diet increased species richness and evenness, while reducing opportunistic pathogens such as Vibrio. Transcriptomic analysis revealed specific activation of the Toll-like receptor signaling pathway and a reduction of immune overstimulation following infection in zebrafish. Our findings demonstrate that the Rec-IFN diet significantly enhanced the host IFN response and alleviated virus-induced damage to intestinal and immune organs, reduced viral load, and decreased mortality. This research offers a protective effect by reducing the severity of infections caused by both DNA virus (CyHV-2) and RNA virus (SVCV). It provides new insights into the application of Rec-IFN microalgae as an effective oral immunotherapeutic strategy for reducing losses from viral infections in aquaculture.
Additional Links: PMID-41802195
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41802195,
year = {2026},
author = {Liu, GP and Li, ZC and Li, Q and Zheng, ZG and Lin, FB and Zhang, GY and Zhang, ZM and Li, S and Li, T and Zhao, JD},
title = {Microalgal delivery of recombinant fish interferon modulates gut microbiota and enhances antiviral immunity in fish.},
journal = {Journal of immunology (Baltimore, Md. : 1950)},
volume = {215},
number = {2},
pages = {},
doi = {10.1093/jimmun/vkaf304},
pmid = {41802195},
issn = {1550-6606},
support = {XDB0730300//Strategic Priority Research Program of the Chinese Academy of Sciences/ ; 92251304//National Natural Science Foundation of China/ ; 202001539//Qidong-SLS Innovation Fund/ ; 32322086//Peking University, National Excellent Youth Science Fund/ ; 32073009//National Natural Science Foundation of China/ ; //Youth Innovation Promotion Association/ ; 2023YFD2400201//National Key Research and Development Program of China/ ; 32173023//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/immunology/drug effects ; Zebrafish/immunology ; *Fish Diseases/immunology ; *Interferons/genetics/immunology/administration & dosage ; Recombinant Proteins/immunology/genetics ; *Microalgae ; *Antiviral Agents ; *Herpesviridae Infections/immunology/veterinary ; Herpesviridae/immunology ; Carps/immunology ; },
abstract = {Viral infections remain a challenge to aquaculture, resulting in severe economic losses and threatening fish health worldwide. As a key immunomodulatory and antiviral factor, interferon (IFN) plays a crucial role in regulating immune responses. We constructed a high-level expression strain of recombinant interferon (Rec-IFN) using Synechococcus sp. PCC 7002, which also served as a delivery system, and evaluated its efficacy as a dietary immunostimulant in gibel carp (Carassius gibelio) and zebrafish (Danio rerio). Analysis of the intestinal microbiome indicated that the Rec-IFN diet promoted beneficial bacteria such as Cetobacterium while reducing opportunistic pathogens including Aeromonas and Vibrio in gibel carp. Notably, after Cyprinid herpesvirus-2 (CyHV-2) infection, the Rec-IFN diet enhanced microbial connectivity, helping to preserve gut microbiota function. In zebrafish, the Rec-IFN diet increased species richness and evenness, while reducing opportunistic pathogens such as Vibrio. Transcriptomic analysis revealed specific activation of the Toll-like receptor signaling pathway and a reduction of immune overstimulation following infection in zebrafish. Our findings demonstrate that the Rec-IFN diet significantly enhanced the host IFN response and alleviated virus-induced damage to intestinal and immune organs, reduced viral load, and decreased mortality. This research offers a protective effect by reducing the severity of infections caused by both DNA virus (CyHV-2) and RNA virus (SVCV). It provides new insights into the application of Rec-IFN microalgae as an effective oral immunotherapeutic strategy for reducing losses from viral infections in aquaculture.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Gastrointestinal Microbiome/immunology/drug effects
Zebrafish/immunology
*Fish Diseases/immunology
*Interferons/genetics/immunology/administration & dosage
Recombinant Proteins/immunology/genetics
*Microalgae
*Antiviral Agents
*Herpesviridae Infections/immunology/veterinary
Herpesviridae/immunology
Carps/immunology
RevDate: 2026-03-09
Discovering naturally occurring antifreeze peptides from microbiome by integrating protein language models and molecular dynamics simulation.
Journal of materials chemistry. B [Epub ahead of print].
Antifreeze peptides inhibit ice crystal growth and recrystallization, and are promising components of cryoprotective formulations for cell, tissue, and food preservation, as well as anti-icing surface coatings. However, the discovery of new antifreeze peptides has been hindered by their sequence diversity and the limited scalability of experimental screening. In this study, we identify novel antifreeze peptide candidates from a microbiome-derived sequence library using ensemble machine learning and molecular dynamics (MD) simulations. We developed an ensemble classifier composed of 10 adapter-tuned protein-language models and a random forest meta-learner. After training on a curated dataset of 73 766 sequences, we applied this ensemble to 56 008 amino acid sequences from an Arctic microbiome library to identify antifreeze peptide candidates. Structural prediction yields a diverse range of conformations for six selected candidates, including α-helices, coils, and combinations of both. To evaluate their functional relevance, atomistic MD simulations were conducted to assess conformational stability and solvent interactions under freezing conditions. One candidate shows persistent helicity, surface amphipathicity, and an organized hydration pattern consistent with structural signatures reported for ice-binding helices. These findings expand the known landscape of antifreeze peptides and highlight a scalable strategy for discovering functional peptides from complex biological sources.
Additional Links: PMID-41801733
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41801733,
year = {2026},
author = {Imam, IA and Morey, T and Jiang, Y and Wang, D and Xu, D and Shao, Q},
title = {Discovering naturally occurring antifreeze peptides from microbiome by integrating protein language models and molecular dynamics simulation.},
journal = {Journal of materials chemistry. B},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5tb02758f},
pmid = {41801733},
issn = {2050-7518},
abstract = {Antifreeze peptides inhibit ice crystal growth and recrystallization, and are promising components of cryoprotective formulations for cell, tissue, and food preservation, as well as anti-icing surface coatings. However, the discovery of new antifreeze peptides has been hindered by their sequence diversity and the limited scalability of experimental screening. In this study, we identify novel antifreeze peptide candidates from a microbiome-derived sequence library using ensemble machine learning and molecular dynamics (MD) simulations. We developed an ensemble classifier composed of 10 adapter-tuned protein-language models and a random forest meta-learner. After training on a curated dataset of 73 766 sequences, we applied this ensemble to 56 008 amino acid sequences from an Arctic microbiome library to identify antifreeze peptide candidates. Structural prediction yields a diverse range of conformations for six selected candidates, including α-helices, coils, and combinations of both. To evaluate their functional relevance, atomistic MD simulations were conducted to assess conformational stability and solvent interactions under freezing conditions. One candidate shows persistent helicity, surface amphipathicity, and an organized hydration pattern consistent with structural signatures reported for ice-binding helices. These findings expand the known landscape of antifreeze peptides and highlight a scalable strategy for discovering functional peptides from complex biological sources.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Impact of proton pump inhibitors on immunotherapy is modulated by prior chemotherapy and linked to gut microbiome-immune cell signatures.
Cancer immunology, immunotherapy : CII, 75(4):.
Proton pump inhibitors (PPIs) are one of the most widely used medications in the world. They have been associated with an altered microbiome, which is demonstrated to be important for immune checkpoint inhibitor (ICI) response. We sought to determine whether PPI use was associated with shorter overall survival (OS) in patients treated with ICIs, and whether these changes were associated with altered microbiomes and immune cell composition. Our retrospective study of patients with advanced cancer (n = 1078) evaluated the impact of PPI use on OS. We also analyzed stool samples from melanoma patients treated with ICIs (n = 42) and stool and blood samples from patients with non-small cell lung cancer (NSCLC) and renal cell carcinoma treated with ICIs (n = 8). With the data from our prospective study, we assessed microbiome composition from stool samples using metagenomic whole-genome shotgun; immune cell populations from blood samples were determined using CyTOF. Associations between PPI use, clinical outcomes, the microbiome, and immune cell populations were evaluated using survival analyses, diversity metrics, and multivariable models. PPI use was associated with shorter OS in patients with advanced cancers treated with ICIs, with the strongest effects seen in melanoma. PPI use was associated with worse clinical outcomes and microbiome alterations in patients with advanced cancers treated with ICIs, suggesting that its use may influence the efficacy of immunotherapy; prospective studies implicate its effect on the microbiome. These findings underscore the importance of considering the microbiome and concomitant medications when to enhance treatment response and efficacy.
Additional Links: PMID-41801404
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41801404,
year = {2026},
author = {Petouhoff, A and Hicks, R and Husain, M and Hoyd, R and Xu, M and Dravillas, C and Patel, SH and Johns, A and Grogan, M and Li, M and Lopez, G and Miah, A and Liu, Y and Muniak, M and Schmidt, M and Das, A and Lathrop, H and Das, P and Secor, A and Haddad, T and Tinoco, G and Carbone, D and Kendra, K and Otterson, GA and Presley, CJ and Mace, T and Spakowicz, D and Owen, DH},
title = {Impact of proton pump inhibitors on immunotherapy is modulated by prior chemotherapy and linked to gut microbiome-immune cell signatures.},
journal = {Cancer immunology, immunotherapy : CII},
volume = {75},
number = {4},
pages = {},
pmid = {41801404},
issn = {1432-0851},
support = {P30CA016058/NH/NIH HHS/United States ; UL1TR002733/TR/NCATS NIH HHS/United States ; Innovator Award 1046611//American Lung Association/ ; Research Scholar Award RSG-23-1023205//American Cancer Society/ ; },
mesh = {Humans ; *Proton Pump Inhibitors/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/drug effects/immunology ; Male ; Female ; Middle Aged ; Aged ; *Immunotherapy/methods ; Retrospective Studies ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; Prospective Studies ; *Neoplasms/drug therapy/immunology/mortality ; Melanoma/drug therapy/immunology ; Carcinoma, Non-Small-Cell Lung/drug therapy/immunology ; },
abstract = {Proton pump inhibitors (PPIs) are one of the most widely used medications in the world. They have been associated with an altered microbiome, which is demonstrated to be important for immune checkpoint inhibitor (ICI) response. We sought to determine whether PPI use was associated with shorter overall survival (OS) in patients treated with ICIs, and whether these changes were associated with altered microbiomes and immune cell composition. Our retrospective study of patients with advanced cancer (n = 1078) evaluated the impact of PPI use on OS. We also analyzed stool samples from melanoma patients treated with ICIs (n = 42) and stool and blood samples from patients with non-small cell lung cancer (NSCLC) and renal cell carcinoma treated with ICIs (n = 8). With the data from our prospective study, we assessed microbiome composition from stool samples using metagenomic whole-genome shotgun; immune cell populations from blood samples were determined using CyTOF. Associations between PPI use, clinical outcomes, the microbiome, and immune cell populations were evaluated using survival analyses, diversity metrics, and multivariable models. PPI use was associated with shorter OS in patients with advanced cancers treated with ICIs, with the strongest effects seen in melanoma. PPI use was associated with worse clinical outcomes and microbiome alterations in patients with advanced cancers treated with ICIs, suggesting that its use may influence the efficacy of immunotherapy; prospective studies implicate its effect on the microbiome. These findings underscore the importance of considering the microbiome and concomitant medications when to enhance treatment response and efficacy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Proton Pump Inhibitors/therapeutic use/pharmacology
*Gastrointestinal Microbiome/drug effects/immunology
Male
Female
Middle Aged
Aged
*Immunotherapy/methods
Retrospective Studies
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
Prospective Studies
*Neoplasms/drug therapy/immunology/mortality
Melanoma/drug therapy/immunology
Carcinoma, Non-Small-Cell Lung/drug therapy/immunology
RevDate: 2026-03-09
CmpDate: 2026-03-09
Earthworm gut microbiome promotes biodegradation of albendazole in soil.
Crop health, 4(1):.
The excretion of the anthelmintic drug albendazole (ALB) from treated animals into the soil, as well as its widespread application as a fungicide, poses a serious ecological risk to the soil environment. In this study, we investigated the degradation of ALB in soil and its bioaccumulation in earthworms, changes in the microbiome and degradation genes, and the effect of zinc oxide nanoparticles on the degradation and enrichment behaviors of ALB and microbial community structure and function. Our findings showed that ALB selectively enriched specific albendazole degradation genes (i.e., hmr and ami) in the earthworm, preferentially activating the pathways associated with sulfur reduction, amination of ALB sulfone, and hydroxylation of ALB. Metagenomic analysis revealed that the relative abundances of ppo, xylA, cutC, and nfsl in the earthworm gut were 0.19-52.64-fold higher in the ALB treatment than in the control, indicating their potential dominance in ALB biodegradation. Network analysis further identified potential bacterial hosts carrying biodegradation genes and albendazole degradation genes. Notably, Sphaerobacter, Saccharothrix, Actinomadura, and Nocardia were recognized as potential dual hosts of biodegradation genes and albendazole degradation genes, displaying a 0.05-1.32-fold elevation in relative abundance in ALB-treated earthworm guts compared to the control. Additionally, ZnO nanoparticles were found to reduce ALB bioaccumulation in earthworms and accelerate its dissipation in soil. These findings provide novel insights into the bioremediation mechanisms of pesticides in soil-earthworm ecosystems.
Additional Links: PMID-41801284
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41801284,
year = {2026},
author = {Wang, J and Ge, H and Liu, Y and Huang, C and Zhang, L and Yu, Y and Xu, L and Fang, H},
title = {Earthworm gut microbiome promotes biodegradation of albendazole in soil.},
journal = {Crop health},
volume = {4},
number = {1},
pages = {},
pmid = {41801284},
issn = {2948-1945},
support = {2023YFD1902903//National Key Research and Development Program of China/ ; 42177252//National Natural Science Foundation of China/ ; 2023C02039-01//Leading Goose" R&D program of Zhejiang Province of China/ ; },
abstract = {The excretion of the anthelmintic drug albendazole (ALB) from treated animals into the soil, as well as its widespread application as a fungicide, poses a serious ecological risk to the soil environment. In this study, we investigated the degradation of ALB in soil and its bioaccumulation in earthworms, changes in the microbiome and degradation genes, and the effect of zinc oxide nanoparticles on the degradation and enrichment behaviors of ALB and microbial community structure and function. Our findings showed that ALB selectively enriched specific albendazole degradation genes (i.e., hmr and ami) in the earthworm, preferentially activating the pathways associated with sulfur reduction, amination of ALB sulfone, and hydroxylation of ALB. Metagenomic analysis revealed that the relative abundances of ppo, xylA, cutC, and nfsl in the earthworm gut were 0.19-52.64-fold higher in the ALB treatment than in the control, indicating their potential dominance in ALB biodegradation. Network analysis further identified potential bacterial hosts carrying biodegradation genes and albendazole degradation genes. Notably, Sphaerobacter, Saccharothrix, Actinomadura, and Nocardia were recognized as potential dual hosts of biodegradation genes and albendazole degradation genes, displaying a 0.05-1.32-fold elevation in relative abundance in ALB-treated earthworm guts compared to the control. Additionally, ZnO nanoparticles were found to reduce ALB bioaccumulation in earthworms and accelerate its dissipation in soil. These findings provide novel insights into the bioremediation mechanisms of pesticides in soil-earthworm ecosystems.},
}
RevDate: 2026-03-09
Playgrounds as microbial interfaces: strategies to enhance soil microbiomes and support healthy childhoods.
mSystems [Epub ahead of print].
Emerging evidence suggests that reduced exposure to biodiversity, including rich environmental microbiota, is associated with negative outcomes in the health and well-being of children. Biodiversity loss not only impacts individual health but also poses significant threats to planetary health. It destabilizes systems that regulate climate, purify air and water, maintain soil fertility, and support plant and microbial life essential for environmental health. Here, we review the scientific evidence on microbiome-supportive strategies in eco-centric, child-friendly playground environments. Investigating how environmental features influence soil microbiomes and exposure pathways could provide insights into how playgrounds function as living interfaces. These are places where environmental microbes shape children's microbial colonization patterns, immune and endocrine regulatory systems, while also contributing to ecosystem services such as biodiversity support and pollutant mitigation-particularly relevant given that many pollutants are known to disrupt immune and endocrine functions in children. These dynamics have far-reaching implications for child well-being, preventive health strategies, physical activity, environmental literacy, and broader sustainability. A multi-omic systems approach offers a critical pathway to uncover the ecological and health-related impacts of nature-associated microbial exposure and characterize host-microbiome interactions underlying immune and endocrine regulation, brain development, cognition, and stress-related disorders. Our review highlights a lack of such integrative studies, underscoring the need to advance this line of research to inform evidence-based, sustainable, and health-promoting urban design.
Additional Links: PMID-41801038
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41801038,
year = {2026},
author = {Manninen, J and Korhonen, A and Johnson, KL and Tahvonen, O and Luukkonen, A and Saarenpää, M and Puhakka, R and Uimonen, L and Kummola, L and Skevaki, C and Renz, H and Rajaniemi, J and Laitinen, OH and Roslund, MI},
title = {Playgrounds as microbial interfaces: strategies to enhance soil microbiomes and support healthy childhoods.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0166225},
doi = {10.1128/msystems.01662-25},
pmid = {41801038},
issn = {2379-5077},
abstract = {Emerging evidence suggests that reduced exposure to biodiversity, including rich environmental microbiota, is associated with negative outcomes in the health and well-being of children. Biodiversity loss not only impacts individual health but also poses significant threats to planetary health. It destabilizes systems that regulate climate, purify air and water, maintain soil fertility, and support plant and microbial life essential for environmental health. Here, we review the scientific evidence on microbiome-supportive strategies in eco-centric, child-friendly playground environments. Investigating how environmental features influence soil microbiomes and exposure pathways could provide insights into how playgrounds function as living interfaces. These are places where environmental microbes shape children's microbial colonization patterns, immune and endocrine regulatory systems, while also contributing to ecosystem services such as biodiversity support and pollutant mitigation-particularly relevant given that many pollutants are known to disrupt immune and endocrine functions in children. These dynamics have far-reaching implications for child well-being, preventive health strategies, physical activity, environmental literacy, and broader sustainability. A multi-omic systems approach offers a critical pathway to uncover the ecological and health-related impacts of nature-associated microbial exposure and characterize host-microbiome interactions underlying immune and endocrine regulation, brain development, cognition, and stress-related disorders. Our review highlights a lack of such integrative studies, underscoring the need to advance this line of research to inform evidence-based, sustainable, and health-promoting urban design.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
[The gut microbiome in obesity: new horizons in personalized medicine].
Terapevticheskii arkhiv, 98(2):92-98.
Currently, disturbances in the composition and metabolic activity of the intestinal microbiota are considered a key modifiable factor in obesity and associated metabolic disorders. This review summarizes data on the characteristics and variability of the microbiota composition in individuals with obesity. The main mechanisms linking dysbiosis to metabolic disorders are discussed: changes in the production of short-chain fatty acids and other microbial metabolites, as well as the contribution of lipopolysaccharide-induced chronic inflammation. The influence of the microbiota on the regulation of appetite and eating behavior through the microbiota-gut-brain axis and intestinal hormones is discussed separately. Current approaches to the diagnosis of dysbiosis and potential strategies for correcting microbiome-associated disorders in obesity in the context of personalized medicine are presented.
Additional Links: PMID-41801026
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41801026,
year = {2026},
author = {Starodubova, AV and Kislyak, OA and Demidova, TY and Nikitin, IG and Leonov, GE},
title = {[The gut microbiome in obesity: new horizons in personalized medicine].},
journal = {Terapevticheskii arkhiv},
volume = {98},
number = {2},
pages = {92-98},
doi = {10.26442/00403660.2026.02.203596},
pmid = {41801026},
issn = {0040-3660},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Obesity/microbiology/metabolism/therapy/physiopathology ; *Precision Medicine/methods ; *Dysbiosis/microbiology ; },
abstract = {Currently, disturbances in the composition and metabolic activity of the intestinal microbiota are considered a key modifiable factor in obesity and associated metabolic disorders. This review summarizes data on the characteristics and variability of the microbiota composition in individuals with obesity. The main mechanisms linking dysbiosis to metabolic disorders are discussed: changes in the production of short-chain fatty acids and other microbial metabolites, as well as the contribution of lipopolysaccharide-induced chronic inflammation. The influence of the microbiota on the regulation of appetite and eating behavior through the microbiota-gut-brain axis and intestinal hormones is discussed separately. Current approaches to the diagnosis of dysbiosis and potential strategies for correcting microbiome-associated disorders in obesity in the context of personalized medicine are presented.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Obesity/microbiology/metabolism/therapy/physiopathology
*Precision Medicine/methods
*Dysbiosis/microbiology
RevDate: 2026-03-09
CmpDate: 2026-03-09
A yeast synthetic biotic platform for delivery of therapeutic nanobodies to ameliorate gastrointestinal inflammation.
Disease models & mechanisms, 19(2):.
