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Human Microbiome
The human microbiome is the set of all microbes that live on or in humans. Together, a human body and its associated microbiomes constitute a human holobiont. Although a human holobiont is mostly mammal by weight, by cell count it is mostly microbial. The number of microbial genes in the associated microbiomes far outnumber the number of human genes in the human genome. Just as humans (and other multicellular eukaryotes) evolved in the constant presence of gravity, so they also evolved in the constant presence of microbes. Consequently, nearly every aspect of human biology has evolved to deal with, and to take advantage of, the existence of associated microbiota. In some cases, the absence of a "normal microbiome" can cause disease, which can be treated by the transplant of a correct microbiome from a healthy donor. For example, fecal transplants are an effective treatment for chronic diarrhea from over abundant Clostridium difficile bacteria in the gut.
Created with PubMed® Query: "human microbiome" NOT pmcbook NOT ispreviousversion
Citations The Papers (from PubMed®)
RevDate: 2025-12-01
STREAMS guidelines: standards for technical reporting in environmental and host-associated microbiome studies.
Nature microbiology, 10(12):3059-3068.
The interdisciplinary nature of microbiome research, coupled with the generation of complex multi-omics data, makes knowledge sharing challenging. The Strengthening the Organization and Reporting of Microbiome Studies (STORMS) guidelines provide a checklist for the reporting of study information, experimental design and analytical methods within a scientific manuscript on human microbiome research. Here, in this Consensus Statement, we present the standards for technical reporting in environmental and host-associated microbiome studies (STREAMS) guidelines. The guidelines expand on STORMS and include 67 items to support the reporting and review of environmental (for example, terrestrial, aquatic, atmospheric and engineered), synthetic and non-human host-associated microbiome studies in a standardized and machine-actionable manner. Based on input from 248 researchers spanning 28 countries, we provide detailed guidance, including comparisons with STORMS, and case studies that demonstrate the usage of the STREAMS guidelines. STREAMS, like STORMS, will be a living community resource updated by the Consortium with consensus-building input of the broader community.
Additional Links: PMID-41326814
PubMed:
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@article {pmid41326814,
year = {2025},
author = {Kelliher, JM and Mirzayi, C and Bordenstein, SR and Oliver, A and Kellogg, CA and Hatcher, EL and Berg, M and Baldrian, P and Aljumaah, M and Miller, CML and Mungall, C and Novak, V and Palucki, A and Smith, E and Tabassum, N and Bonito, G and Brister, JR and Chain, PSG and Chen, M and Degregori, S and Dundore-Arias, JP and Emerson, JB and Moreira C Fernandes, V and Flores, R and Gonzalez, A and Hansen, ZA and Jackson, SA and Moustafa, AM and Northen, TR and Pariente, N and Pett-Ridge, J and Record, S and Reji, L and Reysenbach, AL and Rich, VI and Richardson, L and Roux, S and Schriml, LM and Shabman, RS and Sierra, MA and Sullivan, MB and Sundaramurthy, P and Thibault, KM and Thompson, LR and Tighe, S and Vereen, E and , and Eloe-Fadrosh, EA},
title = {STREAMS guidelines: standards for technical reporting in environmental and host-associated microbiome studies.},
journal = {Nature microbiology},
volume = {10},
number = {12},
pages = {3059-3068},
pmid = {41326814},
issn = {2058-5276},
abstract = {The interdisciplinary nature of microbiome research, coupled with the generation of complex multi-omics data, makes knowledge sharing challenging. The Strengthening the Organization and Reporting of Microbiome Studies (STORMS) guidelines provide a checklist for the reporting of study information, experimental design and analytical methods within a scientific manuscript on human microbiome research. Here, in this Consensus Statement, we present the standards for technical reporting in environmental and host-associated microbiome studies (STREAMS) guidelines. The guidelines expand on STORMS and include 67 items to support the reporting and review of environmental (for example, terrestrial, aquatic, atmospheric and engineered), synthetic and non-human host-associated microbiome studies in a standardized and machine-actionable manner. Based on input from 248 researchers spanning 28 countries, we provide detailed guidance, including comparisons with STORMS, and case studies that demonstrate the usage of the STREAMS guidelines. STREAMS, like STORMS, will be a living community resource updated by the Consortium with consensus-building input of the broader community.},
}
RevDate: 2025-12-01
CmpDate: 2025-12-01
Evaluating the Role of Candida albicans as a Potential Oral Carcinogen.
Interdisciplinary perspectives on infectious diseases, 2025:4057977.