Protein-based pharmaceuticals, such as engineered antibodies, form a major drug class of steadily increasing market share. However, these biologic medicines are costly to manufacture, are subject to strict supply chain and storage constraints, and often require invasive administration routes. Engineered microbes that secrete bioactive products directly within the microbiome milieu may mitigate these challenges. Here, we describe a cell microfactory platform based on the probiotic yeast Saccharomyces boulardii for the production of nanobody biologics in the gastrointestinal (GI) tract. High-level secretion of nanobodies by S. boulardii was achieved by optimizing promoters, secretion signals and antibody formats. In mice, oral gavage of S. boulardii allowed efficient and transient colonization of the colonic compartment, and in situ production of a therapeutic nanobody directed against tumor necrosis factor (TNF). In a mouse model of chemical-induced colitis, GI-delivery of anti-murine TNF nanobody via live S. boulardii improved both survival and disease severity without causing overt perturbation of microbiome composition. These results position S. boulardii as a synthetic biotic platform for the in situ production and delivery of protein-based therapeutics to the GI tract.
Additional Links: PMID-41800924
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800924,
year = {2026},
author = {Palou, R and van der Sloot, AM and Fiebig, AA and Zangara, MT and Sangwan, N and Sánchez-Osuna, M and Ilyas, B and Zubyk, H and Cook, M and Wright, GD and Coombes, BK and Tyers, M},
title = {A yeast synthetic biotic platform for delivery of therapeutic nanobodies to ameliorate gastrointestinal inflammation.},
journal = {Disease models & mechanisms},
volume = {19},
number = {2},
pages = {},
doi = {10.1242/dmm.052620},
pmid = {41800924},
issn = {1754-8411},
support = {//Weston Family Foundation/ ; //Genome Canada/ ; PJT-180315/CAPMC/CIHR/Canada ; FDN-167277/CAPMC/CIHR/Canada ; //Genome Quebec/ ; },
mesh = {Animals ; *Single-Domain Antibodies/therapeutic use/administration & dosage/pharmacology ; *Saccharomyces boulardii/metabolism ; Colitis/pathology/drug therapy/microbiology ; *Inflammation/pathology/drug therapy ; Mice, Inbred C57BL ; Tumor Necrosis Factor-alpha/metabolism/immunology ; *Gastrointestinal Tract/pathology/microbiology ; Mice ; *Drug Delivery Systems ; },
abstract = {Protein-based pharmaceuticals, such as engineered antibodies, form a major drug class of steadily increasing market share. However, these biologic medicines are costly to manufacture, are subject to strict supply chain and storage constraints, and often require invasive administration routes. Engineered microbes that secrete bioactive products directly within the microbiome milieu may mitigate these challenges. Here, we describe a cell microfactory platform based on the probiotic yeast Saccharomyces boulardii for the production of nanobody biologics in the gastrointestinal (GI) tract. High-level secretion of nanobodies by S. boulardii was achieved by optimizing promoters, secretion signals and antibody formats. In mice, oral gavage of S. boulardii allowed efficient and transient colonization of the colonic compartment, and in situ production of a therapeutic nanobody directed against tumor necrosis factor (TNF). In a mouse model of chemical-induced colitis, GI-delivery of anti-murine TNF nanobody via live S. boulardii improved both survival and disease severity without causing overt perturbation of microbiome composition. These results position S. boulardii as a synthetic biotic platform for the in situ production and delivery of protein-based therapeutics to the GI tract.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Single-Domain Antibodies/therapeutic use/administration & dosage/pharmacology
*Saccharomyces boulardii/metabolism
Colitis/pathology/drug therapy/microbiology
*Inflammation/pathology/drug therapy
Mice, Inbred C57BL
Tumor Necrosis Factor-alpha/metabolism/immunology
*Gastrointestinal Tract/pathology/microbiology
Mice
*Drug Delivery Systems
RevDate: 2026-03-09
16S rRNA Amplicon Sequencing of the Intraoperative Surgical Site Demonstrates an Aberrant Microbiota Which Can Predict Colorectal Surgical Site Infection.
ANZ journal of surgery [Epub ahead of print].
INTRODUCTION: Surgical Site Infection (SSI) of an abdominal incision is a dreaded infectious complication following colorectal surgery. Understanding the intraoperative microbiology holds the key to prevention. Genomic sequencing has revolutionised culture-independent techniques, allowing for a more sensitive tool in microbial detection. The purpose of this study is to determine whether an aberrant microbiota is present within the intraoperative surgical site in patients that develop an SSI.
METHODS: The subcutaneous abdominal surgical site of patients undergoing elective bowel resection was opportunistically sampled, following fascial closure. DNA was recovered from the swabs and used for 16S rRNA gene amplicon sequencing. The intraoperative microbiota was compared in those with and without a subsequent SSI with focus on alpha diversity and beta diversity, as well as taxonomic composition.
RESULTS: 16/123 patients developed an SSI. The bacterial profile within the surgical site showed a strong presence of obligate anaerobes in all patients. Chao1, Shannon, and Simpson measures of alpha diversity from the intraoperative swabs were all significantly increased in SSI patients (p = 0.05, 0.05 and 0.05, respectively). Beta diversity demonstrated no significant separation between patients (Bray-Curtis dissimilarity index, PERMANOVA p = 0.394).
CONCLUSIONS: To the best of our knowledge this is the first study to demonstrate an aberrant intraoperative microbiota of the surgical site associated with subsequent infection. Pending validation studies, this provides a target for the strategic manipulation of the surgical site to reduce the burden of infection.
Additional Links: PMID-41800916
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800916,
year = {2026},
author = {Vishnoi, V and Hoedt, EC and Zhao, M and Carroll, R and Kanakaratne, S and Lott, N and Pockney, P and Smith, SR and Keely, S},
title = {16S rRNA Amplicon Sequencing of the Intraoperative Surgical Site Demonstrates an Aberrant Microbiota Which Can Predict Colorectal Surgical Site Infection.},
journal = {ANZ journal of surgery},
volume = {},
number = {},
pages = {},
doi = {10.1111/ans.70578},
pmid = {41800916},
issn = {1445-2197},
support = {Doctor in Training Grant//Avant Foundation/ ; },
abstract = {INTRODUCTION: Surgical Site Infection (SSI) of an abdominal incision is a dreaded infectious complication following colorectal surgery. Understanding the intraoperative microbiology holds the key to prevention. Genomic sequencing has revolutionised culture-independent techniques, allowing for a more sensitive tool in microbial detection. The purpose of this study is to determine whether an aberrant microbiota is present within the intraoperative surgical site in patients that develop an SSI.
METHODS: The subcutaneous abdominal surgical site of patients undergoing elective bowel resection was opportunistically sampled, following fascial closure. DNA was recovered from the swabs and used for 16S rRNA gene amplicon sequencing. The intraoperative microbiota was compared in those with and without a subsequent SSI with focus on alpha diversity and beta diversity, as well as taxonomic composition.
RESULTS: 16/123 patients developed an SSI. The bacterial profile within the surgical site showed a strong presence of obligate anaerobes in all patients. Chao1, Shannon, and Simpson measures of alpha diversity from the intraoperative swabs were all significantly increased in SSI patients (p = 0.05, 0.05 and 0.05, respectively). Beta diversity demonstrated no significant separation between patients (Bray-Curtis dissimilarity index, PERMANOVA p = 0.394).
CONCLUSIONS: To the best of our knowledge this is the first study to demonstrate an aberrant intraoperative microbiota of the surgical site associated with subsequent infection. Pending validation studies, this provides a target for the strategic manipulation of the surgical site to reduce the burden of infection.},
}
RevDate: 2026-03-09
Dysbiosis of fecal virome in pediatric Crohn's disease and its dynamic changes during infliximab therapy.
mSystems [Epub ahead of print].
UNLABELLED: The gut virome is an emerging but underexplored component of the human microbiota, especially in pediatric Crohn's disease (CD). This study aimed to characterize the fecal virome in children with CD and evaluate its association with clinical response to infliximab (IFX) therapy. A total of 85 participants, including 60 pediatric CD patients and 25 healthy controls (HC), were recruited. Among the CD patients, 53 received ≥3 IFX infusions, 41 achieved remission (IFX-R), and 12 did not (IFX-NR). Viral-like particles in fecal samples were enriched and profiled by metagenomic sequencing, while bacterial communities were assessed via 16S rRNA gene sequencing. Pediatric CD patients exhibited significantly reduced viral richness and altered viral community compared to HCs. Functional analyses revealed that CD patients exhibit a shift in fecal virome function from DNA repair to viral replication and assembly. Trans-kingdom correlations were disrupted in CD, particularly between Torque teno viruses and beneficial bacteria, such as Blautia. An integrated machine learning model combining viral and bacterial markers achieved a certain level of diagnostic accuracy for pediatric CD (area under the curve [AUC] = 89.3%). IFX treatment influences the gut virome, with remission associated with higher abundances of Microviridae and Siphoviridae, while Anelloviridae, Myoviridae, and Podoviridae were enriched in IFX-NR at baseline. These findings suggest the virome as a potential biomarker for predicting clinical outcome in pediatric CD, offering a novel avenue for disease diagnosis and personalized treatment strategies.
IMPORTANCE: Crohn's disease (CD) in children poses a growing clinical challenge, with increasing incidence and variable response to biologic therapies such as infliximab (IFX). While gut bacterial dysbiosis has been extensively studied, the role of the gut virome in pediatric CD remains largely unexplored. This study provides the first longitudinal characterization of the fecal virome in children with CD undergoing IFX therapy. We reveal distinct viral community patterns, functional alterations, and virus-bacteria interactions in pediatric CD patients. Notably, integration of virome and bacteriome profiles enhances diagnostic accuracy, offering a promising avenue for predictive biomarker development. Furthermore, virome changes may be associated with the IFX treatment outcomes in children with CD. These findings highlight the gut virome as a critical but overlooked dimension of host-microbiome interactions in pediatric CD, with potential implications for personalized therapy and mechanistic understanding of treatment resistance.
Additional Links: PMID-41800893
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800893,
year = {2026},
author = {Ge, T and Zhao, T and Ruan, Y and Ye, L and Xiao, Y and Xiao, F and Li, Y and Li, X and Wang, R and Hu, H and Lu, C and Sun, H and Zhang, C and Yu, G and Zhang, T},
title = {Dysbiosis of fecal virome in pediatric Crohn's disease and its dynamic changes during infliximab therapy.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0148925},
doi = {10.1128/msystems.01489-25},
pmid = {41800893},
issn = {2379-5077},
abstract = {UNLABELLED: The gut virome is an emerging but underexplored component of the human microbiota, especially in pediatric Crohn's disease (CD). This study aimed to characterize the fecal virome in children with CD and evaluate its association with clinical response to infliximab (IFX) therapy. A total of 85 participants, including 60 pediatric CD patients and 25 healthy controls (HC), were recruited. Among the CD patients, 53 received ≥3 IFX infusions, 41 achieved remission (IFX-R), and 12 did not (IFX-NR). Viral-like particles in fecal samples were enriched and profiled by metagenomic sequencing, while bacterial communities were assessed via 16S rRNA gene sequencing. Pediatric CD patients exhibited significantly reduced viral richness and altered viral community compared to HCs. Functional analyses revealed that CD patients exhibit a shift in fecal virome function from DNA repair to viral replication and assembly. Trans-kingdom correlations were disrupted in CD, particularly between Torque teno viruses and beneficial bacteria, such as Blautia. An integrated machine learning model combining viral and bacterial markers achieved a certain level of diagnostic accuracy for pediatric CD (area under the curve [AUC] = 89.3%). IFX treatment influences the gut virome, with remission associated with higher abundances of Microviridae and Siphoviridae, while Anelloviridae, Myoviridae, and Podoviridae were enriched in IFX-NR at baseline. These findings suggest the virome as a potential biomarker for predicting clinical outcome in pediatric CD, offering a novel avenue for disease diagnosis and personalized treatment strategies.
IMPORTANCE: Crohn's disease (CD) in children poses a growing clinical challenge, with increasing incidence and variable response to biologic therapies such as infliximab (IFX). While gut bacterial dysbiosis has been extensively studied, the role of the gut virome in pediatric CD remains largely unexplored. This study provides the first longitudinal characterization of the fecal virome in children with CD undergoing IFX therapy. We reveal distinct viral community patterns, functional alterations, and virus-bacteria interactions in pediatric CD patients. Notably, integration of virome and bacteriome profiles enhances diagnostic accuracy, offering a promising avenue for predictive biomarker development. Furthermore, virome changes may be associated with the IFX treatment outcomes in children with CD. These findings highlight the gut virome as a critical but overlooked dimension of host-microbiome interactions in pediatric CD, with potential implications for personalized therapy and mechanistic understanding of treatment resistance.},
}
RevDate: 2026-03-11
CmpDate: 2026-03-11
Put your money where your mouth is: Surveillance of antibiotic resistance within the commensal Neisseria.
bioRxiv : the preprint server for biology.
Commensal Neisseria species are major reservoirs of adaptive genetic variation, including antimicrobial resistance, for their pathogenic relatives, yet they remain poorly characterized. This gap limits our ability to anticipate resistance mechanisms that may ultimately emerge Neisseria gonorrhoeae and N. meningitidis. Here, we analyzed 166 novel commensal Neisseria isolates collected from 31 study participants and measured minimum inhibitory concentrations (MICs) for seven antimicrobials: azithromycin, cefixime, ceftriaxone, ciprofloxacin, doxycycline, and gentamicin. Resistance, defined using the Clinical and Laboratory Standards Institute (CLSI) guidelines, was highly prevalent for azithromycin (76%) and doxycycline (52%), while no resistance to gentamicin was observed. High-level doxycycline resistance was always associated with inheritance of tetM. Reduced susceptibility to azithromycin was linked to an MtrD K823E substitution, and reduced susceptibility to ciprofloxacin was associated with GyrA T91I (N. subflava) or S91V (N. mucosa). The PenA 312M mutation was associated with significantly elevated ceftriaxone and cefixime MICs. Across all antimicrobials, MICs varied widely, indicating the presence of additional modulating mutations. Finally, the genetic determinants underlying low-level doxycycline resistance and reduced penicillin susceptibility remain unresolved. Overall, here we continue to build on the foundation of surveillance efforts in the commensal Neisseria, and continue to flesh out what is known and unknown about this early warning system - or canary in the coal mine - for emerging resistance and clinically consequential evolution in pathogenic Neisseria.
Additional Links: PMID-41727074
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41727074,
year = {2026},
author = {Regan, MR and McDevitt, CJ and Robinson, LR and Issifou, S and Wadsworth, CB},
title = {Put your money where your mouth is: Surveillance of antibiotic resistance within the commensal Neisseria.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {41727074},
issn = {2692-8205},
abstract = {Commensal Neisseria species are major reservoirs of adaptive genetic variation, including antimicrobial resistance, for their pathogenic relatives, yet they remain poorly characterized. This gap limits our ability to anticipate resistance mechanisms that may ultimately emerge Neisseria gonorrhoeae and N. meningitidis. Here, we analyzed 166 novel commensal Neisseria isolates collected from 31 study participants and measured minimum inhibitory concentrations (MICs) for seven antimicrobials: azithromycin, cefixime, ceftriaxone, ciprofloxacin, doxycycline, and gentamicin. Resistance, defined using the Clinical and Laboratory Standards Institute (CLSI) guidelines, was highly prevalent for azithromycin (76%) and doxycycline (52%), while no resistance to gentamicin was observed. High-level doxycycline resistance was always associated with inheritance of tetM. Reduced susceptibility to azithromycin was linked to an MtrD K823E substitution, and reduced susceptibility to ciprofloxacin was associated with GyrA T91I (N. subflava) or S91V (N. mucosa). The PenA 312M mutation was associated with significantly elevated ceftriaxone and cefixime MICs. Across all antimicrobials, MICs varied widely, indicating the presence of additional modulating mutations. Finally, the genetic determinants underlying low-level doxycycline resistance and reduced penicillin susceptibility remain unresolved. Overall, here we continue to build on the foundation of surveillance efforts in the commensal Neisseria, and continue to flesh out what is known and unknown about this early warning system - or canary in the coal mine - for emerging resistance and clinically consequential evolution in pathogenic Neisseria.},
}
RevDate: 2026-03-09
Cuticle-associated microbiota in Bactrocera dorsalis suppress fungal infection through immune and chemical defenses.
Pest management science [Epub ahead of print].
BACKGROUND: Cuticular microbial communities influence insect-pathogen interactions, yet their protective roles remain incompletely understood. These microbial defenses are critical in pest species like Bactrocera dorsalis, where microbial symbionts may shape resistance to biological control agents.
RESULTS: We show that the cuticular microbiota of Bactrocera dorsalis enhances resistance to the entomopathogenic fungi (EPF) Beauveria bassiana and Isaria fumosorosea through dual immune and chemical mechanisms. Gnotobiotic assays demonstrate that specific bacterial isolates (Microbacterium, Psychrobacter, and Staphylococcus) promote host survival and defense by stimulating Toll/IMD signaling pathway and up-regulating antimicrobial peptides (AMPs) such as defensin, attacin, and cecropin. In contrast, non-cuticle-associated bacteria (Escherichia coli and Staphylococcus aureus) failed to enhance survival and immune responses, indicating that protection is microbiota-specific rather than a result of general bacterial exposure. In parallel, bacterial volatiles, such as phenol, indole, and eicosane, along with extracellular enzymes including chitinase, cellulase, protease, and lipase, suppressed fungal germination and hyphal growth. Importantly, these protective effects were found to vary with host age, indicating age-dependent modulation of microbiota-mediated defense.
CONCLUSIONS: Our findings revealed that cuticle-associated bacteria protect their host through complementary immune and chemical pathways. These microbiota act as an active barrier, and microbial metabolism interacts with host immune signaling. By distinguishing specific cuticle-derived effects from non-specific bacterial stimulation, this study highlighted the role of microbiota in modulating fungal susceptibility and supports their application in developing next-generation biocontrol strategies in pest management. © 2026 Society of Chemical Industry.
Additional Links: PMID-41800606
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800606,
year = {2026},
author = {Kabir, K and Afzal, I and Haider, K and Naiem, F and Li, X and Zhang, H},
title = {Cuticle-associated microbiota in Bactrocera dorsalis suppress fungal infection through immune and chemical defenses.},
journal = {Pest management science},
volume = {},
number = {},
pages = {},
doi = {10.1002/ps.70704},
pmid = {41800606},
issn = {1526-4998},
support = {//This study was supported by the National Natural Science Foundation of China (No. 32220103009), the China Agriculture Research System of MOF and MARA (CARS-26), and the Hubei Hongshan Laboratory./ ; },
abstract = {BACKGROUND: Cuticular microbial communities influence insect-pathogen interactions, yet their protective roles remain incompletely understood. These microbial defenses are critical in pest species like Bactrocera dorsalis, where microbial symbionts may shape resistance to biological control agents.
RESULTS: We show that the cuticular microbiota of Bactrocera dorsalis enhances resistance to the entomopathogenic fungi (EPF) Beauveria bassiana and Isaria fumosorosea through dual immune and chemical mechanisms. Gnotobiotic assays demonstrate that specific bacterial isolates (Microbacterium, Psychrobacter, and Staphylococcus) promote host survival and defense by stimulating Toll/IMD signaling pathway and up-regulating antimicrobial peptides (AMPs) such as defensin, attacin, and cecropin. In contrast, non-cuticle-associated bacteria (Escherichia coli and Staphylococcus aureus) failed to enhance survival and immune responses, indicating that protection is microbiota-specific rather than a result of general bacterial exposure. In parallel, bacterial volatiles, such as phenol, indole, and eicosane, along with extracellular enzymes including chitinase, cellulase, protease, and lipase, suppressed fungal germination and hyphal growth. Importantly, these protective effects were found to vary with host age, indicating age-dependent modulation of microbiota-mediated defense.
CONCLUSIONS: Our findings revealed that cuticle-associated bacteria protect their host through complementary immune and chemical pathways. These microbiota act as an active barrier, and microbial metabolism interacts with host immune signaling. By distinguishing specific cuticle-derived effects from non-specific bacterial stimulation, this study highlighted the role of microbiota in modulating fungal susceptibility and supports their application in developing next-generation biocontrol strategies in pest management. © 2026 Society of Chemical Industry.},
}
RevDate: 2026-03-09
Application of Artificial Intelligence-Powered Research in Gastrointestinal Pathophysiology: Unveiling Intestinal Pathobionts and Microbiota Dysbiosis.
Journal of physiological investigation [Epub ahead of print].
Additional Links: PMID-41800525
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800525,
year = {2026},
author = {Pai, YC and Yu, LC},
title = {Application of Artificial Intelligence-Powered Research in Gastrointestinal Pathophysiology: Unveiling Intestinal Pathobionts and Microbiota Dysbiosis.},
journal = {Journal of physiological investigation},
volume = {},
number = {},
pages = {},
pmid = {41800525},
issn = {2950-6344},
}
RevDate: 2026-03-09
Host-mediated Remodeling of the Gut Microbiota in Energy Homeostasis and Environmental Resilience.
Journal of physiological investigation pii:02275668-990000000-00060 [Epub ahead of print].
Additional Links: PMID-41800490
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800490,
year = {2026},
author = {Weng, YH and Chen, PC and Ruan, JW},
title = {Host-mediated Remodeling of the Gut Microbiota in Energy Homeostasis and Environmental Resilience.},
journal = {Journal of physiological investigation},
volume = {},
number = {},
pages = {},
doi = {10.4103/ejpi.EJPI-D-25-00028},
pmid = {41800490},
issn = {2950-6344},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Carrier-free supramolecular architectonics of quercetin-berberine for safety-redefined therapy of ulcerative colitis.
Materials today. Bio, 37:102970.
Ulcerative colitis (UC) poses significant clinical management challenges due to the limited efficacy and substantial safety burdens of existing treatments. This study develops a carrier-free supramolecular nanoassembly (QB) composed solely of quercetin (QU) and berberine (BBR), reshaping the safety-efficacy profile of these natural drugs at the nanoscale. Spectroscopic characterization and molecular dynamics simulations reveal that QU and BBR synergistically self-assemble into stable nanoparticles driven primarily by hydrogen bonding and π-π stacking, resulting in a highly negative surface charge and superior colloidal stability. In vitro and in vivo experiments demonstrate that QB markedly reduces BBR's cytotoxicity, expanding its therapeutic dose window by approximately 16-fold, while concurrently enhancing anti-inflammatory, antioxidant, and epithelial barrier repair effects in LPS-stimulated macrophages and DSS-induced UC mice. In vivo fluorescence imaging and tissue distribution indicate selective accumulation of orally administered QB in the inflamed colon and spleen, suggesting dual local intestinal and systemic immune modulatory capabilities. Transcriptomic and gut microbiome analyses further uncover QB's coordinated downregulation of inflammation-related signaling pathways, upregulation of metabolic and antioxidant modules, and restoration of microbial diversity and community homeostasis. Compared to QU or BBR monotherapy and 5-aminosalicylic acid, QB exhibits superior overall efficacy in alleviating colitis symptoms and tissue damage, with excellent biocompatibility, offering a scalable platform for safety-redefined, multidimensional precision interventions in UC based on natural small-molecule self-assembly.
Additional Links: PMID-41800457
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800457,
year = {2026},
author = {Zhang, X and Fu, Y and Liu, S and Zhang, J and Xu, F and Zhang, C and Wang, Y and Huo, C},
title = {Carrier-free supramolecular architectonics of quercetin-berberine for safety-redefined therapy of ulcerative colitis.},
journal = {Materials today. Bio},
volume = {37},
number = {},
pages = {102970},
pmid = {41800457},
issn = {2590-0064},
abstract = {Ulcerative colitis (UC) poses significant clinical management challenges due to the limited efficacy and substantial safety burdens of existing treatments. This study develops a carrier-free supramolecular nanoassembly (QB) composed solely of quercetin (QU) and berberine (BBR), reshaping the safety-efficacy profile of these natural drugs at the nanoscale. Spectroscopic characterization and molecular dynamics simulations reveal that QU and BBR synergistically self-assemble into stable nanoparticles driven primarily by hydrogen bonding and π-π stacking, resulting in a highly negative surface charge and superior colloidal stability. In vitro and in vivo experiments demonstrate that QB markedly reduces BBR's cytotoxicity, expanding its therapeutic dose window by approximately 16-fold, while concurrently enhancing anti-inflammatory, antioxidant, and epithelial barrier repair effects in LPS-stimulated macrophages and DSS-induced UC mice. In vivo fluorescence imaging and tissue distribution indicate selective accumulation of orally administered QB in the inflamed colon and spleen, suggesting dual local intestinal and systemic immune modulatory capabilities. Transcriptomic and gut microbiome analyses further uncover QB's coordinated downregulation of inflammation-related signaling pathways, upregulation of metabolic and antioxidant modules, and restoration of microbial diversity and community homeostasis. Compared to QU or BBR monotherapy and 5-aminosalicylic acid, QB exhibits superior overall efficacy in alleviating colitis symptoms and tissue damage, with excellent biocompatibility, offering a scalable platform for safety-redefined, multidimensional precision interventions in UC based on natural small-molecule self-assembly.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Health benefits of Bifidobacterium animalis subsp. lactis BB-12 in infants and children: a mini-review.
Frontiers in microbiology, 17:1773473.
The colonization of the infant gut microbiome during the critical window of 0-3 years is influenced by a multitude of prenatal, environmental and host factors, and may be crucial for life-long health. The infant gut microbiome is highly dynamic, with bifidobacteria-dominance generally established during birth and lactation, followed by transition to a more stable and adult-like composition reached around 3 years of age. Bifidobacteria-dominance in infancy is considered protective as they not only display both anti-inflammatory and immunomodulatory effects but also foster the establishment of other beneficial species via cross-feeding interactions. As predominance of bifidobacteria is considered the marker of a healthy breastfed infant, the use of bifidobacteria-based probiotics for the prevention of gut dysbiosis and related conditions has been investigated. This clinically oriented summary highlights the unmet research needs of Bifidobacterium animalis subsp. lactis, BB-12[®] (BB-12), a well-studied probiotic added to baby formulas, dietary supplements, and fermented milk products; several potentially beneficial attributes, including acid and bile tolerance, strong adherence properties, pathogen inhibition, and immune modulation are considered. Clinical studies have demonstrated the safety and beneficial effects of BB-12 in infants and children across multiple disorders and highlight the need for improved clinical and regulatory guidelines.
Additional Links: PMID-41800422
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800422,
year = {2026},
author = {Bueno, CPAR and DomÃnguez, AC and Guyonnet, D and Pouteau, E},
title = {Health benefits of Bifidobacterium animalis subsp. lactis BB-12 in infants and children: a mini-review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1773473},
pmid = {41800422},
issn = {1664-302X},
abstract = {The colonization of the infant gut microbiome during the critical window of 0-3 years is influenced by a multitude of prenatal, environmental and host factors, and may be crucial for life-long health. The infant gut microbiome is highly dynamic, with bifidobacteria-dominance generally established during birth and lactation, followed by transition to a more stable and adult-like composition reached around 3 years of age. Bifidobacteria-dominance in infancy is considered protective as they not only display both anti-inflammatory and immunomodulatory effects but also foster the establishment of other beneficial species via cross-feeding interactions. As predominance of bifidobacteria is considered the marker of a healthy breastfed infant, the use of bifidobacteria-based probiotics for the prevention of gut dysbiosis and related conditions has been investigated. This clinically oriented summary highlights the unmet research needs of Bifidobacterium animalis subsp. lactis, BB-12[®] (BB-12), a well-studied probiotic added to baby formulas, dietary supplements, and fermented milk products; several potentially beneficial attributes, including acid and bile tolerance, strong adherence properties, pathogen inhibition, and immune modulation are considered. Clinical studies have demonstrated the safety and beneficial effects of BB-12 in infants and children across multiple disorders and highlight the need for improved clinical and regulatory guidelines.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Dynamic remodeling of skin microbiota during healthy homeostatic and wound repair conditions.
Frontiers in microbiology, 17:1781606.
The skin microbiota is a fundamental component of the cutaneous ecosystem and plays an important role in maintaining skin homeostasis through immune education, maintenance of the skin barrier, colonization resistance, and regulation of the physiological environment under healthy conditions. Skin injury disrupts this balanced microbial ecosystem, resulting in marked changes in the local microenvironment. However, the processes by which skin microbiota reorganise following injury and contribute to the restoration of a remodelled homeostatic ecosystem after wound repair are not fully understood. This review synthesizes current knowledge on host-microbiota interactions across the dynamic transition from healthy skin to wounded skin and to remodeled homeostatic skin. We highlight the functions of commensal microorganisms during the inflammatory, proliferative, and remodeling phases of wound healing, with a particular focus on their roles in the resolution of inflammation, tissue regeneration and barrier restoration. Finally, we discuss emerging microbiota-based therapeutic opportunities for wound management and outline key challenges and future research directions aimed at promoting long-term restoration of skin microbial homeostasis.
Additional Links: PMID-41800418
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800418,
year = {2026},
author = {Ye, H and Wong, A and Chen, X and Sun, W and He, H and Li, X and Wu, J},
title = {Dynamic remodeling of skin microbiota during healthy homeostatic and wound repair conditions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1781606},
pmid = {41800418},
issn = {1664-302X},
abstract = {The skin microbiota is a fundamental component of the cutaneous ecosystem and plays an important role in maintaining skin homeostasis through immune education, maintenance of the skin barrier, colonization resistance, and regulation of the physiological environment under healthy conditions. Skin injury disrupts this balanced microbial ecosystem, resulting in marked changes in the local microenvironment. However, the processes by which skin microbiota reorganise following injury and contribute to the restoration of a remodelled homeostatic ecosystem after wound repair are not fully understood. This review synthesizes current knowledge on host-microbiota interactions across the dynamic transition from healthy skin to wounded skin and to remodeled homeostatic skin. We highlight the functions of commensal microorganisms during the inflammatory, proliferative, and remodeling phases of wound healing, with a particular focus on their roles in the resolution of inflammation, tissue regeneration and barrier restoration. Finally, we discuss emerging microbiota-based therapeutic opportunities for wound management and outline key challenges and future research directions aimed at promoting long-term restoration of skin microbial homeostasis.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Impact of non-standardized reporting on reproducibility, usability, and integration in nasopharyngeal metagenomic research: a systematic review.
Frontiers in microbiology, 17:1707004.
INTRODUCTION: The nasopharyngeal microbiome plays a critical role in respiratory health and disease and is a major focus of metagenomic research. However, inconsistent reporting practices across studies limit reproducibility, dataset usability, and cross-study integration, thereby reducing the overall scientific value of publicly available nasopharyn.
METHODS: A systematic review was conducted to evaluate the impact of non-standardized reporting on reproducibility, usability, and integration of nasopharyngeal metagenomic datasets. A total of 988 studies were screened, and 227 manuscripts met predefined inclusion and exclusion criteria for full-text review. Methodological reproducibility, metadata completeness, and compatibility between reported laboratory methods and deposited datasets were assessed. Reproducible datasets were further analyzed to evaluate the interchangeability of nasopharyngeal aspirates and nasopharyngeal swabs.
RESULTS: Only 78 studies (34%) contained methods sections sufficient for reproducibility, and of these, 33 studies (15%) provided analytically sufficient metadata to support secondary analysis. Mismatches between reported laboratory methods and deposited datasets were identified in 4% of studies. These deficiencies were primarily attributed to incomplete methodological reporting, inaccessible or insufficient metadata, and incompatible file formats. Comparative analysis of reproducible datasets demonstrated significant differences in microbial profiles between nasopharyngeal aspirates and nasopharyngeal swabs, confirming that these specimen types are not interchangeable within a study.
DISCUSSION: The findings demonstrate that inadequate reporting standards substantially impair the reproducibility, reuse, and integration of nasopharyngeal metagenomic data. The observed methodological and metadata inconsistencies limit the reliability of downstream analyses and cross-study comparisons. Standardized reporting guidelines are urgently needed to improve transparency, ensure reproducibility, and enhance the integrative potential of nasopharyngeal microbiome research. Adoption of comprehensive and consistent reporting practices would significantly strengthen the scientific rigor and utility of metagenomic studies in this field.
Additional Links: PMID-41800416
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800416,
year = {2026},
author = {Bustos, ML and Song, K and Brochu, HN and Zhang, Q and Iyer, LK and Icenhour, CR},
title = {Impact of non-standardized reporting on reproducibility, usability, and integration in nasopharyngeal metagenomic research: a systematic review.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1707004},
pmid = {41800416},
issn = {1664-302X},
abstract = {INTRODUCTION: The nasopharyngeal microbiome plays a critical role in respiratory health and disease and is a major focus of metagenomic research. However, inconsistent reporting practices across studies limit reproducibility, dataset usability, and cross-study integration, thereby reducing the overall scientific value of publicly available nasopharyn.
METHODS: A systematic review was conducted to evaluate the impact of non-standardized reporting on reproducibility, usability, and integration of nasopharyngeal metagenomic datasets. A total of 988 studies were screened, and 227 manuscripts met predefined inclusion and exclusion criteria for full-text review. Methodological reproducibility, metadata completeness, and compatibility between reported laboratory methods and deposited datasets were assessed. Reproducible datasets were further analyzed to evaluate the interchangeability of nasopharyngeal aspirates and nasopharyngeal swabs.
RESULTS: Only 78 studies (34%) contained methods sections sufficient for reproducibility, and of these, 33 studies (15%) provided analytically sufficient metadata to support secondary analysis. Mismatches between reported laboratory methods and deposited datasets were identified in 4% of studies. These deficiencies were primarily attributed to incomplete methodological reporting, inaccessible or insufficient metadata, and incompatible file formats. Comparative analysis of reproducible datasets demonstrated significant differences in microbial profiles between nasopharyngeal aspirates and nasopharyngeal swabs, confirming that these specimen types are not interchangeable within a study.
DISCUSSION: The findings demonstrate that inadequate reporting standards substantially impair the reproducibility, reuse, and integration of nasopharyngeal metagenomic data. The observed methodological and metadata inconsistencies limit the reliability of downstream analyses and cross-study comparisons. Standardized reporting guidelines are urgently needed to improve transparency, ensure reproducibility, and enhance the integrative potential of nasopharyngeal microbiome research. Adoption of comprehensive and consistent reporting practices would significantly strengthen the scientific rigor and utility of metagenomic studies in this field.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Plant-soil-microbiome interactions: mechanisms, advances, and challenges in sustainable agriculture and healthy agroecosystems.
Frontiers in microbiology, 17:1762743.
The focus of this article is to summarize current knowledge of plant-associated microbiomes, which play a key role in plant health and in maintaining soil quality. Such microbiomes, comprising bacteria, fungi, archaea, algae, nematodes, and protists, perform various functions, including nutrient transformation, pathogen protection, and stress mitigation. Microbial communities are commonly used as an indicator of ecosystem health. Soil microbiome diversity depends on environmental factors (including biotic and abiotic stresses), which can alter microbial composition, thereby modifying microbial interactions and plant resilience. Biofertilizers, biopreparations, and microbial inoculants or consortia have been utilized in agriculture to enhance soil properties, such as microbial diversity and enzymatic activity, and to prime plant immune responses, thereby promoting plant growth and health. Biofertilizers can significantly help plants adapt to environmental stresses and climate change, mitigating drought stress and reducing greenhouse gas emissions. Recent advances in DNA sequencing technologies, the computing power available to scientists, and the development of bioinformatics tools have made microbial community studies widely accessible. These tools enable the research and modeling of changes in the soil microbiome, plant disease susceptibility, and soil health. Multi-omics approaches to microbiomes are key to characterizing the microbiome and predicting plant diseases. Future research should focus primarily on understanding the interactions among soil, plants, and microbiomes. This approach will help develop climate-resilient plants and improve the health and functionality of agroecosystems. Key efforts closely aligned with the European Union's goals and biodiversity strategies for sustainable agriculture and soil health restoration, as presented in this review, include studying the structures and functions of soil microbiomes, developing new assays, and designing and investigating microbial consortia to restore healthy communities. These strategies address contemporary challenges in agriculture, including vertical and urban farming and superfood production.
Additional Links: PMID-41800415
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800415,
year = {2026},
author = {Panek, J and Gryta, A and Maj, W and Mącik, M and Oszust, K and Pertile, G and Pylak, M and Siegieda, D and Hallama, M and Hatano, R and Kandeler, E and Pathan, SI and Pietramellara, G and Malusa, E and Weber, J and Turnau, K and Różalska, S and Frąc, M},
title = {Plant-soil-microbiome interactions: mechanisms, advances, and challenges in sustainable agriculture and healthy agroecosystems.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1762743},
pmid = {41800415},
issn = {1664-302X},
abstract = {The focus of this article is to summarize current knowledge of plant-associated microbiomes, which play a key role in plant health and in maintaining soil quality. Such microbiomes, comprising bacteria, fungi, archaea, algae, nematodes, and protists, perform various functions, including nutrient transformation, pathogen protection, and stress mitigation. Microbial communities are commonly used as an indicator of ecosystem health. Soil microbiome diversity depends on environmental factors (including biotic and abiotic stresses), which can alter microbial composition, thereby modifying microbial interactions and plant resilience. Biofertilizers, biopreparations, and microbial inoculants or consortia have been utilized in agriculture to enhance soil properties, such as microbial diversity and enzymatic activity, and to prime plant immune responses, thereby promoting plant growth and health. Biofertilizers can significantly help plants adapt to environmental stresses and climate change, mitigating drought stress and reducing greenhouse gas emissions. Recent advances in DNA sequencing technologies, the computing power available to scientists, and the development of bioinformatics tools have made microbial community studies widely accessible. These tools enable the research and modeling of changes in the soil microbiome, plant disease susceptibility, and soil health. Multi-omics approaches to microbiomes are key to characterizing the microbiome and predicting plant diseases. Future research should focus primarily on understanding the interactions among soil, plants, and microbiomes. This approach will help develop climate-resilient plants and improve the health and functionality of agroecosystems. Key efforts closely aligned with the European Union's goals and biodiversity strategies for sustainable agriculture and soil health restoration, as presented in this review, include studying the structures and functions of soil microbiomes, developing new assays, and designing and investigating microbial consortia to restore healthy communities. These strategies address contemporary challenges in agriculture, including vertical and urban farming and superfood production.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Multi-site microbiota crosstalk in the postmenopausal: from dysbiosis mechanisms to precision interventions.
Frontiers in microbiology, 17:1702700.
Persistent estrogen deficiency in postmenopause reshapes the gut-vaginal-urinary ecosystems, contributing to multisystem dysfunction through interconnected dysbiosis. Cross-niche microbial interactions amplify systemic risks: gut-derived toxins are linked to vascular inflammation, vaginal dysbiosis facilitates urinary pathogen colonization, and bile acid disruption impairs bone-immune homeostasis. This review synthesizes current mechanistic evidence illustrating how microbial networks propagate postmenopausal comorbidities. We propose the framework of "Postmenopausal Microbiota Network Medicine" which integrates microbial dynamics with host omics to transition from symptomatic management toward root-cause interception by strengthening microbial network resilience.
Additional Links: PMID-41800413
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800413,
year = {2026},
author = {Fang, J and He, X and Zhou, J},
title = {Multi-site microbiota crosstalk in the postmenopausal: from dysbiosis mechanisms to precision interventions.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1702700},
pmid = {41800413},
issn = {1664-302X},
abstract = {Persistent estrogen deficiency in postmenopause reshapes the gut-vaginal-urinary ecosystems, contributing to multisystem dysfunction through interconnected dysbiosis. Cross-niche microbial interactions amplify systemic risks: gut-derived toxins are linked to vascular inflammation, vaginal dysbiosis facilitates urinary pathogen colonization, and bile acid disruption impairs bone-immune homeostasis. This review synthesizes current mechanistic evidence illustrating how microbial networks propagate postmenopausal comorbidities. We propose the framework of "Postmenopausal Microbiota Network Medicine" which integrates microbial dynamics with host omics to transition from symptomatic management toward root-cause interception by strengthening microbial network resilience.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Microbial succession and tissue-specific restructuring of bacterial and fungal communities during post-harvest onion bulb rotting.
Frontiers in microbiology, 17:1776996.
Despite being a relatively hardy bulb crop with a longer shelf life than many fresh vegetables, onions are susceptible to substantial postharvest losses due to microbial spoilage. This study used high-throughput amplicon sequencing to characterize the bacterial and fungal microbiomes associated with healthy (HB), mildly rotten (MRB), and severely rotten (SRB) onion bulbs. Microbial communities were analysed across three distinct bulb tissues comprising neck tissue (NT), outer scale (OS), and central tissue (CT), to generate stage-specific and tissue-specific microbiome profiles. The microbial community analysis based on over 2 million Illumina NGS reads revealed the presence of 85 bacterial OTUs and 53 fungal OTUs across nine bulb samples. Bulb deterioration was marked by pronounced microbial succession, with bacterial diversity increasing from healthy bulbs (8 genera) to mildly rotten bulbs (36 genera), followed by a sharp decline in severely rotten bulbs (11 genera). Several bacterial genera, including Lactobacillus, Novosphingobium, Sphingobium, Pluralibacter, Acetobacter, Gluconobacter and Pantoea, emerged exclusively in rotten bulbs and were absent in healthy tissues, indicating their association with the onion bulb rot. The microbiome of SRB was marked by an overwhelming dominance of Lactobacillus (33.2% in SRB-CT, 16.9% in SRB-NT, 10.8% in SRB-OS), Acetobacter (16.1% in SRB-CT, 15.6% in SRB-NT, 7.0% in SRB-OS), Carnimonas (57.0% in SRB-NT), and Gluconobacter (14.5% in SRB-OS). Fungal communities exhibited a similar successional pattern: healthy bulbs showed negligible fungal presence except in the neck tissue (HB-NT), whereas mildly rotten bulbs showed a sharp increase in fungal diversity dominated by Meyerozyma (21.7%), Blastobotrys (13.3%), and Penicillium (7.0%). In severely rotten bulbs, fungal diversity declined, with Pichia (48.3%) and Kazachstania (8.6%) becoming dominant. Differential abundance analysis using edgeR identified six bacterial genera (Lactobacillus, Novosphingobium, Acetobacter, Pluralibacter, Carnimonas, and Dysgonomonas) and two fungal genera (Pichia and Kazachstania) that exhibited significant stage-dependent shifts during bulb rot progression. Alpha- and beta-diversity analyses revealed strong tissue-specific structuring of fungal communities, identifying the neck region as the primary fungal succession zone. Overall, this study elucidates the ecological restructuring of bacterial and fungal communities during onion bulb deterioration, and would pave the way for devising microbiome-informed interventions to reduce postharvest losses in onions.