Oral cavity cancers, especially oral squamous cell carcinoma (OSCC), are a major subset of head and neck malignancies. Increasing evidence indicates that oral microbiota, particularly Candida albicans (C. albicans), plays a significant role in OSCC development and progression. While C. albicans is normally a commensal organism in the human microbiome, it can become pathogenic under certain conditions. The carcinogenic potential of C. albicans contributes to oral cancer by acting both as a co-factor and a direct pathogen. This involves complex interactions with the host immune system and the expression of multiple virulence factors. The dynamic relationship between C. albicans and its host influences disease outcomes and cancer progression. This review focuses on key virulence mechanisms of C. albicans, including adhesion to host cells, secretion of hydrolytic enzymes, production of carcinogenic metabolites, induction of chronic inflammation, and release of candidalysin, a cytolytic peptide toxin. Understanding these factors is essential to clarify how C. albicans promotes OSCC initiation and progression. Improved knowledge of C. albicans virulence may lead to targeted therapies, preventive strategies, and novel biomarkers for early detection, ultimately enhancing treatment outcomes and prognosis for patients with oral cavity cancers.
Additional Links: PMID-41322070
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@article {pmid41322070,
year = {2025},
author = {Amirinia, F and Motamedi, M and Ardi, P and Jabrodini, A},
title = {Evaluating the Role of Candida albicans as a Potential Oral Carcinogen.},
journal = {Interdisciplinary perspectives on infectious diseases},
volume = {2025},
number = {},
pages = {4057977},
pmid = {41322070},
issn = {1687-708X},
abstract = {Oral cavity cancers, especially oral squamous cell carcinoma (OSCC), are a major subset of head and neck malignancies. Increasing evidence indicates that oral microbiota, particularly Candida albicans (C. albicans), plays a significant role in OSCC development and progression. While C. albicans is normally a commensal organism in the human microbiome, it can become pathogenic under certain conditions. The carcinogenic potential of C. albicans contributes to oral cancer by acting both as a co-factor and a direct pathogen. This involves complex interactions with the host immune system and the expression of multiple virulence factors. The dynamic relationship between C. albicans and its host influences disease outcomes and cancer progression. This review focuses on key virulence mechanisms of C. albicans, including adhesion to host cells, secretion of hydrolytic enzymes, production of carcinogenic metabolites, induction of chronic inflammation, and release of candidalysin, a cytolytic peptide toxin. Understanding these factors is essential to clarify how C. albicans promotes OSCC initiation and progression. Improved knowledge of C. albicans virulence may lead to targeted therapies, preventive strategies, and novel biomarkers for early detection, ultimately enhancing treatment outcomes and prognosis for patients with oral cavity cancers.},
}
RevDate: 2025-12-01
CmpDate: 2025-12-01
Lactobacillus johnsonii Synthesizes Chenodeoxycholic Acid to Reduce Susceptibility to High-Fat Diet-Induced Colorectal Cancer.
Cancer research, 85(23):4600-4615.
UNLABELLED: High-fat diet (HFD) is positively correlated with colorectal cancer, but there are notable interindividual differences in susceptibility to the tumor-promoting effects of HFD. A better understanding of the mechanisms that modulate the outcomes of HFD could help inform precision prevention strategies for colorectal cancer. In this study, we found a key role for the gut microbiota in the individual differences observed in the tumor-promoting effects of HFD. Analysis of the gut bacteria enriched in mice resistant to HFD-induced cancer identified Lactobacillus johnsonii as an effective protector. Colonization of L. johnsonii increased intestinal chenodeoxycholic acid (CDCA) concentrations in HFD-exposed mice, which decelerated HFD-induced colorectal cancer progression. Mechanistically, L. johnsonii converted conjugated bile acid to CDCA via bile salt hydrolase, and CDCA induced mitochondrial dysfunction and oxidative stress to promote apoptosis, effectively suppressing tumor development. These results establish the gut microbiota as a mediator of interindividual differences in cancer susceptibility induced by HFD and reveal a probiotic strategy with the ability to inhibit tumorigenesis, suggesting a possible route to reduce HFD-induced colorectal cancer progression.
SIGNIFICANCE: Investigation of bacteria-host interactions that alter cancer susceptibility uncovers suppression of high-fat diet-induced colorectal cancer by Lactobacillus johnsonii, offering a translational approach to improve cancer prevention. See related commentary by Dalal and Shah, p. 4579.