Additional Links: PMID-41800410
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800410,
year = {2026},
author = {Kumar, S and Dutta, R and Auji, R and Wackchaure, GC and Jayalakshmi, K and Karuppaiah, V and Mahajan, V},
title = {Microbial succession and tissue-specific restructuring of bacterial and fungal communities during post-harvest onion bulb rotting.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1776996},
pmid = {41800410},
issn = {1664-302X},
abstract = {Despite being a relatively hardy bulb crop with a longer shelf life than many fresh vegetables, onions are susceptible to substantial postharvest losses due to microbial spoilage. This study used high-throughput amplicon sequencing to characterize the bacterial and fungal microbiomes associated with healthy (HB), mildly rotten (MRB), and severely rotten (SRB) onion bulbs. Microbial communities were analysed across three distinct bulb tissues comprising neck tissue (NT), outer scale (OS), and central tissue (CT), to generate stage-specific and tissue-specific microbiome profiles. The microbial community analysis based on over 2 million Illumina NGS reads revealed the presence of 85 bacterial OTUs and 53 fungal OTUs across nine bulb samples. Bulb deterioration was marked by pronounced microbial succession, with bacterial diversity increasing from healthy bulbs (8 genera) to mildly rotten bulbs (36 genera), followed by a sharp decline in severely rotten bulbs (11 genera). Several bacterial genera, including Lactobacillus, Novosphingobium, Sphingobium, Pluralibacter, Acetobacter, Gluconobacter and Pantoea, emerged exclusively in rotten bulbs and were absent in healthy tissues, indicating their association with the onion bulb rot. The microbiome of SRB was marked by an overwhelming dominance of Lactobacillus (33.2% in SRB-CT, 16.9% in SRB-NT, 10.8% in SRB-OS), Acetobacter (16.1% in SRB-CT, 15.6% in SRB-NT, 7.0% in SRB-OS), Carnimonas (57.0% in SRB-NT), and Gluconobacter (14.5% in SRB-OS). Fungal communities exhibited a similar successional pattern: healthy bulbs showed negligible fungal presence except in the neck tissue (HB-NT), whereas mildly rotten bulbs showed a sharp increase in fungal diversity dominated by Meyerozyma (21.7%), Blastobotrys (13.3%), and Penicillium (7.0%). In severely rotten bulbs, fungal diversity declined, with Pichia (48.3%) and Kazachstania (8.6%) becoming dominant. Differential abundance analysis using edgeR identified six bacterial genera (Lactobacillus, Novosphingobium, Acetobacter, Pluralibacter, Carnimonas, and Dysgonomonas) and two fungal genera (Pichia and Kazachstania) that exhibited significant stage-dependent shifts during bulb rot progression. Alpha- and beta-diversity analyses revealed strong tissue-specific structuring of fungal communities, identifying the neck region as the primary fungal succession zone. Overall, this study elucidates the ecological restructuring of bacterial and fungal communities during onion bulb deterioration, and would pave the way for devising microbiome-informed interventions to reduce postharvest losses in onions.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Divergent sucker-corm endophytic microbiota underpins the progressive decline of Fusarium-wilt incidence in resistant bananas across ratoon cycles.
Frontiers in microbiology, 17:1676292.
Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), threatens global banana production. Resistant cultivars exhibit reduced disease incidence after successive ratoon cycles, but the underlying micro-ecological mechanisms remain unclear. This study represents the first longitudinal analysis of corm endophytic microbiota across ratoon cycles in banana, revealing temporal dynamics that underpin progressive disease resistance. A three-cycle field trial with three biological replicates per cultivar per cycle was conducted in a Foc-infested orchard in Guangxi, China. Corm tissues were sampled from resistant ('Bao Dao Jiao' and 'Gui Jiao 9') and susceptible 'Williams B6' bananas (n = 3 biological replicates per group) at plant crop (cycle 1) and third ratoon (cycle 3). 16S rRNA amplicons were sequenced via Illumina NovaSeq. Alpha- and beta-diversity, taxonomic composition, and predicted functions (PICRUSt2) were analyzed. Resistant cultivars maintained significantly higher Chao1 and Shannon indices than the susceptible cultivar, with divergence intensified across ratoon cycles (p < 0.05). Community structure was shaped primarily by cultivar rather than maternal health status. Resistant genotypes enriched Proteobacteria and Actinobacteria, alongside beneficial genera (Halomonas, Nesterenkonia, Aliihoeflea). Functional predictions revealed enrichment in carbohydrate metabolism, membrane transport, and xenobiotic degradation pathways in resistant cultivars. Disease incidence declined significantly from 34-39% (cycle 1) to 4-8% (cycle 3) in resistant cultivars, whereas susceptible cultivars remained at 44-59%. Resistant bananas continuously recruit beneficial endophytes during ratooning, assembling a stable microbiome that reinforces Fusarium wilt resistance. These findings provide microbial targets for breeding and biocontrol strategies.
Additional Links: PMID-41800399
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800399,
year = {2026},
author = {Xiang, S and Tian, D and Chen, J and He, Z and Wei, L and Qin, L and Li, C and Li, B},
title = {Divergent sucker-corm endophytic microbiota underpins the progressive decline of Fusarium-wilt incidence in resistant bananas across ratoon cycles.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1676292},
pmid = {41800399},
issn = {1664-302X},
abstract = {Fusarium wilt of banana, caused by Fusarium oxysporum f. sp. cubense (Foc), threatens global banana production. Resistant cultivars exhibit reduced disease incidence after successive ratoon cycles, but the underlying micro-ecological mechanisms remain unclear. This study represents the first longitudinal analysis of corm endophytic microbiota across ratoon cycles in banana, revealing temporal dynamics that underpin progressive disease resistance. A three-cycle field trial with three biological replicates per cultivar per cycle was conducted in a Foc-infested orchard in Guangxi, China. Corm tissues were sampled from resistant ('Bao Dao Jiao' and 'Gui Jiao 9') and susceptible 'Williams B6' bananas (n = 3 biological replicates per group) at plant crop (cycle 1) and third ratoon (cycle 3). 16S rRNA amplicons were sequenced via Illumina NovaSeq. Alpha- and beta-diversity, taxonomic composition, and predicted functions (PICRUSt2) were analyzed. Resistant cultivars maintained significantly higher Chao1 and Shannon indices than the susceptible cultivar, with divergence intensified across ratoon cycles (p < 0.05). Community structure was shaped primarily by cultivar rather than maternal health status. Resistant genotypes enriched Proteobacteria and Actinobacteria, alongside beneficial genera (Halomonas, Nesterenkonia, Aliihoeflea). Functional predictions revealed enrichment in carbohydrate metabolism, membrane transport, and xenobiotic degradation pathways in resistant cultivars. Disease incidence declined significantly from 34-39% (cycle 1) to 4-8% (cycle 3) in resistant cultivars, whereas susceptible cultivars remained at 44-59%. Resistant bananas continuously recruit beneficial endophytes during ratooning, assembling a stable microbiome that reinforces Fusarium wilt resistance. These findings provide microbial targets for breeding and biocontrol strategies.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Trehalose-mediated reshaping of the rhizosphere microbiome drives tea root rot progression.
Frontiers in microbiology, 17:1787317.
Tea (Camellia sinensis [L.] Kuntze) is one of the most economically important crops and as a traditional medicinal plant in the world. The long-term continuous cropping and inappropriate management have led to frequent outbreaks of soil-borne diseases such as root rot, which pose a serious threat to the sustainable development of the tea industry. However, the pathogenesis of tea root rot remains poorly understood. In this study, two novel pathogen fungi, Paraconiothyrium cyclothyrioides F8 and Apiotrichum sporotrichoides F17, were isolated and identified from diseased tea roots. Microbiome analysis revealed significant restructuring of the rhizosphere microbial community in diseased tea plants, with a significant reduction in the abundance of Basidiomycota and marked enrichment of pathogen such as Fusarium and Apiotrichum. Meanwhile, the abundances of beneficial fungi (e.g., Saitozyma and Trichoderma) and bacteria (e.g., Bacillus and Sporosarcina) were significantly decreased. Further investigation demonstrated that root exudate trehalose exhibited prominent bidirectional regulatory effect through promoted the growth of pathogen, while simultaneously inhibiting biofilm formation, rhizosphere colonization at specific concentrations and weakened the biocontrol functions of the beneficial antagonistic bacteria Sporosarcina pasteurii T21 and Lysinibacillus sp. T23, facilitating the formation of a rhizosphere chemical environment that "aids enemies and harms allies" and thereby exacerbating disease occurrence. This study emphasized the dominant role of plant metabolites such as trehalose in driving the assembly of rhizosphere microbial communities from a disease-suppressive to a disease-conducive state, as well as in disease development. The findings provide a novel theoretical perspective for the microbiological regulation of tea root rot and offer theoretical and practical bases for tea root rot disease green prevention and control.
Additional Links: PMID-41800398
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800398,
year = {2026},
author = {Zhu, Q and Chen, B and Hu, W and Huang, Y and Wang, S and Feng, M and Zhao, J and Yu, M and Li, M and Gong, X},
title = {Trehalose-mediated reshaping of the rhizosphere microbiome drives tea root rot progression.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1787317},
pmid = {41800398},
issn = {1664-302X},
abstract = {Tea (Camellia sinensis [L.] Kuntze) is one of the most economically important crops and as a traditional medicinal plant in the world. The long-term continuous cropping and inappropriate management have led to frequent outbreaks of soil-borne diseases such as root rot, which pose a serious threat to the sustainable development of the tea industry. However, the pathogenesis of tea root rot remains poorly understood. In this study, two novel pathogen fungi, Paraconiothyrium cyclothyrioides F8 and Apiotrichum sporotrichoides F17, were isolated and identified from diseased tea roots. Microbiome analysis revealed significant restructuring of the rhizosphere microbial community in diseased tea plants, with a significant reduction in the abundance of Basidiomycota and marked enrichment of pathogen such as Fusarium and Apiotrichum. Meanwhile, the abundances of beneficial fungi (e.g., Saitozyma and Trichoderma) and bacteria (e.g., Bacillus and Sporosarcina) were significantly decreased. Further investigation demonstrated that root exudate trehalose exhibited prominent bidirectional regulatory effect through promoted the growth of pathogen, while simultaneously inhibiting biofilm formation, rhizosphere colonization at specific concentrations and weakened the biocontrol functions of the beneficial antagonistic bacteria Sporosarcina pasteurii T21 and Lysinibacillus sp. T23, facilitating the formation of a rhizosphere chemical environment that "aids enemies and harms allies" and thereby exacerbating disease occurrence. This study emphasized the dominant role of plant metabolites such as trehalose in driving the assembly of rhizosphere microbial communities from a disease-suppressive to a disease-conducive state, as well as in disease development. The findings provide a novel theoretical perspective for the microbiological regulation of tea root rot and offer theoretical and practical bases for tea root rot disease green prevention and control.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
OmniCorr: an R-package for visualizing putative host-microbiome interactions using multi-omics data.
Bioinformatics advances, 6(1):vbag057.
Holo-omics leverages omics datasets to explore the interactions between hosts and their associated microbiomes. Although the generation of omics data from matching host and microbiome samples is steadily increasing, there remains a scarcity of computational tools capable of integrating and visualizing this data to facilitate the prediction and interpretation of host-microbiome interactions. We present OmniCorr, an R package designed to: (i) manage the complexity of omics data by clustering co-varying features (e.g. genes, proteins, and metabolites) into modules, (ii) visualize correlations of these modules across different omics layers, host-microbiome interfaces, and metadata, and (iii) identify statistically significant associations indicative of putative host-microbiome interactions. OmniCorr's utility is demonstrated using datasets from two systems: (i) Atlantic salmon, integrating host transcriptomics with metagenomics and metatranscriptomics to explore dietary impacts, and (ii) cattle, combining host proteomics with metaproteomics to investigate methane emission variability. Availability and implementation: OmniCorr is freely available at https://github.com/shashank-KU/OmniCorr.
Additional Links: PMID-41800387
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800387,
year = {2026},
author = {Gupta, S and Quarato, V and Lai, W and Kobel, CM and Aho, VTE and Vera-Ponce de León, A and La Rosa, SL and Sandve, SR and Pope, PB and Hvidsten, TR},
title = {OmniCorr: an R-package for visualizing putative host-microbiome interactions using multi-omics data.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag057},
pmid = {41800387},
issn = {2635-0041},
abstract = {Holo-omics leverages omics datasets to explore the interactions between hosts and their associated microbiomes. Although the generation of omics data from matching host and microbiome samples is steadily increasing, there remains a scarcity of computational tools capable of integrating and visualizing this data to facilitate the prediction and interpretation of host-microbiome interactions. We present OmniCorr, an R package designed to: (i) manage the complexity of omics data by clustering co-varying features (e.g. genes, proteins, and metabolites) into modules, (ii) visualize correlations of these modules across different omics layers, host-microbiome interfaces, and metadata, and (iii) identify statistically significant associations indicative of putative host-microbiome interactions. OmniCorr's utility is demonstrated using datasets from two systems: (i) Atlantic salmon, integrating host transcriptomics with metagenomics and metatranscriptomics to explore dietary impacts, and (ii) cattle, combining host proteomics with metaproteomics to investigate methane emission variability. Availability and implementation: OmniCorr is freely available at https://github.com/shashank-KU/OmniCorr.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
TAGINE: fast taxonomy-based feature engineering for microbiome analysis.
Bioinformatics advances, 6(1):vbag056.
SUMMARY: TAGINE is a feature engineering algorithm that leverages the microbial taxonomic tree to optimize feature sets in microbiome data for predictive modeling. The algorithm starts with features at high taxonomic levels and iteratively splits them into lower-level clades in cases where it improves predictive accuracy, ultimately producing a feature set spanning multiple taxonomic levels. This approach aims to markedly reduce the number of features while preserving biological relevance and interpretability. We compare TAGINE's performance to other standard and taxonomy-based feature engineering methods on several different datasets, and show that TAGINE yields more compact feature sets and is orders of magnitude faster than other methods, while maintaining predictive accuracy.
TAGINE is freely available under the MIT license with source code available at https://github.com/borenstein-lab/tagine_fe.
Additional Links: PMID-41800386
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800386,
year = {2026},
author = {Baum, S and Meshulam, I and Algavi, YM and Peleg, O and Borenstein, E},
title = {TAGINE: fast taxonomy-based feature engineering for microbiome analysis.},
journal = {Bioinformatics advances},
volume = {6},
number = {1},
pages = {vbag056},
pmid = {41800386},
issn = {2635-0041},
abstract = {SUMMARY: TAGINE is a feature engineering algorithm that leverages the microbial taxonomic tree to optimize feature sets in microbiome data for predictive modeling. The algorithm starts with features at high taxonomic levels and iteratively splits them into lower-level clades in cases where it improves predictive accuracy, ultimately producing a feature set spanning multiple taxonomic levels. This approach aims to markedly reduce the number of features while preserving biological relevance and interpretability. We compare TAGINE's performance to other standard and taxonomy-based feature engineering methods on several different datasets, and show that TAGINE yields more compact feature sets and is orders of magnitude faster than other methods, while maintaining predictive accuracy.
TAGINE is freely available under the MIT license with source code available at https://github.com/borenstein-lab/tagine_fe.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut-Lung Microbiota Axis Shapes the Immune Microenvironment and Immunotherapeutic Response in Lung Cancer.
International journal of biological sciences, 22(5):2265-2284.
The gut-lung axis microbiota plays a pivotal role in shaping the tumor immune microenvironment (TIME) and regulating immunotherapeutic responses in lung cancer. This review highlights that pulmonary and gut microbial dysbiosis drives lung cancer development through inducing chronic inflammation, remodeling the immune microenvironment, and reprogramming metabolism. Lung cancer patients exhibit distinct microbial signatures characterized by altered microbiotal diversity and enrichment of specific taxa like Streptococcus, Veillonella, and Bacteroidetes in the airways, along with gut microbial shifts involving decreased Firmicutes/Bacteroidetes ratio. These microbial alterations promote tumor progression via activation of pro-inflammatory pathways (e.g., interleukin-17 (IL-17)/interleukin-23 (IL-23) axis) and suppression of antitumor immunity.Notably, the gut-lung microbiome exerts a profound impact on immunotherapeutic efficacy: responders are enriched with beneficial microbes like Akkermansia muciniphila and Bifidobacterium that enhance CD8[+] T cell responses, while non-responders show elevated levels of Gammaproteobacteria and Fusobacterium associated with immunosuppression. Regulatory mechanisms include systemic immune modulation by microbial metabolites such as short-chain fatty acids, as well as activation of key signaling pathways including cGAS-STING and CD40L-CD40/NF-κB. Emerging translational applications encompass lung cancer diagnosis and immunotherapeutic response prediction via microbial biomarkers, as well as therapeutic interventions including fecal microbiota transplantation (FMT) and probiotic supplementation. Future studies should clarify microbe-host interaction mechanisms and develop personalized microbiota-based strategies to overcome immunotherapy resistance, offering the potential to revolutionize precision oncology through integrating microbiota modulation with conventional therapies.
Additional Links: PMID-41800246
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800246,
year = {2026},
author = {Liu, Y and Wang, S and Xiang, X and Du, Y and Xue, Q and Niu, Y and Peng, W and Ye, L and Zhou, Q},
title = {Gut-Lung Microbiota Axis Shapes the Immune Microenvironment and Immunotherapeutic Response in Lung Cancer.},
journal = {International journal of biological sciences},
volume = {22},
number = {5},
pages = {2265-2284},
pmid = {41800246},
issn = {1449-2288},
mesh = {Humans ; *Lung Neoplasms/immunology/therapy/microbiology ; *Gastrointestinal Microbiome/physiology/immunology ; *Tumor Microenvironment/immunology ; *Immunotherapy/methods ; *Lung/microbiology/immunology ; Dysbiosis ; Animals ; },
abstract = {The gut-lung axis microbiota plays a pivotal role in shaping the tumor immune microenvironment (TIME) and regulating immunotherapeutic responses in lung cancer. This review highlights that pulmonary and gut microbial dysbiosis drives lung cancer development through inducing chronic inflammation, remodeling the immune microenvironment, and reprogramming metabolism. Lung cancer patients exhibit distinct microbial signatures characterized by altered microbiotal diversity and enrichment of specific taxa like Streptococcus, Veillonella, and Bacteroidetes in the airways, along with gut microbial shifts involving decreased Firmicutes/Bacteroidetes ratio. These microbial alterations promote tumor progression via activation of pro-inflammatory pathways (e.g., interleukin-17 (IL-17)/interleukin-23 (IL-23) axis) and suppression of antitumor immunity.Notably, the gut-lung microbiome exerts a profound impact on immunotherapeutic efficacy: responders are enriched with beneficial microbes like Akkermansia muciniphila and Bifidobacterium that enhance CD8[+] T cell responses, while non-responders show elevated levels of Gammaproteobacteria and Fusobacterium associated with immunosuppression. Regulatory mechanisms include systemic immune modulation by microbial metabolites such as short-chain fatty acids, as well as activation of key signaling pathways including cGAS-STING and CD40L-CD40/NF-κB. Emerging translational applications encompass lung cancer diagnosis and immunotherapeutic response prediction via microbial biomarkers, as well as therapeutic interventions including fecal microbiota transplantation (FMT) and probiotic supplementation. Future studies should clarify microbe-host interaction mechanisms and develop personalized microbiota-based strategies to overcome immunotherapy resistance, offering the potential to revolutionize precision oncology through integrating microbiota modulation with conventional therapies.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Lung Neoplasms/immunology/therapy/microbiology
*Gastrointestinal Microbiome/physiology/immunology
*Tumor Microenvironment/immunology
*Immunotherapy/methods
*Lung/microbiology/immunology
Dysbiosis
Animals
RevDate: 2026-03-09
CmpDate: 2026-03-09
Harnessing the Gut Microbiota to Improve Cancer Immunotherapy: Focus on Lung Cancer.
Immune network, 26(1):e7.
The gut microbiota has emerged as a key orchestrator of systemic immunity, capable of reshaping the tumor microenvironment and modulating responses to cancer immunotherapy via the gut-lung axis. While immune checkpoint blockade (ICB) has revolutionized lung cancer treatment, a significant proportion of patients fail to respond. Accumulating evidence suggests that intestinal microbial composition modulates antitumor immunity, yet clinical associations between specific microbial taxa and ICB outcomes often show inconsistencies across cohorts. In this review, we synthesize current mechanistic insights into how gut microbial metabolites and structural components modulate pulmonary immune surveillance. We critically examine the clinical landscape of microbiome signatures in non-small cell lung cancer (NSCLC), highlighting how species- and strain-level heterogeneity contributes to divergent findings. Finally, we discuss translational strategies-ranging from fecal microbiota transplantation to rationally designed bacterial consortia and engineered probiotics-and propose a roadmap for integrating multi-omics with microbiome engineering to overcome current limitations and optimize precision immunotherapy.
Additional Links: PMID-41800020
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800020,
year = {2026},
author = {Park, U and Heo, JY and Chun, SM and Lee, JC and Lee, SH and Lee, SW},
title = {Harnessing the Gut Microbiota to Improve Cancer Immunotherapy: Focus on Lung Cancer.},
journal = {Immune network},
volume = {26},
number = {1},
pages = {e7},
pmid = {41800020},
issn = {1598-2629},
abstract = {The gut microbiota has emerged as a key orchestrator of systemic immunity, capable of reshaping the tumor microenvironment and modulating responses to cancer immunotherapy via the gut-lung axis. While immune checkpoint blockade (ICB) has revolutionized lung cancer treatment, a significant proportion of patients fail to respond. Accumulating evidence suggests that intestinal microbial composition modulates antitumor immunity, yet clinical associations between specific microbial taxa and ICB outcomes often show inconsistencies across cohorts. In this review, we synthesize current mechanistic insights into how gut microbial metabolites and structural components modulate pulmonary immune surveillance. We critically examine the clinical landscape of microbiome signatures in non-small cell lung cancer (NSCLC), highlighting how species- and strain-level heterogeneity contributes to divergent findings. Finally, we discuss translational strategies-ranging from fecal microbiota transplantation to rationally designed bacterial consortia and engineered probiotics-and propose a roadmap for integrating multi-omics with microbiome engineering to overcome current limitations and optimize precision immunotherapy.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review.
International journal of clinical pediatric dentistry, 19(2):278-284.
AIM AND BACKGROUND: The oral cavity harbors a diverse microbiota that significantly influences oral health and disease. Conventional microbiological techniques have limitations in detecting the full range of microbial species, particularly those that are uncultivable. Metagenomics, through culture-independent, high-throughput sequencing methods, offers a comprehensive approach to studying oral microbial diversity. This narrative review aims to evaluate the role of metagenomics in exploring the oral microbiome and its association with dental diseases.
METHODS: This review systematically synthesized current literature and research on metagenomic technologies, including 16S ribosomal RNA (rRNA) sequencing, shotgun metagenomics, metatranscriptomics, metaproteomics, and metabolomics. It highlighted their principles, diagnostic capabilities, and limitations in analyzing microbial communities in caries, endodontic infections, and periodontitis. It also reviewed auxiliary tools such as quantitative polymerase chain reaction (qPCR), microarrays, fluorescence in situ hybridization (FISH), and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and discussed the integration of artificial intelligence (AI) in metagenomic data interpretation.
RESULTS: Metagenomic studies have expanded the scope of known microbial species involved in dental caries beyond Streptococcus mutans, highlighting the contributions of Lactobacillus, Veillonella, Actinomyces, and Candida albicans. In endodontics, resistant species such as Enterococcus faecalis, Porphyromonas endodontalis, and Fusobacterium nucleatum are implicated in persistent infections. In periodontitis, a dysbiotic microbial shift has been associated with the presence of complex microbial consortia, including red and orange complex bacteria.
CONCLUSION: Metagenomics is a powerful diagnostic tool that provides an in-depth characterization of the complex microbial ecosystem of the oral cavity. It offers diagnostic potential through early and accurate detection of pathogenic shifts, promotes personalized treatment planning, and opens avenues for the development of potential biomarkers of disease progression.
CLINICAL SIGNIFICANCE: The integration of metagenomics into dental practice can revolutionize caries risk assessment, treatment precision, and disease prevention strategies. Although challenges such as high cost, data complexity, and lack of standardization remain, ongoing advancements in sequencing technologies and bioinformatics are expected to enhance its accessibility and clinical relevance.
HOW TO CITE THIS ARTICLE: Walia T, Srivastava N, Shetty RM, et al. Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review. Int J Clin Pediatr Dent 2026;19(2):278-284.
Additional Links: PMID-41800013
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41800013,
year = {2026},
author = {Walia, T and Srivastava, N and Shetty, RM and Rana, V},
title = {Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review.},
journal = {International journal of clinical pediatric dentistry},
volume = {19},
number = {2},
pages = {278-284},
pmid = {41800013},
issn = {0974-7052},
abstract = {AIM AND BACKGROUND: The oral cavity harbors a diverse microbiota that significantly influences oral health and disease. Conventional microbiological techniques have limitations in detecting the full range of microbial species, particularly those that are uncultivable. Metagenomics, through culture-independent, high-throughput sequencing methods, offers a comprehensive approach to studying oral microbial diversity. This narrative review aims to evaluate the role of metagenomics in exploring the oral microbiome and its association with dental diseases.
METHODS: This review systematically synthesized current literature and research on metagenomic technologies, including 16S ribosomal RNA (rRNA) sequencing, shotgun metagenomics, metatranscriptomics, metaproteomics, and metabolomics. It highlighted their principles, diagnostic capabilities, and limitations in analyzing microbial communities in caries, endodontic infections, and periodontitis. It also reviewed auxiliary tools such as quantitative polymerase chain reaction (qPCR), microarrays, fluorescence in situ hybridization (FISH), and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS), and discussed the integration of artificial intelligence (AI) in metagenomic data interpretation.
RESULTS: Metagenomic studies have expanded the scope of known microbial species involved in dental caries beyond Streptococcus mutans, highlighting the contributions of Lactobacillus, Veillonella, Actinomyces, and Candida albicans. In endodontics, resistant species such as Enterococcus faecalis, Porphyromonas endodontalis, and Fusobacterium nucleatum are implicated in persistent infections. In periodontitis, a dysbiotic microbial shift has been associated with the presence of complex microbial consortia, including red and orange complex bacteria.
CONCLUSION: Metagenomics is a powerful diagnostic tool that provides an in-depth characterization of the complex microbial ecosystem of the oral cavity. It offers diagnostic potential through early and accurate detection of pathogenic shifts, promotes personalized treatment planning, and opens avenues for the development of potential biomarkers of disease progression.
CLINICAL SIGNIFICANCE: The integration of metagenomics into dental practice can revolutionize caries risk assessment, treatment precision, and disease prevention strategies. Although challenges such as high cost, data complexity, and lack of standardization remain, ongoing advancements in sequencing technologies and bioinformatics are expected to enhance its accessibility and clinical relevance.
HOW TO CITE THIS ARTICLE: Walia T, Srivastava N, Shetty RM, et al. Metagenomics as an Effective Diagnostic Approach for Exploring Oral Microbial Diversity and Dental Diseases: A Narrative Review. Int J Clin Pediatr Dent 2026;19(2):278-284.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Evaluation of Agolin® Pig on sow and piglet performance and sow fecal microbial communities during lactation.
Translational animal science, 10:txag023.
Essential oils are increasingly evaluated as alternatives to antibiotics in swine nutrition. This pilot study investigated the effects of Agolin Pig, a blend of microencapsulated essential oils, on sow performance, piglet growth, and sow fecal microbiota during lactation. Twenty-five sows were randomly assigned to either a control group (CON; n = 13) or a treatment group supplemented with Agolin Pig (AGO; n = 12; 200 ppm) from two weeks pre-farrowing through lactation. Diets for both groups met NRC (2012) nutrient requirements. Sow average daily feed intake (ADFI), body weight, body condition score (BCS), and Knauer Caliper measurements were collected at baseline, one week post-farrowing, and weaning. Piglet average daily gain (ADG) was recorded throughout lactation. Sow fecal samples were collected on d-14, d-7, d0, d8, and d16 relative to farrowing for microbiome analysis. Performance data were analyzed using PROC GLM or MIXED (SAS 9.4), with parity, number nursed, number weaned, and lactation week included as covariates. Microbiota data were analyzed in QIIME2 (v2022.8) and R (v4.2.3). Agolin Pig supplementation did not affect sow ADFI, piglet ADG, or colostrum and milk composition. However, AGO sows lost significantly less body condition during lactation, as measured by the Knauer Caliper (P = 0.010). Beta diversity differed between treatments on d8 (P = 0.029) and tended to differ on d16 (P = 0.066). Additionally, Clostridium and Streptococcus increased in CON but not AGO sows on d8 and d16, respectively. In summary, Agolin Pig supplementation reduced body condition loss and altered sow fecal microbiota diversity during lactation. These findings highlight the potential of essential oils to support sow health and productivity and warrant confirmation in larger studies.
Additional Links: PMID-41799843
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799843,
year = {2026},
author = {Fisk, AE and Dong, WX and Johnson, TA and Harlow, K and Scaff, TJ and DeDecker, AE and Hoogland, MJ and Parsley, MA and Richert, BT and Stewart, KR},
title = {Evaluation of Agolin® Pig on sow and piglet performance and sow fecal microbial communities during lactation.},
journal = {Translational animal science},
volume = {10},
number = {},
pages = {txag023},
pmid = {41799843},
issn = {2573-2102},
abstract = {Essential oils are increasingly evaluated as alternatives to antibiotics in swine nutrition. This pilot study investigated the effects of Agolin Pig, a blend of microencapsulated essential oils, on sow performance, piglet growth, and sow fecal microbiota during lactation. Twenty-five sows were randomly assigned to either a control group (CON; n = 13) or a treatment group supplemented with Agolin Pig (AGO; n = 12; 200 ppm) from two weeks pre-farrowing through lactation. Diets for both groups met NRC (2012) nutrient requirements. Sow average daily feed intake (ADFI), body weight, body condition score (BCS), and Knauer Caliper measurements were collected at baseline, one week post-farrowing, and weaning. Piglet average daily gain (ADG) was recorded throughout lactation. Sow fecal samples were collected on d-14, d-7, d0, d8, and d16 relative to farrowing for microbiome analysis. Performance data were analyzed using PROC GLM or MIXED (SAS 9.4), with parity, number nursed, number weaned, and lactation week included as covariates. Microbiota data were analyzed in QIIME2 (v2022.8) and R (v4.2.3). Agolin Pig supplementation did not affect sow ADFI, piglet ADG, or colostrum and milk composition. However, AGO sows lost significantly less body condition during lactation, as measured by the Knauer Caliper (P = 0.010). Beta diversity differed between treatments on d8 (P = 0.029) and tended to differ on d16 (P = 0.066). Additionally, Clostridium and Streptococcus increased in CON but not AGO sows on d8 and d16, respectively. In summary, Agolin Pig supplementation reduced body condition loss and altered sow fecal microbiota diversity during lactation. These findings highlight the potential of essential oils to support sow health and productivity and warrant confirmation in larger studies.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiota and metabolic characteristics in subthreshold depression based on multi-omics.
Frontiers in psychiatry, 17:1760479.
BACKGROUND: Subthreshold depression (SD) is an intermediate state between normal mood and major depressive disorder (MDD), but its biological underpinnings remain insufficiently understood. Increasing evidence suggests that gut microbiota and host metabolic alterations may contribute to early depressive pathophysiology.
METHODS: We performed full-length 16S rRNA gene sequencing and LC-MS-based untargeted metabolomics on stool and plasma samples obtained from SD subjects and healthy controls. Microbial diversity, taxonomic composition, metabolic pathway alterations, and gut microbiota-metabolite associations were analyzed using bioinformatics pipelines, KEGG annotation, and Spearman correlation analysis.
RESULTS: SD patients exhibited marked gut microbial disturbances, including reduced microbial diversity and altered abundances of key genera such as decreased Eubacterium hallii group, Blautia, Dorea, and Agathobacter, and increased Escherichia-Shigella, Monoglobus, and Lachnoclostridium. Metabolomic profiling identified widespread metabolic perturbations, mainly affecting lipid metabolism, steroid hormone biosynthesis, and amino acid pathways. Exploratory correlation analysis indicated that beneficial taxa (e.g., Eubacterium hallii group and Blautia) were positively associated with specific glycerophospholipid and steroid hormone metabolites, whereas inverse associations were observed for other lipid-related metabolites.
CONCLUSION: This integrative microbiome-metabolome analysis demonstrates that SD is accompanied by early disruptions in gut microbial composition and systemic metabolism, particularly within lipid-related pathways. These findings suggest that gut microbiota dysbiosis may reflect early metabolic dysregulation and depression-related biological vulnerability in SD and highlight the gut microbiota as a candidate biological target for early identification and intervention.
Additional Links: PMID-41799813
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799813,
year = {2026},
author = {Xian, J and Wang, L and Shang, R and Sun, M and Yua, HJ and Zhang, X and Cheng, B and Wang, SJ and Tan, QW},
title = {Gut microbiota and metabolic characteristics in subthreshold depression based on multi-omics.},
journal = {Frontiers in psychiatry},
volume = {17},
number = {},
pages = {1760479},
pmid = {41799813},
issn = {1664-0640},
abstract = {BACKGROUND: Subthreshold depression (SD) is an intermediate state between normal mood and major depressive disorder (MDD), but its biological underpinnings remain insufficiently understood. Increasing evidence suggests that gut microbiota and host metabolic alterations may contribute to early depressive pathophysiology.
METHODS: We performed full-length 16S rRNA gene sequencing and LC-MS-based untargeted metabolomics on stool and plasma samples obtained from SD subjects and healthy controls. Microbial diversity, taxonomic composition, metabolic pathway alterations, and gut microbiota-metabolite associations were analyzed using bioinformatics pipelines, KEGG annotation, and Spearman correlation analysis.
RESULTS: SD patients exhibited marked gut microbial disturbances, including reduced microbial diversity and altered abundances of key genera such as decreased Eubacterium hallii group, Blautia, Dorea, and Agathobacter, and increased Escherichia-Shigella, Monoglobus, and Lachnoclostridium. Metabolomic profiling identified widespread metabolic perturbations, mainly affecting lipid metabolism, steroid hormone biosynthesis, and amino acid pathways. Exploratory correlation analysis indicated that beneficial taxa (e.g., Eubacterium hallii group and Blautia) were positively associated with specific glycerophospholipid and steroid hormone metabolites, whereas inverse associations were observed for other lipid-related metabolites.
CONCLUSION: This integrative microbiome-metabolome analysis demonstrates that SD is accompanied by early disruptions in gut microbial composition and systemic metabolism, particularly within lipid-related pathways. These findings suggest that gut microbiota dysbiosis may reflect early metabolic dysregulation and depression-related biological vulnerability in SD and highlight the gut microbiota as a candidate biological target for early identification and intervention.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Periodontal disease and neuroinflammation in multiple sclerosis: a systematic review of current evidence.
Frontiers in dental medicine, 7:1701357.
BACKGROUND: Multiple Sclerosis (MS) is a chronic, immune-mediated neurological disorder characterized by demyelination and neurodegeneration. Emerging evidence suggests a link between MS and Periodontal Diseases (PD) through shared immune-inflammatory pathways. This review assesses the association between periodontal diseases and multiple sclerosis, focusing on immune-inflammatory interactions and clinical correlations. Despite emerging evidence, the strength of association remains unclear due to methodological heterogeneity.
AIM: To review and evaluate the literature on the epidemiological association between PD and MS in adults.
MATERIALS AND METHODS: A systematic search was conducted in PubMed, Scopus, and Cochrane. Studies with full text articles that are available in English, without time restrictions, that assessed periodontitis, oral microbiome, and salivary biomarkers in relation to MS were included. Observational studies evaluating clinical, microbiological, or immunological associations were selected. Data extraction covered periodontal parameters, salivary biomarkers, periodontal pathogens and disease severity. The risk of bias was evaluated using Newcastle-Ottawa Scale.
RESULTS: The findings indicated that patients with MS had poorer periodontal health, when compared to healthy controls. Dysbiosis in the oral microbiome was observed, with a higher abundance of periodontal pathogens. Patients with MS exhibited elevated neutrophil-lymphocyte ratios and total oxidative stress, indicating a potential link between systemic inflammation and periodontal dysbiosis. While some studies established positive association between PD and MS, others highlighted the need for further investigation due to inconsistent findings in periodontal parameters between MS patients and controls.
CONCLUSION: Despite methodological heterogeneity, the available limited evidence indicates the association between periodontitis and MS. This highlights the need for standardized periodontal assessments in research involving MS and suggests that periodontal care may hold potential as an adjunct in management of MS.
Additional Links: PMID-41799794
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799794,
year = {2026},
author = {Santhanakrishnan, S and Kannappan, K and Krithika, C and Sridhar, C and Mahendra, J},
title = {Periodontal disease and neuroinflammation in multiple sclerosis: a systematic review of current evidence.},
journal = {Frontiers in dental medicine},
volume = {7},
number = {},
pages = {1701357},
pmid = {41799794},
issn = {2673-4915},
abstract = {BACKGROUND: Multiple Sclerosis (MS) is a chronic, immune-mediated neurological disorder characterized by demyelination and neurodegeneration. Emerging evidence suggests a link between MS and Periodontal Diseases (PD) through shared immune-inflammatory pathways. This review assesses the association between periodontal diseases and multiple sclerosis, focusing on immune-inflammatory interactions and clinical correlations. Despite emerging evidence, the strength of association remains unclear due to methodological heterogeneity.
AIM: To review and evaluate the literature on the epidemiological association between PD and MS in adults.
MATERIALS AND METHODS: A systematic search was conducted in PubMed, Scopus, and Cochrane. Studies with full text articles that are available in English, without time restrictions, that assessed periodontitis, oral microbiome, and salivary biomarkers in relation to MS were included. Observational studies evaluating clinical, microbiological, or immunological associations were selected. Data extraction covered periodontal parameters, salivary biomarkers, periodontal pathogens and disease severity. The risk of bias was evaluated using Newcastle-Ottawa Scale.
RESULTS: The findings indicated that patients with MS had poorer periodontal health, when compared to healthy controls. Dysbiosis in the oral microbiome was observed, with a higher abundance of periodontal pathogens. Patients with MS exhibited elevated neutrophil-lymphocyte ratios and total oxidative stress, indicating a potential link between systemic inflammation and periodontal dysbiosis. While some studies established positive association between PD and MS, others highlighted the need for further investigation due to inconsistent findings in periodontal parameters between MS patients and controls.
CONCLUSION: Despite methodological heterogeneity, the available limited evidence indicates the association between periodontitis and MS. This highlights the need for standardized periodontal assessments in research involving MS and suggests that periodontal care may hold potential as an adjunct in management of MS.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut Microbiota Signatures and Potential Mediators in the Trajectory of Age-related Macular Degeneration: A Phased Atlas by Genetic Inference.
International journal of medical sciences, 23(3):950-962.
PURPOSE: To depict an atlas of stage-stratified gut microbiota (GM) signatures and intermediatory metabolites, inflammatory proteins, and immune cell traits, governing the AMD trajectory.
METHODS: We deployed bidirectional two-sample Mendelian randomization (TSMR) integrating GWAS data of 207 GM taxa from the Dutch Microbiome Project (N = 7,738), and multiple AMD stages/subtypes, including 'Macular degeneration (senile) of retina', 'Early AMD', 'Disease progression to GA/CNV', 'Dry AMD includes GA', and 'Wet AMD', encapsulating the disease trajectory (N > 410,000), complemented by multivariable MR (MVMR) mediation analysis of 1,400 circulating metabolites, 731 immune cell traits, and 91 inflammatory proteins.
RESULTS: We identified 12/8/5/2/9/8 genetically predicted causal GM taxa of various AMD stages/subtypes as a stage-stratified GM signature across the AMD trajectory, among which g.Ruminococcaceae and s.Ruminococcaceae_bacterium_D16 were the sole shared GM taxa in triple AMD stages, while s.Bacteroides eggerthii, c.Gammaproteobacteria, s.Dorea and s.Ruminococcus_obeum influence dual AMD stages. Bidirectional analysis revealed that f.Streptococcaceae, g.Erysipelotrichaceae_noname, g.Streptococcus, s.Streptococcus_thermophilus, g.Ruminococcaceae_noname, and s.Ruminococcaceae_bacterium_D16 exhibited genetically reciprocal causation with AMD. We also proposed that Firmicutes may exhibit stage-specific duality depending on their constituent members and AMD stages. Several understudied GM from p.Actinobacteria and p.Verrucomicrobia have been implicated as AMD-associated taxa for the first time. Key metabolites, immune cell traits, and inflammatory proteins were established as significant mediators of GM-AMD links.
CONCLUSIONS: This first phased atlas uncovers GM effects over the AMD course, identifying potential microbial and biochemical targets for intervening in disease development.
Additional Links: PMID-41799763
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799763,
year = {2026},
author = {Zhou, Y and Wang, Z and Huang, C and Yu, X and Chen, J and Jiang, X and Dong, J and Peng, Q and Li, L and Song, X and Lu, X},
title = {Gut Microbiota Signatures and Potential Mediators in the Trajectory of Age-related Macular Degeneration: A Phased Atlas by Genetic Inference.},
journal = {International journal of medical sciences},
volume = {23},
number = {3},
pages = {950-962},
pmid = {41799763},
issn = {1449-1907},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics/immunology ; *Macular Degeneration/genetics/microbiology/immunology/pathology ; Mendelian Randomization Analysis ; Genome-Wide Association Study ; Disease Progression ; Polymorphism, Single Nucleotide ; },
abstract = {PURPOSE: To depict an atlas of stage-stratified gut microbiota (GM) signatures and intermediatory metabolites, inflammatory proteins, and immune cell traits, governing the AMD trajectory.
METHODS: We deployed bidirectional two-sample Mendelian randomization (TSMR) integrating GWAS data of 207 GM taxa from the Dutch Microbiome Project (N = 7,738), and multiple AMD stages/subtypes, including 'Macular degeneration (senile) of retina', 'Early AMD', 'Disease progression to GA/CNV', 'Dry AMD includes GA', and 'Wet AMD', encapsulating the disease trajectory (N > 410,000), complemented by multivariable MR (MVMR) mediation analysis of 1,400 circulating metabolites, 731 immune cell traits, and 91 inflammatory proteins.