Additional Links: PMID-40953220
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PubMed:
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@article {pmid40953220,
year = {2025},
author = {Liu, C and Lai, P and Hu, J and Yin, S and Guo, S and Liu, D and Yu, J and Liang, D and Chen, G and Xing, M and Luo, Z and He, X and Gong, J and Lan, P and He, Z},
title = {Lactobacillus johnsonii Synthesizes Chenodeoxycholic Acid to Reduce Susceptibility to High-Fat Diet-Induced Colorectal Cancer.},
journal = {Cancer research},
volume = {85},
number = {23},
pages = {4600-4615},
doi = {10.1158/0008-5472.CAN-25-0879},
pmid = {40953220},
issn = {1538-7445},
support = {2022YFA1304000//National Key Research and Development Program of China (NKPs)/ ; 2024B1111150001//Guangdong Provincial Department of Science and Technology (GDSTC)/ ; 2021B1212040017//Guangdong Provincial Department of Science and Technology (GDSTC)/ ; 2020B1111170004//Guangdong Gastrointestinal Disease Research Center/ ; 82273346//National Natural Science Foundation of China (NSFC)/ ; U21A20344//National Natural Science Foundation of China (NSFC)/ ; 2023WST03//Sun Yat-sen University (SYSU)/ ; //National Key Clinical Specialty Discipline Construction Program of China (National Key Clinical Specialty Construction Programs of China)/ ; //Guangdong Cheung Kong Foundation/ ; B2302036//Shenzhen Government ()/ ; },
mesh = {Animals ; *Colorectal Neoplasms/etiology/prevention & control/microbiology/pathology/metabolism ; *Diet, High-Fat/adverse effects ; Mice ; Gastrointestinal Microbiome ; *Chenodeoxycholic Acid/metabolism/biosynthesis ; *Lactobacillus johnsonii/metabolism ; Mice, Inbred C57BL ; Humans ; Probiotics ; Male ; Disease Susceptibility ; Apoptosis ; Oxidative Stress ; },
abstract = {UNLABELLED: High-fat diet (HFD) is positively correlated with colorectal cancer, but there are notable interindividual differences in susceptibility to the tumor-promoting effects of HFD. A better understanding of the mechanisms that modulate the outcomes of HFD could help inform precision prevention strategies for colorectal cancer. In this study, we found a key role for the gut microbiota in the individual differences observed in the tumor-promoting effects of HFD. Analysis of the gut bacteria enriched in mice resistant to HFD-induced cancer identified Lactobacillus johnsonii as an effective protector. Colonization of L. johnsonii increased intestinal chenodeoxycholic acid (CDCA) concentrations in HFD-exposed mice, which decelerated HFD-induced colorectal cancer progression. Mechanistically, L. johnsonii converted conjugated bile acid to CDCA via bile salt hydrolase, and CDCA induced mitochondrial dysfunction and oxidative stress to promote apoptosis, effectively suppressing tumor development. These results establish the gut microbiota as a mediator of interindividual differences in cancer susceptibility induced by HFD and reveal a probiotic strategy with the ability to inhibit tumorigenesis, suggesting a possible route to reduce HFD-induced colorectal cancer progression.
SIGNIFICANCE: Investigation of bacteria-host interactions that alter cancer susceptibility uncovers suppression of high-fat diet-induced colorectal cancer by Lactobacillus johnsonii, offering a translational approach to improve cancer prevention. See related commentary by Dalal and Shah, p. 4579.},
}
MeSH Terms:
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Animals
*Colorectal Neoplasms/etiology/prevention & control/microbiology/pathology/metabolism
*Diet, High-Fat/adverse effects
Mice
Gastrointestinal Microbiome
*Chenodeoxycholic Acid/metabolism/biosynthesis
*Lactobacillus johnsonii/metabolism
Mice, Inbred C57BL
Humans
Probiotics
Male
Disease Susceptibility
Apoptosis
Oxidative Stress
RevDate: 2025-11-30
Gut microbe alleviates stress-related cancer metastasis by oleic acid degradation.
Gut pii:gutjnl-2025-335627 [Epub ahead of print].
BACKGROUND: Chronic stress is a known risk factor for cancer metastasis. However, the underlying mechanisms, particularly those involving the gut microbiota and their metabolites, remain unclear.
OBJECTIVE: To investigate whether gut microbiota dysbiosis and metabolic alterations mediate the sustained pro-metastatic effects of chronic stress, even after normalisation of stress hormone levels.
DESIGN: Multiple metastatic models were performed after stress cessation. Shotgun metagenomics and metabolomics were performed to assess changes in microbiota and metabolites. The effects of Bifidobacterium animalis and oleic acid (OA) on metastasis were evaluated in vivo and in vitro. Moreover, we explored how B. animalis degraded OA. Mechanistically, we discovered the interaction between corticosteroids and gut bacteria through guanine metabolism assays. Human samples were collected from patients with colorectal cancer (CRC) with varying perceived stress scores and metastatic status for validation.