RESULTS: We identified 12/8/5/2/9/8 genetically predicted causal GM taxa of various AMD stages/subtypes as a stage-stratified GM signature across the AMD trajectory, among which g.Ruminococcaceae and s.Ruminococcaceae_bacterium_D16 were the sole shared GM taxa in triple AMD stages, while s.Bacteroides eggerthii, c.Gammaproteobacteria, s.Dorea and s.Ruminococcus_obeum influence dual AMD stages. Bidirectional analysis revealed that f.Streptococcaceae, g.Erysipelotrichaceae_noname, g.Streptococcus, s.Streptococcus_thermophilus, g.Ruminococcaceae_noname, and s.Ruminococcaceae_bacterium_D16 exhibited genetically reciprocal causation with AMD. We also proposed that Firmicutes may exhibit stage-specific duality depending on their constituent members and AMD stages. Several understudied GM from p.Actinobacteria and p.Verrucomicrobia have been implicated as AMD-associated taxa for the first time. Key metabolites, immune cell traits, and inflammatory proteins were established as significant mediators of GM-AMD links.
CONCLUSIONS: This first phased atlas uncovers GM effects over the AMD course, identifying potential microbial and biochemical targets for intervening in disease development.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/genetics/immunology
*Macular Degeneration/genetics/microbiology/immunology/pathology
Mendelian Randomization Analysis
Genome-Wide Association Study
Disease Progression
Polymorphism, Single Nucleotide
RevDate: 2026-03-09
CmpDate: 2026-03-09
Human milk oligosaccharides promote synaptogenesis and neurite outgrowth in human cortical organoids.
Biochemistry and biophysics reports, 45:102529.
The first 1000 days of a child's life represent a critical window for brain development, during which nutrition exerts profound effects on the trajectories of neurodevelopment. Human Milk Oligosaccharides (HMOs), a major component of human milk, are largely indigestible by infants and are known to influence immunity, microbiome composition, and gut-brain signaling, but their direct role in neurodevelopment remains poorly understood. Here, we investigated the impact of HMOs on human cortical organoids, a physiologically relevant in vitro model of early brain development. We found that HMO treatment significantly enhanced neurite outgrowth and synaptogenesis in a dose-dependent manner. Global proteomic profiling further demonstrated the upregulation of proteins associated with neuronal differentiation, synaptic maturation, and cytoskeletal remodeling. Our findings suggest that HMOs can influence neurodevelopmental processes and highlight a potential role for maternal milk components in early brain development.
Additional Links: PMID-41799697
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799697,
year = {2026},
author = {Bulcão V C, L and Moreira, NCS and Carvalho, PC and Luz, IS and de S da G Fischer, J and Tsu, BL and Sejane, K and Savo, C and Martins, AMA and Bode, L and Muotri, AR},
title = {Human milk oligosaccharides promote synaptogenesis and neurite outgrowth in human cortical organoids.},
journal = {Biochemistry and biophysics reports},
volume = {45},
number = {},
pages = {102529},
pmid = {41799697},
issn = {2405-5808},
abstract = {The first 1000 days of a child's life represent a critical window for brain development, during which nutrition exerts profound effects on the trajectories of neurodevelopment. Human Milk Oligosaccharides (HMOs), a major component of human milk, are largely indigestible by infants and are known to influence immunity, microbiome composition, and gut-brain signaling, but their direct role in neurodevelopment remains poorly understood. Here, we investigated the impact of HMOs on human cortical organoids, a physiologically relevant in vitro model of early brain development. We found that HMO treatment significantly enhanced neurite outgrowth and synaptogenesis in a dose-dependent manner. Global proteomic profiling further demonstrated the upregulation of proteins associated with neuronal differentiation, synaptic maturation, and cytoskeletal remodeling. Our findings suggest that HMOs can influence neurodevelopmental processes and highlight a potential role for maternal milk components in early brain development.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
The Role of the Gut Microbiome in Clinical Outcomes of Colorectal Cancer: A Systematic Review (2020-2025).
Oncology research, 34(3):3.
BACKGROUND: The Colorectal Cancer (CRC) pathogenesis and therapeutic efficacy are influenced by the gut microbiome, making it a promising biomarker for predicting treatment responses and adverse effects. This systematic review aims to outline the gut microbiome composition in individuals with CRC undergoing the same therapeutic regimen and evaluate interindividual microbiome profile variations to better understand how these differences may influence therapeutic outcomes.
METHODS: Key studies investigating the microbiome's role in therapeutic approaches for CRC were searched in both PubMed and Cochrane databases on 12 and 22 March 2025, respectively. Eligible studies included free full-text English-language randomized clinical trials and human observational studies reporting on gut microbiome composition and treatment outcomes. RoB 2 and ROBINS-I were employed in the evaluation of bias for randomized trials and observational studies, respectively. Data extracted was narratively analyzed.
RESULTS: Six studies involving a total of 361 individuals were included. Therapeutic interventions, either standard treatments and/or those targeting the gut microbiome, generally increased probiotic taxa and reduced pro-carcinogenic bacteria. However, no consistent pattern of improved clinical outcomes was observed, suggesting that treatment mechanisms, the tumor's nature, and individual characteristics play critical roles in microbiome modulation.
CONCLUSION: The gut microbiome holds significant potential in clinical settings. Nonetheless, further research is needed to better understand its functional aspects and to consider the influence of treatment mechanisms, the tumor's nature, and individual characteristics as modulators, in order to optimize clinical outcomes.
Additional Links: PMID-41799504
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799504,
year = {2026},
author = {Santos, I and Liberal, J and Teixeira, P and Martins, D and Mendes, F},
title = {The Role of the Gut Microbiome in Clinical Outcomes of Colorectal Cancer: A Systematic Review (2020-2025).},
journal = {Oncology research},
volume = {34},
number = {3},
pages = {3},
pmid = {41799504},
issn = {1555-3906},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/therapy ; *Gastrointestinal Microbiome ; Treatment Outcome ; Probiotics/therapeutic use ; Randomized Controlled Trials as Topic ; },
abstract = {BACKGROUND: The Colorectal Cancer (CRC) pathogenesis and therapeutic efficacy are influenced by the gut microbiome, making it a promising biomarker for predicting treatment responses and adverse effects. This systematic review aims to outline the gut microbiome composition in individuals with CRC undergoing the same therapeutic regimen and evaluate interindividual microbiome profile variations to better understand how these differences may influence therapeutic outcomes.
METHODS: Key studies investigating the microbiome's role in therapeutic approaches for CRC were searched in both PubMed and Cochrane databases on 12 and 22 March 2025, respectively. Eligible studies included free full-text English-language randomized clinical trials and human observational studies reporting on gut microbiome composition and treatment outcomes. RoB 2 and ROBINS-I were employed in the evaluation of bias for randomized trials and observational studies, respectively. Data extracted was narratively analyzed.
RESULTS: Six studies involving a total of 361 individuals were included. Therapeutic interventions, either standard treatments and/or those targeting the gut microbiome, generally increased probiotic taxa and reduced pro-carcinogenic bacteria. However, no consistent pattern of improved clinical outcomes was observed, suggesting that treatment mechanisms, the tumor's nature, and individual characteristics play critical roles in microbiome modulation.
CONCLUSION: The gut microbiome holds significant potential in clinical settings. Nonetheless, further research is needed to better understand its functional aspects and to consider the influence of treatment mechanisms, the tumor's nature, and individual characteristics as modulators, in order to optimize clinical outcomes.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Colorectal Neoplasms/microbiology/therapy
*Gastrointestinal Microbiome
Treatment Outcome
Probiotics/therapeutic use
Randomized Controlled Trials as Topic
RevDate: 2026-03-09
CmpDate: 2026-03-09
Human Leukocyte Antigen Alleles and Oral Microbiome Association With Antibody-mediated Rejection in Living-donor Liver Transplant Patients.
Journal of clinical and experimental hepatology, 16(3):103494.
BACKGROUND/AIMS: Antibody-mediated rejection (ABMR) is an important cause of graft dysfunction after liver transplantation, yet the combined influence of human leukocyte antigen (HLA) immunogenetics and the oral microbiome on ABMR risk is not well defined.
METHODS: In this prospective cohort of 180 living donor-recipient pairs, pre-transplant 16S ribosomal ribonucleic acid sequences and high-resolution HLA genotyping were done. The human leukocyte antigen epitope mismatch algorithm quantified amino acid and solvent-accessible mismatches. Oral microbiome profiles were generated using the Divisive Amplicon Denoising Algorithm (DADA2) and quantitative insights into microbial ecology version 2 (QIIME2). Associations between HLA alleles and microbial taxa were assessed using generalized linear models and linear discriminant analysis effect size (LEfSe). ABMR was diagnosed as per Banff criteria over one year.
RESULTS: ABMR was diagnosed in 15 patients. These patients had significantly higher mismatch burdens at HLA-DPB1, DQB1, and DRB1 than non-ABMR recipients. Across the cohort, 68 HLA alleles demonstrated distinct microbial associations at phylum, family, and genus levels. Alleles such as HLA-DRB108, HLA-DPB1575, and HLA-C05 were linked to differential abundance of Actinobacteriota, Campylobacterota, and Fusobacteriota, respectively. Genus-level analyses revealed strong allele-specific associations with Veillonella, Enterobacter, Streptococcus, and other immunomodulatory taxa. LEfSe identified HLA-DQB106 and HLA-DQB1∗104 as associated with enrichment of Enterobacter, Citrobacter europaeus, Bacteroides plebeius, Rothia dentocariosa, Megasphaera, and Burkholderiaceae-microbial signatures also prominent in ABMR cases.
CONCLUSION: Class II HLA mismatch burden and allele-specific oral microbial signatures are closely linked to ABMR. Combined HLA-microbiome profiling may enhance early risk stratification and inform targeted peri-transplant microbial interventions.
Additional Links: PMID-41799378
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799378,
year = {2026},
author = {Kaur, M and Babu, R and Baweja, S and Gupta, R and Singh, SP and Pamecha, V and Bihari, C},
title = {Human Leukocyte Antigen Alleles and Oral Microbiome Association With Antibody-mediated Rejection in Living-donor Liver Transplant Patients.},
journal = {Journal of clinical and experimental hepatology},
volume = {16},
number = {3},
pages = {103494},
pmid = {41799378},
issn = {0973-6883},
abstract = {BACKGROUND/AIMS: Antibody-mediated rejection (ABMR) is an important cause of graft dysfunction after liver transplantation, yet the combined influence of human leukocyte antigen (HLA) immunogenetics and the oral microbiome on ABMR risk is not well defined.
METHODS: In this prospective cohort of 180 living donor-recipient pairs, pre-transplant 16S ribosomal ribonucleic acid sequences and high-resolution HLA genotyping were done. The human leukocyte antigen epitope mismatch algorithm quantified amino acid and solvent-accessible mismatches. Oral microbiome profiles were generated using the Divisive Amplicon Denoising Algorithm (DADA2) and quantitative insights into microbial ecology version 2 (QIIME2). Associations between HLA alleles and microbial taxa were assessed using generalized linear models and linear discriminant analysis effect size (LEfSe). ABMR was diagnosed as per Banff criteria over one year.
RESULTS: ABMR was diagnosed in 15 patients. These patients had significantly higher mismatch burdens at HLA-DPB1, DQB1, and DRB1 than non-ABMR recipients. Across the cohort, 68 HLA alleles demonstrated distinct microbial associations at phylum, family, and genus levels. Alleles such as HLA-DRB108, HLA-DPB1575, and HLA-C05 were linked to differential abundance of Actinobacteriota, Campylobacterota, and Fusobacteriota, respectively. Genus-level analyses revealed strong allele-specific associations with Veillonella, Enterobacter, Streptococcus, and other immunomodulatory taxa. LEfSe identified HLA-DQB106 and HLA-DQB1∗104 as associated with enrichment of Enterobacter, Citrobacter europaeus, Bacteroides plebeius, Rothia dentocariosa, Megasphaera, and Burkholderiaceae-microbial signatures also prominent in ABMR cases.
CONCLUSION: Class II HLA mismatch burden and allele-specific oral microbial signatures are closely linked to ABMR. Combined HLA-microbiome profiling may enhance early risk stratification and inform targeted peri-transplant microbial interventions.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Bacterial vesicles-initiated in-situ spray-polymerized coating enables synergistic antibacterial-photothermal functionality for accelerating wound healing.
Theranostics, 16(9):4566-4579.
BACKGROUND: Although microbial therapies can address the harm to beneficial bacteria and microbiome balance caused by traditional antibacterial treatments in skin damage and infection, their pathogenic potential limits clinical application. Bacterial extracellular vesicles (BEVs) offer a safer alternative by targeting microbes and modulating immunity.
METHODS: Lactobacillus reuteri-derived BEVs (LBEVs) are functionalized with Fe [3+] via electrostatic adsorption, and co-sprayed with pyrrole monomers onto wounds to initiate oxidative polymerization and then form conformal polypyrrole coatings (LBEVs-PPy). Thanks to the natural antibacterial activity of LBEVs, the LBEVs-PPy coating could inhibit the growth of pathogens efficiently. Furthermore, the mild hyperthermia induced by PPy's NIR-triggered photothermal activation significantly upregulates the expression of angiogenic regulators.
RESULTS: In vitro, LBEVs effectively inhibited the growth of S. aureus, E. coli, and S. epidermidis, demonstrating potent antibacterial efficacy. Following mild hyperthermia (42 °C for 1 h), HUVECs showed elevated expression of angiogenic regulators, including VEGFA and ANGPT1. This treatment also activates HSP90/p-eNOS pathway in HUVECs, thereby accelerating angiogenesis. In a mouse model of skin damage and infection, LBEVs-PPy coating significantly accelerates wound healing through synergistic mechanisms that integrate the antibacterial activity of LBEVs and the photothermal effect of PPy.
CONCLUSIONS: Our research developed an in-situ spray-polymerized coating integrating antibacterial and photothermal modalities, thus presenting a promising biotherapeutic platform for clinical wound management and tissue regeneration.
Additional Links: PMID-41799196
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41799196,
year = {2026},
author = {Wang, D and Liang, S and Ai, Z and Kong, Q and Xing, D and Cao, Z and Geng, Z},
title = {Bacterial vesicles-initiated in-situ spray-polymerized coating enables synergistic antibacterial-photothermal functionality for accelerating wound healing.},
journal = {Theranostics},
volume = {16},
number = {9},
pages = {4566-4579},
pmid = {41799196},
issn = {1838-7640},
mesh = {Animals ; *Wound Healing/drug effects ; *Anti-Bacterial Agents/pharmacology ; Mice ; Humans ; *Extracellular Vesicles/chemistry/metabolism ; Escherichia coli/drug effects ; Human Umbilical Vein Endothelial Cells ; Polymers/chemistry/pharmacology ; *Photothermal Therapy/methods ; Staphylococcus aureus/drug effects ; Pyrroles/chemistry/pharmacology ; Disease Models, Animal ; Skin ; Neovascularization, Physiologic/drug effects ; Staphylococcus epidermidis/drug effects ; },
abstract = {BACKGROUND: Although microbial therapies can address the harm to beneficial bacteria and microbiome balance caused by traditional antibacterial treatments in skin damage and infection, their pathogenic potential limits clinical application. Bacterial extracellular vesicles (BEVs) offer a safer alternative by targeting microbes and modulating immunity.
METHODS: Lactobacillus reuteri-derived BEVs (LBEVs) are functionalized with Fe [3+] via electrostatic adsorption, and co-sprayed with pyrrole monomers onto wounds to initiate oxidative polymerization and then form conformal polypyrrole coatings (LBEVs-PPy). Thanks to the natural antibacterial activity of LBEVs, the LBEVs-PPy coating could inhibit the growth of pathogens efficiently. Furthermore, the mild hyperthermia induced by PPy's NIR-triggered photothermal activation significantly upregulates the expression of angiogenic regulators.
RESULTS: In vitro, LBEVs effectively inhibited the growth of S. aureus, E. coli, and S. epidermidis, demonstrating potent antibacterial efficacy. Following mild hyperthermia (42 °C for 1 h), HUVECs showed elevated expression of angiogenic regulators, including VEGFA and ANGPT1. This treatment also activates HSP90/p-eNOS pathway in HUVECs, thereby accelerating angiogenesis. In a mouse model of skin damage and infection, LBEVs-PPy coating significantly accelerates wound healing through synergistic mechanisms that integrate the antibacterial activity of LBEVs and the photothermal effect of PPy.
CONCLUSIONS: Our research developed an in-situ spray-polymerized coating integrating antibacterial and photothermal modalities, thus presenting a promising biotherapeutic platform for clinical wound management and tissue regeneration.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Wound Healing/drug effects
*Anti-Bacterial Agents/pharmacology
Mice
Humans
*Extracellular Vesicles/chemistry/metabolism
Escherichia coli/drug effects
Human Umbilical Vein Endothelial Cells
Polymers/chemistry/pharmacology
*Photothermal Therapy/methods
Staphylococcus aureus/drug effects
Pyrroles/chemistry/pharmacology
Disease Models, Animal
Skin
Neovascularization, Physiologic/drug effects
Staphylococcus epidermidis/drug effects
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiome dysregulation is associated with segmental glomerulosclerosis in IgA nephropathy: insights from Oxford classification-based microbiome profiling.
Frontiers in cellular and infection microbiology, 16:1644626.
BACKGROUND: IgA nephropathy (IgAN) is a common immune-complex-mediated glomerulonephritis with segmental glomerulosclerosis (S lesion, S1 in Oxford classification) being an independent predictor of poor renal prognosis, where 20%-40% of IgAN-S1 patients progress to end-stage renal disease, but its pathogenesis is unclear.
METHODS: This study enrolled 12 IgAN-S0 (without segmental sclerosis) and 19 IgAN-S1 (with segmental sclerosis) patients, performed 16S rRNA gene sequencing on fecal samples, and analyzed gut microbiota composition and functions.
RESULTS: S1 had enriched Firmicutes and Patescibacteria while S0 had more Proteobacteria, Campylobacterota, and Desulfobacterota; LEfSe analysis identified Subdoligranulum and unclassified_Erysipelotrichaceae_UCG-003 as S1-specific biomarkers and Phascolarctobacterium, Streptococcus_parasanguinis, and Proteobacteria as S0 biomarkers (P<0.05). Functional prediction showed S1 was enriched in pro-inflammatory pathways like endoplasmic reticulum stress and secondary bile acid biosynthesis, while S0 had activated protective pathways such as cytochrome P450 drug metabolism and ubiquitin system.
CONCLUSIONS: This study reveals gut microbiota dysregulation is closely associated with IgAN segmental sclerosis, with S1 showing pro-inflammatory microbial profiles and S0 retaining protective functions, providing new insights into gut-kidney axis mechanisms and potential microbiome-targeted therapies for IgAN.
Additional Links: PMID-41798752
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41798752,
year = {2026},
author = {Lu, B and Zhang, A and Wu, M and Chen, S and Wang, Y and Wang, J and Huang, M and Zhu, Y and Liu, H and Zhu, F and Zeng, X and Chen, S and Zhou, X and Lin, R},
title = {Gut microbiome dysregulation is associated with segmental glomerulosclerosis in IgA nephropathy: insights from Oxford classification-based microbiome profiling.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1644626},
pmid = {41798752},
issn = {2235-2988},
mesh = {Humans ; *Glomerulonephritis, IGA/microbiology/pathology ; *Gastrointestinal Microbiome ; Male ; RNA, Ribosomal, 16S/genetics ; Female ; Adult ; Feces/microbiology ; *Bacteria/classification/genetics/isolation & purification ; *Glomerulosclerosis, Focal Segmental/microbiology/pathology ; Middle Aged ; Biomarkers ; Dysbiosis ; DNA, Bacterial/genetics ; },
abstract = {BACKGROUND: IgA nephropathy (IgAN) is a common immune-complex-mediated glomerulonephritis with segmental glomerulosclerosis (S lesion, S1 in Oxford classification) being an independent predictor of poor renal prognosis, where 20%-40% of IgAN-S1 patients progress to end-stage renal disease, but its pathogenesis is unclear.
METHODS: This study enrolled 12 IgAN-S0 (without segmental sclerosis) and 19 IgAN-S1 (with segmental sclerosis) patients, performed 16S rRNA gene sequencing on fecal samples, and analyzed gut microbiota composition and functions.
RESULTS: S1 had enriched Firmicutes and Patescibacteria while S0 had more Proteobacteria, Campylobacterota, and Desulfobacterota; LEfSe analysis identified Subdoligranulum and unclassified_Erysipelotrichaceae_UCG-003 as S1-specific biomarkers and Phascolarctobacterium, Streptococcus_parasanguinis, and Proteobacteria as S0 biomarkers (P<0.05). Functional prediction showed S1 was enriched in pro-inflammatory pathways like endoplasmic reticulum stress and secondary bile acid biosynthesis, while S0 had activated protective pathways such as cytochrome P450 drug metabolism and ubiquitin system.
CONCLUSIONS: This study reveals gut microbiota dysregulation is closely associated with IgAN segmental sclerosis, with S1 showing pro-inflammatory microbial profiles and S0 retaining protective functions, providing new insights into gut-kidney axis mechanisms and potential microbiome-targeted therapies for IgAN.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Glomerulonephritis, IGA/microbiology/pathology
*Gastrointestinal Microbiome
Male
RNA, Ribosomal, 16S/genetics
Female
Adult
Feces/microbiology
*Bacteria/classification/genetics/isolation & purification
*Glomerulosclerosis, Focal Segmental/microbiology/pathology
Middle Aged
Biomarkers
Dysbiosis
DNA, Bacterial/genetics
RevDate: 2026-03-09
CmpDate: 2026-03-09
Predicting inter-microbial host specificity in oral biofilms using a lightweight relation-aware knowledge graph model.
Frontiers in cellular and infection microbiology, 16:1775191.
INTRODUCTION: The human oral cavity hosts a complex microbial ecosystem of bacteria, viruses, bacteriophages, and other microorganisms forming biofilms in different niches. Phage-bacteria host specificity is crucial in shaping microbial community, stability, and dysbiosis. mapping this specificity is limited by experimental constraints and traditional methods can't capture ecological complexity. The goal is to create a graph-based model that treats inter-microbial host specificity as a relational learning problem, integrating taxonomic, ecological, and infection data into a knowledge graph. This improves phage-bacteria host predictions and reveals microbial hubs and interaction patterns related to periodontal disease dysbiosis.
METHODS: This study introduces a lightweight, relation-aware knowledge graph for predicting microbial host specificity in oral biofilms. We built a heterogeneous graph of the oral microbiome, incorporating microbial taxa, anatomical sites, taxonomic hierarchies, enrichment patterns, and INFECTS relationships. The dataset includes 500 viral taxa across four oral niches, with 21,338 significant co-occurrence relationships and various biological features. To learn meaningful representations, we combined graph embeddings with microbial features. We developed a relation-aware graph neural network, IK-BRNet, to efficiently encode ecological and interaction semantics.
RESULTS: Model performance was evaluated against a conventional Graph Attention Network (GAT) using stratified training, validation, and test splits with class imbalance correction. IK-BRNet demonstrated faster convergence and superior discrimination ability, achieving a higher AUC-ROC (0.929 vs. 0.904) and markedly improved sensitivity for disease-associated viral taxa (93.8% vs. 56.3%). While the baseline GAT achieved higher accuracy and specificity, IK-BRNet consistently reduced false negatives, thereby improving its ability to detect disease-related microbial signals. Site-specific predictions confirmed biological validity, with the highest disease scores for dental plaque-associated viruses and lower scores in healthy niches such as the tongue and buccal mucosa.
CONCLSUION: This study shows that relation-aware graph learning offers a meaningful and efficient way to model inter-microbial host specificity in oral biofilms. The framework improves oral microbiome network inference and supports disease screening, ecological analysis, and microbiome-based dentistry.
Additional Links: PMID-41798747
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41798747,
year = {2026},
author = {Natarajan, PM and Varma, SR and Kodangattil Narayanan, J and Odeh, R},
title = {Predicting inter-microbial host specificity in oral biofilms using a lightweight relation-aware knowledge graph model.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1775191},
pmid = {41798747},
issn = {2235-2988},
mesh = {*Mouth/microbiology/virology ; *Biofilms/growth & development ; Humans ; Microbiota ; *Bacteria/classification ; *Host Specificity ; Neural Networks, Computer ; Bacteriophages/physiology ; Periodontal Diseases/microbiology ; Dysbiosis/microbiology ; },
abstract = {INTRODUCTION: The human oral cavity hosts a complex microbial ecosystem of bacteria, viruses, bacteriophages, and other microorganisms forming biofilms in different niches. Phage-bacteria host specificity is crucial in shaping microbial community, stability, and dysbiosis. mapping this specificity is limited by experimental constraints and traditional methods can't capture ecological complexity. The goal is to create a graph-based model that treats inter-microbial host specificity as a relational learning problem, integrating taxonomic, ecological, and infection data into a knowledge graph. This improves phage-bacteria host predictions and reveals microbial hubs and interaction patterns related to periodontal disease dysbiosis.
METHODS: This study introduces a lightweight, relation-aware knowledge graph for predicting microbial host specificity in oral biofilms. We built a heterogeneous graph of the oral microbiome, incorporating microbial taxa, anatomical sites, taxonomic hierarchies, enrichment patterns, and INFECTS relationships. The dataset includes 500 viral taxa across four oral niches, with 21,338 significant co-occurrence relationships and various biological features. To learn meaningful representations, we combined graph embeddings with microbial features. We developed a relation-aware graph neural network, IK-BRNet, to efficiently encode ecological and interaction semantics.
RESULTS: Model performance was evaluated against a conventional Graph Attention Network (GAT) using stratified training, validation, and test splits with class imbalance correction. IK-BRNet demonstrated faster convergence and superior discrimination ability, achieving a higher AUC-ROC (0.929 vs. 0.904) and markedly improved sensitivity for disease-associated viral taxa (93.8% vs. 56.3%). While the baseline GAT achieved higher accuracy and specificity, IK-BRNet consistently reduced false negatives, thereby improving its ability to detect disease-related microbial signals. Site-specific predictions confirmed biological validity, with the highest disease scores for dental plaque-associated viruses and lower scores in healthy niches such as the tongue and buccal mucosa.
CONCLSUION: This study shows that relation-aware graph learning offers a meaningful and efficient way to model inter-microbial host specificity in oral biofilms. The framework improves oral microbiome network inference and supports disease screening, ecological analysis, and microbiome-based dentistry.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Mouth/microbiology/virology
*Biofilms/growth & development
Humans
Microbiota
*Bacteria/classification
*Host Specificity
Neural Networks, Computer
Bacteriophages/physiology
Periodontal Diseases/microbiology
Dysbiosis/microbiology
RevDate: 2026-03-09
CmpDate: 2026-03-09
Diabetes Mellitus Accelerates Alzheimer's Disease Development by Affecting the Gut Microbiome.
BioMed research international, 2026:9974079.
Increasing evidence suggests a link between Alzheimer's disease (AD) and diabetes mellitus (DM). However, the precise mechanisms by which DM contributes to AD remain unclear. This study is aimed at elucidating the potential role of DM in the early stages of AD. Accordingly, a streptozotocin (STZ)-induced diabetic 5 × familial AD (FAD) mouse model was established. Immunohistochemistry and positron emission tomography/computed tomography (PET/CT) scanning were performed to examine amyloid beta (Aβ) deposition in the brain. The integrity of the colonic epithelium was assessed using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunofluorescence staining. Microbial diversity analysis was conducted for 5 × FAD mice with and without STZ-induced DM to determine shifts in intestinal flora profiles. After oral administration of butyrate to STZ-treated 5 × FAD mice, we observed that Aβ deposition in the brain was decreased, and the intestinal flora improved. Immunohistochemistry and PET/CT findings revealed a marked increase in Aβ formation in the brains of 5 × FAD mice treated with STZ. qRT-PCR and immunofluorescence staining revealed severe intestinal barrier dysfunction in these mice. Gut microbiota sequencing indicated significant dysbiosis in STZ-treated 5 × FAD mice, characterized by a reduction in short-chain fatty acid (SCFA)-producing species. After oral administration of butyrate, Aβ deposition in the brains of STZ-treated 5 × FAD mice was significantly reduced, and beneficial changes occurred in the intestinal flora, including increases in bacteria associated with SCFA production and neurological function. Dysregulation of the gut microbiome may exacerbate cerebral amyloidosis during AD pathogenesis. Microbes associated with SCFA production may play a beneficial role in AD treatment, and butyrate supplementation can significantly delay AD progression.
Additional Links: PMID-41798687
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41798687,
year = {2026},
author = {He, Q and Zhao, Z and Jiang, D and Fei, A},
title = {Diabetes Mellitus Accelerates Alzheimer's Disease Development by Affecting the Gut Microbiome.},
journal = {BioMed research international},
volume = {2026},
number = {},
pages = {9974079},
pmid = {41798687},
issn = {2314-6141},
mesh = {*Gastrointestinal Microbiome/physiology/drug effects ; *Alzheimer Disease/microbiology/pathology/metabolism ; Animals ; Mice ; Brain/metabolism/pathology/diagnostic imaging ; Amyloid beta-Peptides/metabolism ; *Diabetes Mellitus, Experimental/microbiology/complications ; Male ; Butyrates/pharmacology ; Disease Models, Animal ; Positron Emission Tomography Computed Tomography ; Mice, Inbred C57BL ; Fatty Acids, Volatile/metabolism ; },
abstract = {Increasing evidence suggests a link between Alzheimer's disease (AD) and diabetes mellitus (DM). However, the precise mechanisms by which DM contributes to AD remain unclear. This study is aimed at elucidating the potential role of DM in the early stages of AD. Accordingly, a streptozotocin (STZ)-induced diabetic 5 × familial AD (FAD) mouse model was established. Immunohistochemistry and positron emission tomography/computed tomography (PET/CT) scanning were performed to examine amyloid beta (Aβ) deposition in the brain. The integrity of the colonic epithelium was assessed using quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and immunofluorescence staining. Microbial diversity analysis was conducted for 5 × FAD mice with and without STZ-induced DM to determine shifts in intestinal flora profiles. After oral administration of butyrate to STZ-treated 5 × FAD mice, we observed that Aβ deposition in the brain was decreased, and the intestinal flora improved. Immunohistochemistry and PET/CT findings revealed a marked increase in Aβ formation in the brains of 5 × FAD mice treated with STZ. qRT-PCR and immunofluorescence staining revealed severe intestinal barrier dysfunction in these mice. Gut microbiota sequencing indicated significant dysbiosis in STZ-treated 5 × FAD mice, characterized by a reduction in short-chain fatty acid (SCFA)-producing species. After oral administration of butyrate, Aβ deposition in the brains of STZ-treated 5 × FAD mice was significantly reduced, and beneficial changes occurred in the intestinal flora, including increases in bacteria associated with SCFA production and neurological function. Dysregulation of the gut microbiome may exacerbate cerebral amyloidosis during AD pathogenesis. Microbes associated with SCFA production may play a beneficial role in AD treatment, and butyrate supplementation can significantly delay AD progression.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Gastrointestinal Microbiome/physiology/drug effects
*Alzheimer Disease/microbiology/pathology/metabolism
Animals
Mice
Brain/metabolism/pathology/diagnostic imaging
Amyloid beta-Peptides/metabolism
*Diabetes Mellitus, Experimental/microbiology/complications
Male
Butyrates/pharmacology
Disease Models, Animal
Positron Emission Tomography Computed Tomography
Mice, Inbred C57BL
Fatty Acids, Volatile/metabolism
RevDate: 2026-03-09
CmpDate: 2026-03-09
Fecal microbiota transplantation in ulcerative colitis: evidence, mechanisms, and practice considerations.
Therapeutic advances in gastroenterology, 19:17562848261426284.
Ulcerative colitis (UC) is a chronic inflammatory bowel disease strongly associated with intestinal dysbiosis, reduced microbial diversity, and disrupted microbial metabolite profiles. Fecal microbiota transplantation (FMT) aims to restore microbial homeostasis and has shown a signal of benefit for induction of remission in some trials, but results are heterogeneous and long-term maintenance efficacy remains uncertain. In this narrative review, we synthesize randomized controlled trials (RCTs), systematic reviews/meta-analyses, and recent guideline and regulatory updates on FMT in UC, and integrate mechanistic insights from microbiome and metabolomics research. Across RCTs, intensive lower-gastrointestinal regimens using pooled, multidonor material, and/or anaerobic processing have most consistently achieved modestly higher steroid-free clinical and endoscopic remission than placebo in mild-to-moderate UC (approximately 25%-32% vs 5%-10% in representative studies), whereas upper-gastrointestinal delivery or oral lyophilized formulations and highly restrictive donor selection have yielded mixed or negative results. Mechanistically, responders commonly demonstrate engraftment of short-chain fatty acid producing taxa and restoration of secondary bile acid pathways. Safety profiles in trials are generally comparable to placebo for common mild adverse events, but rare severe transmissions (e.g., multidrug-resistant Escherichia coli and SARS-CoV-2) have driven stricter donor screening and have limited routine use outside regulated programs. Current guidelines recommend against FMT for UC outside clinical trials. Future work should prioritize standardized protocols, biomarker-guided personalization, combination strategies (diet/priming), and development of defined microbial therapeutics to improve efficacy and safety.
Additional Links: PMID-41798257
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41798257,
year = {2026},
author = {Liu, J and Wu, X},
title = {Fecal microbiota transplantation in ulcerative colitis: evidence, mechanisms, and practice considerations.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261426284},
pmid = {41798257},
issn = {1756-283X},
abstract = {Ulcerative colitis (UC) is a chronic inflammatory bowel disease strongly associated with intestinal dysbiosis, reduced microbial diversity, and disrupted microbial metabolite profiles. Fecal microbiota transplantation (FMT) aims to restore microbial homeostasis and has shown a signal of benefit for induction of remission in some trials, but results are heterogeneous and long-term maintenance efficacy remains uncertain. In this narrative review, we synthesize randomized controlled trials (RCTs), systematic reviews/meta-analyses, and recent guideline and regulatory updates on FMT in UC, and integrate mechanistic insights from microbiome and metabolomics research. Across RCTs, intensive lower-gastrointestinal regimens using pooled, multidonor material, and/or anaerobic processing have most consistently achieved modestly higher steroid-free clinical and endoscopic remission than placebo in mild-to-moderate UC (approximately 25%-32% vs 5%-10% in representative studies), whereas upper-gastrointestinal delivery or oral lyophilized formulations and highly restrictive donor selection have yielded mixed or negative results. Mechanistically, responders commonly demonstrate engraftment of short-chain fatty acid producing taxa and restoration of secondary bile acid pathways. Safety profiles in trials are generally comparable to placebo for common mild adverse events, but rare severe transmissions (e.g., multidrug-resistant Escherichia coli and SARS-CoV-2) have driven stricter donor screening and have limited routine use outside regulated programs. Current guidelines recommend against FMT for UC outside clinical trials. Future work should prioritize standardized protocols, biomarker-guided personalization, combination strategies (diet/priming), and development of defined microbial therapeutics to improve efficacy and safety.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
The impact of gut microbiota on leukemia and prospects for novel therapies.
Infectious medicine, 5(1):100239.
The Human Microbiome Project has underscored the pivotal role of the gut microbiome in human health, revealing its potential influence on leukemia development, progression, and treatment response. This review summarizes evidence on microbiome-targeted therapies such as probiotics, fecal microbiota transplantation, antimicrobial peptides, and nanoparticles. These approaches may improve leukemia treatment outcomes through immune and metabolic modulation and reduced toxicity. Although emerging data suggest beneficial effects, most findings remain correlative and limited by small, heterogeneous studies. Further mechanistic and clinical research is required to clarify causal pathways, standardize interventions, and evaluate long-term safety. Personalized microbiome-based strategies that integrate molecular and immunologic profiling may ultimately refine leukemia management and improve survival.
Additional Links: PMID-41797849
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797849,
year = {2026},
author = {Jalalifar, S and Bajelan, B and Mohammadi, R and Ghafoury, R and Kalhori, Z and Pooshang-Bagheri, K and Nekouian, R and Faranoush, M},
title = {The impact of gut microbiota on leukemia and prospects for novel therapies.},
journal = {Infectious medicine},
volume = {5},
number = {1},
pages = {100239},
pmid = {41797849},
issn = {2772-431X},
abstract = {The Human Microbiome Project has underscored the pivotal role of the gut microbiome in human health, revealing its potential influence on leukemia development, progression, and treatment response. This review summarizes evidence on microbiome-targeted therapies such as probiotics, fecal microbiota transplantation, antimicrobial peptides, and nanoparticles. These approaches may improve leukemia treatment outcomes through immune and metabolic modulation and reduced toxicity. Although emerging data suggest beneficial effects, most findings remain correlative and limited by small, heterogeneous studies. Further mechanistic and clinical research is required to clarify causal pathways, standardize interventions, and evaluate long-term safety. Personalized microbiome-based strategies that integrate molecular and immunologic profiling may ultimately refine leukemia management and improve survival.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Cold exposure and human metabolism: A heterogeneous response across tissues and organs.
Temperature (Austin, Tex.), 13(1):15-50.
Cold-induced metabolic responses across human organs and tissues vary markedly and do not regulate metabolism uniformly. The magnitude and nature of these responses differ depending on the type of cold exposure, ranging from mild surface cooling and beta-adrenergic stimulation to deep tissue cooling impacting intracellular biophysical and metabolic properties. Upregulating brown adipose tissue (BAT) activity has been proposed to improve whole-body metabolism. Despite its high metabolic activity, BAT mass is typically only 50-100 g and may contribute less than 1% of total heat production during thermogenesis. In contrast, skeletal muscles and white adipocytes may play greater roles in thermogenic and metabolic regulation. Cold exposure triggers a cascade of metabolic responses across tissues, extending beyond fuel partitioning and the regulation of uncoupling proteins. It also alters gene expression, protein synthesis, and metabolic pathways. In response to cold, the body increases sympathetic nervous system activity, leading to peripheral vasoconstriction and energy substrate mobilization. Brown adipocytes increase mitochondrial uncoupling to produce heat, while skeletal muscle contributes through shivering and non-shivering thermogenesis. The liver adjusts glucose production and lipid metabolism, the heart and circulatory system adapt to altered hemodynamic demands, and the kidneys modify fluid balance. Endocrine systems, including the thyroid, amplify thermogenic capacity, and the brain integrates thermal sensing with behavioral responses. Cold exposure also modulates immune function, cytokine profiles and inflammatory pathways across tissues, and shifts in gut microbiome composition influence nutrient absorption, bile acid metabolism and energy homeostasis. These coordinated tissue-specific adaptations enable the maintenance of core temperature during cold stress.
Additional Links: PMID-41797814
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797814,
year = {2026},
author = {Tetzlaff, EJ and Hancock, C and Waddell, L and Gagnon, SS and Mäkelä, KA and Karhu, T and Peltonen, JE and Herzig, KH and Gagnon, DD},
title = {Cold exposure and human metabolism: A heterogeneous response across tissues and organs.},
journal = {Temperature (Austin, Tex.)},
volume = {13},
number = {1},
pages = {15-50},
pmid = {41797814},
issn = {2332-8940},
abstract = {Cold-induced metabolic responses across human organs and tissues vary markedly and do not regulate metabolism uniformly. The magnitude and nature of these responses differ depending on the type of cold exposure, ranging from mild surface cooling and beta-adrenergic stimulation to deep tissue cooling impacting intracellular biophysical and metabolic properties. Upregulating brown adipose tissue (BAT) activity has been proposed to improve whole-body metabolism. Despite its high metabolic activity, BAT mass is typically only 50-100 g and may contribute less than 1% of total heat production during thermogenesis. In contrast, skeletal muscles and white adipocytes may play greater roles in thermogenic and metabolic regulation. Cold exposure triggers a cascade of metabolic responses across tissues, extending beyond fuel partitioning and the regulation of uncoupling proteins. It also alters gene expression, protein synthesis, and metabolic pathways. In response to cold, the body increases sympathetic nervous system activity, leading to peripheral vasoconstriction and energy substrate mobilization. Brown adipocytes increase mitochondrial uncoupling to produce heat, while skeletal muscle contributes through shivering and non-shivering thermogenesis. The liver adjusts glucose production and lipid metabolism, the heart and circulatory system adapt to altered hemodynamic demands, and the kidneys modify fluid balance. Endocrine systems, including the thyroid, amplify thermogenic capacity, and the brain integrates thermal sensing with behavioral responses. Cold exposure also modulates immune function, cytokine profiles and inflammatory pathways across tissues, and shifts in gut microbiome composition influence nutrient absorption, bile acid metabolism and energy homeostasis. These coordinated tissue-specific adaptations enable the maintenance of core temperature during cold stress.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut microbiota and sarcoidosis: a concise review.
Frontiers in medicine, 13:1747012.
Microbial involvement in sarcoidosis pathogenesis is suggested by the observation that histological findings in sarcoid granulomas are like those of leprosy, tuberculosis and parasitic infection. Some studies have shown that the lung microbiome in patients with sarcoidosis is different from healthy individuals. Results are conflicting, reporting an abundance or decrease in bacterial and fungal species. The altered composition of the microbiome in sarcoidosis can contribute to the formation of granulomas, typical lesions of the disease, through interactions with the host immune system. However, no single microbe has been clearly demonstrated as a cause of sarcoidosis, several microorganisms have been involved in the formation of granulomas and are under study. In fact, various microorganisms have been detected in sarcoid granulomas and in the tissue of different organs. Microorganisms were demonstrated at the genomic level and only a few studies showed microbial presence using bacteriological or proteomic methods. A possible microbial involvement in sarcoidosis pathogenesis is further supported by studies reporting innate immune system activation and increased inflammatory cytokines secretion. Of note, a meta-analysis involving over 6,000 patients identified a strong association between Cutibacterium acnes and Mycobacterium tuberculosis and sarcoidosis. Interestingly, some studies have compared microbiomes in sarcoidosis with chronic respiratory conditions like chronic obstructive pulmonary disease, asthma, interstitial lung disease, and occupational lung diseases. Little is known whether gut microbiota alteration plays a causal role in the development of these diseases or is a consequence of a shared risk factor profile. However, current evidence does not conclusively support the causative role of microbes in sarcoidosis. Furthermore, research is studying the role of intestinal microbiomes in sarcoidosis with some studies showing that the restoration of the intestinal microbiome could be a possible therapeutic approach. The aims of the review are: (1) to clarify microbial involvement in sarcoidosis pathogenesis, (2) to describe microbiota in lungs of patients with sarcoidosis and to compare the data with other interstitial lung diseases.
Additional Links: PMID-41797790
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797790,
year = {2026},
author = {Carbone, RG and Puppo, F and Tapson, VF},
title = {Gut microbiota and sarcoidosis: a concise review.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1747012},
pmid = {41797790},
issn = {2296-858X},
abstract = {Microbial involvement in sarcoidosis pathogenesis is suggested by the observation that histological findings in sarcoid granulomas are like those of leprosy, tuberculosis and parasitic infection. Some studies have shown that the lung microbiome in patients with sarcoidosis is different from healthy individuals. Results are conflicting, reporting an abundance or decrease in bacterial and fungal species. The altered composition of the microbiome in sarcoidosis can contribute to the formation of granulomas, typical lesions of the disease, through interactions with the host immune system. However, no single microbe has been clearly demonstrated as a cause of sarcoidosis, several microorganisms have been involved in the formation of granulomas and are under study. In fact, various microorganisms have been detected in sarcoid granulomas and in the tissue of different organs. Microorganisms were demonstrated at the genomic level and only a few studies showed microbial presence using bacteriological or proteomic methods. A possible microbial involvement in sarcoidosis pathogenesis is further supported by studies reporting innate immune system activation and increased inflammatory cytokines secretion. Of note, a meta-analysis involving over 6,000 patients identified a strong association between Cutibacterium acnes and Mycobacterium tuberculosis and sarcoidosis. Interestingly, some studies have compared microbiomes in sarcoidosis with chronic respiratory conditions like chronic obstructive pulmonary disease, asthma, interstitial lung disease, and occupational lung diseases. Little is known whether gut microbiota alteration plays a causal role in the development of these diseases or is a consequence of a shared risk factor profile. However, current evidence does not conclusively support the causative role of microbes in sarcoidosis. Furthermore, research is studying the role of intestinal microbiomes in sarcoidosis with some studies showing that the restoration of the intestinal microbiome could be a possible therapeutic approach. The aims of the review are: (1) to clarify microbial involvement in sarcoidosis pathogenesis, (2) to describe microbiota in lungs of patients with sarcoidosis and to compare the data with other interstitial lung diseases.},
}
RevDate: 2026-03-09
CmpDate: 2026-03-09
Gut Microbiome Dysbiosis Promotes Gallstone Formation via Bile Acid Metabolic Disorder: A Multiomics Study.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 40(6):e71656.
Gallstone disease is a common global digestive disorder. This study intends to analyze gut microbiota-gallstone disease interactions, to inform disease mechanism and microbiota-targeted prevention and treatment strategies. Participants were recruited from health check-up populations, outpatients, and inpatients. Basic information and biological samples were collected: fecal samples for metagenomic sequencing, and serum samples for bile acid metabolism detection. A total of 62 gallstone patients and 62 healthy controls were enrolled in this study. Compared with the control group, gallstone patients exhibited increased level of bile salt hydrolase (BSH)-producing bacteria, including the genera Bacteroides, Enterococcus, Bifidobacterium, and the family Lactobacillaceae. Further KEGG analysis revealed that the significantly enriched signaling pathways in the gallstone patients were mainly related to bile acid biosynthesis, lipid and bile acid precursor metabolism. Subsequently, we found that in gallstone patients, the levels of hydrophobic bile acids, (e.g., lithocholic acid, LCA), was increased, while the levels of hydrophilic bile acids taurolithocholic acid (TLCA) were decreased. In the correlation analysis between differential bile acids and differential bacterial species, Bacteroides intestinalis was positively correlated with LCA, while Bacteroides fragilis was negatively correlated with TLCA. These results further confirm the role of BSH-active bacteria in bile acid dysregulation. This study proposes the "intestinal microbiota imbalance-bile acid metabolic disorder-gallbladder stone formation" axis, and confirms that gallstone patients exhibit intestinal dysbiosis, which leads to bile acid dysregulation. Furthermore, the accumulation of hydrophobic bile acids is identified as a key factor in gallbladder stone formation.
Additional Links: PMID-41797508
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797508,
year = {2026},
author = {Huang, C and Xiao, W and Zhao, J and Zhong, R and Gao, L and Ma, H and Tian, L and Yue, P and Lin, Y and He, Q and Xia, B and Yuan, J and Yang, M and Meng, W},
title = {Gut Microbiome Dysbiosis Promotes Gallstone Formation via Bile Acid Metabolic Disorder: A Multiomics Study.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {6},
pages = {e71656},
pmid = {41797508},
issn = {1530-6860},
support = {82204123//MOST | National Natural Science Foundation of China (NSFC)/ ; 82473707//MOST | National Natural Science Foundation of China (NSFC)/ ; LCYSSQ20220823091203008//Funding of Shenzhen Clinical Research Center for Gastroenterlogy (Gastrointestinal Surgery)/ ; 2022YFC2407405//MOST | National Key Research and Development Program of China (NKPs)/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Bile Acids and Salts/metabolism ; *Dysbiosis/microbiology/metabolism/complications ; *Gallstones/microbiology/metabolism/etiology ; Male ; Female ; Middle Aged ; Feces/microbiology ; Adult ; Aged ; Multiomics ; Amidohydrolases ; },
abstract = {Gallstone disease is a common global digestive disorder. This study intends to analyze gut microbiota-gallstone disease interactions, to inform disease mechanism and microbiota-targeted prevention and treatment strategies. Participants were recruited from health check-up populations, outpatients, and inpatients. Basic information and biological samples were collected: fecal samples for metagenomic sequencing, and serum samples for bile acid metabolism detection. A total of 62 gallstone patients and 62 healthy controls were enrolled in this study. Compared with the control group, gallstone patients exhibited increased level of bile salt hydrolase (BSH)-producing bacteria, including the genera Bacteroides, Enterococcus, Bifidobacterium, and the family Lactobacillaceae. Further KEGG analysis revealed that the significantly enriched signaling pathways in the gallstone patients were mainly related to bile acid biosynthesis, lipid and bile acid precursor metabolism. Subsequently, we found that in gallstone patients, the levels of hydrophobic bile acids, (e.g., lithocholic acid, LCA), was increased, while the levels of hydrophilic bile acids taurolithocholic acid (TLCA) were decreased. In the correlation analysis between differential bile acids and differential bacterial species, Bacteroides intestinalis was positively correlated with LCA, while Bacteroides fragilis was negatively correlated with TLCA. These results further confirm the role of BSH-active bacteria in bile acid dysregulation. This study proposes the "intestinal microbiota imbalance-bile acid metabolic disorder-gallbladder stone formation" axis, and confirms that gallstone patients exhibit intestinal dysbiosis, which leads to bile acid dysregulation. Furthermore, the accumulation of hydrophobic bile acids is identified as a key factor in gallbladder stone formation.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/physiology
*Bile Acids and Salts/metabolism
*Dysbiosis/microbiology/metabolism/complications
*Gallstones/microbiology/metabolism/etiology
Male
Female
Middle Aged
Feces/microbiology
Adult
Aged
Multiomics
Amidohydrolases
RevDate: 2026-03-09
CmpDate: 2026-03-09
Human Intestinal Microbiota Composition Shapes Model Polyfluoroalkyl Substance Biotransformation.
Chembiochem : a European journal of chemical biology, 27(5):e202500905.
6:2 polyfluoroalkyl phosphate diester (6:2 diPAP) is a prevalent environmental contaminant to which humans are regularly exposed. Environmental microbes can biotransform 6:2 diPAP, and the human gut microbiome can biotransform its congener, 8:2 monoPAP. While the human gut microbiome is highly variable between individuals, potential variability in PAP biotransformation has yet to be assessed. We address this gap using six cohorts (A-F) to examine in vitro biotransformation of 6:2 diPAP by the human gut microbiome. Biotransformation pathways of 6:2 diPAP and their connections to the composition of microbial taxa were assessed using gas chromatography mass spectrometry (GC-MS), liquid chromatography tandem mass spectrometry (LC-MS/MS) and 16S rRNA amplicon sequencing. All cohorts biotransformed 6:2 diPAP but differed in their downstream perfluoroalkyl acid (PFAA) profiles, suggesting diverse biotransformation pathways. Microbial community analysis showed similar alpha diversity across cohorts, while the degree of difference between cohorts varied. The analysis confirmed the initial composition of each cohort's microbial community had a bearing on products stemming from 6:2 diPAP transformation, likely driven by low-abundance microbial taxa. These findings underscore the complexity of microbe-mediated polyfluoroalkyl substance (PFAS) transformation and highlight the need for mechanistic studies that identify the genetic controls governing PFAS transformations in the gut microbiome.
Additional Links: PMID-41797364
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797364,
year = {2026},
author = {Peskett, ST and Grégoire, DS and Rand, AA},
title = {Human Intestinal Microbiota Composition Shapes Model Polyfluoroalkyl Substance Biotransformation.},
journal = {Chembiochem : a European journal of chemical biology},
volume = {27},
number = {5},
pages = {e202500905},
pmid = {41797364},
issn = {1439-7633},
support = {RGPIN-2018-05330//Natural Science and Engineering Research Council/ ; NFRFE-2023-00695//New Frontiers in Research Fund/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; Biotransformation ; RNA, Ribosomal, 16S/genetics ; Tandem Mass Spectrometry ; *Organophosphates/metabolism/chemistry ; *Fluorocarbons/metabolism ; },
abstract = {6:2 polyfluoroalkyl phosphate diester (6:2 diPAP) is a prevalent environmental contaminant to which humans are regularly exposed. Environmental microbes can biotransform 6:2 diPAP, and the human gut microbiome can biotransform its congener, 8:2 monoPAP. While the human gut microbiome is highly variable between individuals, potential variability in PAP biotransformation has yet to be assessed. We address this gap using six cohorts (A-F) to examine in vitro biotransformation of 6:2 diPAP by the human gut microbiome. Biotransformation pathways of 6:2 diPAP and their connections to the composition of microbial taxa were assessed using gas chromatography mass spectrometry (GC-MS), liquid chromatography tandem mass spectrometry (LC-MS/MS) and 16S rRNA amplicon sequencing. All cohorts biotransformed 6:2 diPAP but differed in their downstream perfluoroalkyl acid (PFAA) profiles, suggesting diverse biotransformation pathways. Microbial community analysis showed similar alpha diversity across cohorts, while the degree of difference between cohorts varied. The analysis confirmed the initial composition of each cohort's microbial community had a bearing on products stemming from 6:2 diPAP transformation, likely driven by low-abundance microbial taxa. These findings underscore the complexity of microbe-mediated polyfluoroalkyl substance (PFAS) transformation and highlight the need for mechanistic studies that identify the genetic controls governing PFAS transformations in the gut microbiome.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome
Biotransformation
RNA, Ribosomal, 16S/genetics
Tandem Mass Spectrometry
*Organophosphates/metabolism/chemistry
*Fluorocarbons/metabolism
RevDate: 2026-03-09
Infertility and Periodontitis: Are We Connecting the Right Dots?.
Journal of dental research [Epub ahead of print].
Infertility is an increasing global health concern. Growing evidence suggests that systemic inflammatory conditions, including periodontal disease, may contribute to impaired reproductive outcomes. This narrative review highlights recent conceptual advances linking periodontal disease with male and female infertility, focusing on biological mechanisms (i.e., microbial translocation, chronic inflammation, immune dysregulation, oxidative stress, and epigenetic modifications). The review critically examines available studies focusing on scientific quality, design, and clinical relevance. In females, periodontal disease has been associated with idiopathic infertility and polycystic ovary syndrome. These conditions are characterized by immune dysregulation and low-grade systemic inflammation. In males, impaired semen parameters and idiopathic infertility have been linked to poor periodontal status. Despite growing interest, existing studies are largely associative and limited by methodological heterogeneity, insufficient control for confounders, and a lack of standardized outcome measures. This review proposes a framework for improved future research strategies addressing these shortcomings to clarify causality and therapeutic potential.
Additional Links: PMID-41797218
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797218,
year = {2026},
author = {Wetzel, C and Bumm, CV and Becker, J and Schwendicke, F and Folwaczny, M and Werner, N},
title = {Infertility and Periodontitis: Are We Connecting the Right Dots?.},
journal = {Journal of dental research},
volume = {},
number = {},
pages = {220345261416502},
doi = {10.1177/00220345261416502},
pmid = {41797218},
issn = {1544-0591},
abstract = {Infertility is an increasing global health concern. Growing evidence suggests that systemic inflammatory conditions, including periodontal disease, may contribute to impaired reproductive outcomes. This narrative review highlights recent conceptual advances linking periodontal disease with male and female infertility, focusing on biological mechanisms (i.e., microbial translocation, chronic inflammation, immune dysregulation, oxidative stress, and epigenetic modifications). The review critically examines available studies focusing on scientific quality, design, and clinical relevance. In females, periodontal disease has been associated with idiopathic infertility and polycystic ovary syndrome. These conditions are characterized by immune dysregulation and low-grade systemic inflammation. In males, impaired semen parameters and idiopathic infertility have been linked to poor periodontal status. Despite growing interest, existing studies are largely associative and limited by methodological heterogeneity, insufficient control for confounders, and a lack of standardized outcome measures. This review proposes a framework for improved future research strategies addressing these shortcomings to clarify causality and therapeutic potential.},
}
RevDate: 2026-03-09
Silkworm excrement-immobilized bacteria for synergistic remediation of phthalate esters in agricultural soil.
Journal of hazardous materials, 507:141703 pii:S0304-3894(26)00681-3 [Epub ahead of print].
The widespread contamination of agricultural soils by phthalate esters (PAEs) poses serious risks to ecosystem and human health. While microbial remediation is a promising solution, the poor survival and performance of free degrading bacteria in complex soil environments limit its practical application. To address this challenge, we develop a novel immobilized inoculant by leveraging silkworm excrement (SE), an agricultural by-product, as a carrier for the efficient PAE-degrader Pseudomonas aeruginosa PS1. This microbe-immobilized silkworm excrement (MSE) was thoroughly characterized and validated by pot experiments. The results showed that MSE treatment significantly reduced PAEs in both soil and choysum (Brassica parachinensis L.), with PAEs detected little in shoots (edible parts), significantly outperforming the treatments of free bacteria or SE alone. The enhanced remediation was linked to MSE-induced improvements in soil health, including increased pH, organic matter, and ammonium nitrogen. Crucially, high-throughput sequencing revealed that MSE application selectively enriched key PAE-degrading bacterial phyla, particularly Proteobacteria and Bacteroidetes, thereby reshaping the soil microbiome into a more effective remediation consortium. This study presents a sustainable and efficient bioaugmentation strategy for transforming a waste product into a functional inoculant, offering a viable solution for the in-situ remediation of PAE-contaminated soils.
Additional Links: PMID-41797118
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41797118,
year = {2026},
author = {Chen, YH and Du, H and Liu, YX and Xu, K and Ye, JC and Liu, BL and Feng, NX and Xiang, L and Li, YW and Cai, QY and Mo, CH and Zhao, HM},
title = {Silkworm excrement-immobilized bacteria for synergistic remediation of phthalate esters in agricultural soil.},
journal = {Journal of hazardous materials},
volume = {507},
number = {},
pages = {141703},
doi = {10.1016/j.jhazmat.2026.141703},
pmid = {41797118},
issn = {1873-3336},
abstract = {The widespread contamination of agricultural soils by phthalate esters (PAEs) poses serious risks to ecosystem and human health. While microbial remediation is a promising solution, the poor survival and performance of free degrading bacteria in complex soil environments limit its practical application. To address this challenge, we develop a novel immobilized inoculant by leveraging silkworm excrement (SE), an agricultural by-product, as a carrier for the efficient PAE-degrader Pseudomonas aeruginosa PS1. This microbe-immobilized silkworm excrement (MSE) was thoroughly characterized and validated by pot experiments. The results showed that MSE treatment significantly reduced PAEs in both soil and choysum (Brassica parachinensis L.), with PAEs detected little in shoots (edible parts), significantly outperforming the treatments of free bacteria or SE alone. The enhanced remediation was linked to MSE-induced improvements in soil health, including increased pH, organic matter, and ammonium nitrogen. Crucially, high-throughput sequencing revealed that MSE application selectively enriched key PAE-degrading bacterial phyla, particularly Proteobacteria and Bacteroidetes, thereby reshaping the soil microbiome into a more effective remediation consortium. This study presents a sustainable and efficient bioaugmentation strategy for transforming a waste product into a functional inoculant, offering a viable solution for the in-situ remediation of PAE-contaminated soils.},
}
RevDate: 2026-03-09
Role of the gut microbiome in shaping drug response in immunocompromised hosts.
Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases pii:S1198-743X(26)00104-7 [Epub ahead of print].
BACKGROUND: There is an increasing amount of evidence on microbiome-drug interactions in several clinical settings, including in immunocompromised patients. The gut microbiome has been shown to directly and indirectly influence drug efficacy and toxicity, offering high potential for clinical translation.
OBJECTIVES: This narrative review aims to provide an up-to-date overview of the relationship between gut microbes and drugs, with a focus on immu1no-chemotherapy in immunocompromised hosts, including oncological and transplant patients.
SOURCES: We searched PubMed to identify relevant literature in English up to February 2026, as well as included articles known to the authors (prioritising clinical studies wherever possible).
CONTENT: For commonly used anticancer drugs in untargeted conventional chemotherapy, gut microbes may directly activate prodrugs, inactivate biologically active drugs, and/or interfere with their toxicity. Furthermore, indirect mechanisms of immune system modulation have been shown to enhance or worsen therapeutic outcomes, including in targeted immunotherapy. For immunosuppressants in transplant recipients, there is less available evidence overall. Nevertheless, existing studies support the role of the gut microbiome in influencing pharmacokinetics, including enterohepatic recirculation, also through modulation of host drug-metabolising enzymes. Notably, some studies have demonstrated the potential of targeted microbiome manipulation to improve therapeutic outcomes. However, most of this information derives from small, heterogeneous studies, including animal models and in vitro studies.
IMPLICATIONS: The translational implications of microbiome research in pharmacology are of paramount importance. Well-designed clinical studies and the integration of in vivo and ex vivo models will be essential for advancing knowledge and providing mechanistic insights into microbiome-drug interactions. In parallel, advanced computational approaches such as artificial intelligence and machine learning tools will facilitate the analysis of complex microbiome data. These approaches will help identify clinically relevant microbial signatures, including high-risk microbiome-drug interactions. This will enable the development of personalised precision strategies to improve clinical outcomes and prolong disease-free survival.
Additional Links: PMID-41796961
Publisher:
PubMed:
Citation:
show bibtex listing
hide bibtex listing
@article {pmid41796961,
year = {2026},
author = {Bejaoui, S and D'Amico, F and Turroni, S},
title = {Role of the gut microbiome in shaping drug response in immunocompromised hosts.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2026.02.026},
pmid = {41796961},
issn = {1469-0691},
abstract = {BACKGROUND: There is an increasing amount of evidence on microbiome-drug interactions in several clinical settings, including in immunocompromised patients. The gut microbiome has been shown to directly and indirectly influence drug efficacy and toxicity, offering high potential for clinical translation.
OBJECTIVES: This narrative review aims to provide an up-to-date overview of the relationship between gut microbes and drugs, with a focus on immu1no-chemotherapy in immunocompromised hosts, including oncological and transplant patients.
SOURCES: We searched PubMed to identify relevant literature in English up to February 2026, as well as included articles known to the authors (prioritising clinical studies wherever possible).
CONTENT: For commonly used anticancer drugs in untargeted conventional chemotherapy, gut microbes may directly activate prodrugs, inactivate biologically active drugs, and/or interfere with their toxicity. Furthermore, indirect mechanisms of immune system modulation have been shown to enhance or worsen therapeutic outcomes, including in targeted immunotherapy. For immunosuppressants in transplant recipients, there is less available evidence overall. Nevertheless, existing studies support the role of the gut microbiome in influencing pharmacokinetics, including enterohepatic recirculation, also through modulation of host drug-metabolising enzymes. Notably, some studies have demonstrated the potential of targeted microbiome manipulation to improve therapeutic outcomes. However, most of this information derives from small, heterogeneous studies, including animal models and in vitro studies.
IMPLICATIONS: The translational implications of microbiome research in pharmacology are of paramount importance. Well-designed clinical studies and the integration of in vivo and ex vivo models will be essential for advancing knowledge and providing mechanistic insights into microbiome-drug interactions. In parallel, advanced computational approaches such as artificial intelligence and machine learning tools will facilitate the analysis of complex microbiome data. These approaches will help identify clinically relevant microbial signatures, including high-risk microbiome-drug interactions. This will enable the development of personalised precision strategies to improve clinical outcomes and prolong disease-free survival.},
}
▼ ▼ LOAD NEXT 100 CITATIONS
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.
ESP Goal
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.
ESP Usage
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.
ESP Content
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.
ESP Help
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.
ESP Plans
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.
ESP Picks from Around the Web (updated 28 JUL 2024 )
Old Science
Weird Science
Treating Disease with Fecal Transplantation
Fossils of miniature humans (hobbits) discovered in Indonesia
Paleontology
Dinosaur tail, complete with feathers, found preserved in amber.
Astronomy
Mysterious fast radio burst (FRB) detected in the distant universe.
Big Data & Informatics
Big Data: Buzzword or Big Deal?
Hacking the genome: Identifying anonymized human subjects using publicly available data.