RESULTS: Mice that underwent chronic stress exhibited increased metastasis even after hormone levels recovered. The gut microenvironment was altered, with a significant reduction in B. animalis and an increase in OA. B. animalis administration reduced OA levels and suppressed metastasis, while OA supplementation had the opposite effect. B. animalis expresses oleate hydratase, an enzyme that degrades OA. Stress hormones inhibited B. animalis by altering guanine metabolism in the intestinal epithelium. In patients, high stress was associated with more OA, lower B. animalis levels and increased metastasis.
CONCLUSIONS: Chronic stress promotes metastasis by altering microbiota and increasing OA. Targeting B. animalis and OA may help prevent stress-related tumour progression.
Additional Links: PMID-41320324
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PubMed:
Citation:
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@article {pmid41320324,
year = {2025},
author = {Liu, C and Gong, J and Luo, Z and Lai, P and Guo, S and Liang, D and Chen, G and Xing, M and Yu, J and Xie, Y and Liu, D and Zeng, W and He, Z and Lan, P},
title = {Gut microbe alleviates stress-related cancer metastasis by oleic acid degradation.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-335627},
pmid = {41320324},
issn = {1468-3288},
abstract = {BACKGROUND: Chronic stress is a known risk factor for cancer metastasis. However, the underlying mechanisms, particularly those involving the gut microbiota and their metabolites, remain unclear.
OBJECTIVE: To investigate whether gut microbiota dysbiosis and metabolic alterations mediate the sustained pro-metastatic effects of chronic stress, even after normalisation of stress hormone levels.
DESIGN: Multiple metastatic models were performed after stress cessation. Shotgun metagenomics and metabolomics were performed to assess changes in microbiota and metabolites. The effects of Bifidobacterium animalis and oleic acid (OA) on metastasis were evaluated in vivo and in vitro. Moreover, we explored how B. animalis degraded OA. Mechanistically, we discovered the interaction between corticosteroids and gut bacteria through guanine metabolism assays. Human samples were collected from patients with colorectal cancer (CRC) with varying perceived stress scores and metastatic status for validation.
RESULTS: Mice that underwent chronic stress exhibited increased metastasis even after hormone levels recovered. The gut microenvironment was altered, with a significant reduction in B. animalis and an increase in OA. B. animalis administration reduced OA levels and suppressed metastasis, while OA supplementation had the opposite effect. B. animalis expresses oleate hydratase, an enzyme that degrades OA. Stress hormones inhibited B. animalis by altering guanine metabolism in the intestinal epithelium. In patients, high stress was associated with more OA, lower B. animalis levels and increased metastasis.
CONCLUSIONS: Chronic stress promotes metastasis by altering microbiota and increasing OA. Targeting B. animalis and OA may help prevent stress-related tumour progression.},
}
RevDate: 2025-11-29
Intratumoral microbiome composition and its role in tumor recurrence in primary liver cancer.
Journal of the Formosan Medical Association = Taiwan yi zhi pii:S0929-6646(25)00638-2 [Epub ahead of print].
BACKGROUND: The human microbiome is increasingly recognized as a factor in cancer development, though its role in primary liver cancer (PLC) remains unclear. This retrospective cohort study examines tissue-specific microbiota differences between hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), and explores their association with tumor recurrence in PLC.
METHODS: Clinical data from 116 patients (85 HCC and 31 age-matched CCA) were analyzed. Fresh frozen samples underwent RNAscope™ ISH assay for microbial RNA detection, while the MiSeq platform targeted 16 S ribosomal RNA. Microbiome functional pathways were explored with Tax4Fun2, and predictors of recurrence were identified through logistic regression analysis.
RESULTS: Microbial RNA was detected within liver sinusoids, the basal lamina of intrahepatic bile ducts, and hepatocyte cytosol. 16 S ribosomal RNA analysis revealed differences in microbiome composition, including a distinct Firmicutes/Bacteroidetes ratio between CCA and HCC patients. Specific functional pathways were differentially enriched between the two groups. LEfSe and logistic regression analyses identified Aquabacterium spp. as a potential marker for HCC recurrence (OR, 14.77; 95 % CI, 1.07-203.94; p = 0.044). Increased abundances of Brevundimonas spp. (OR, 3.1 E+17; 95 % CI, 4.3 E+3-2.2 E+31; p = 0.013), Novosphingobium spp. (OR, 3.5 E+20; 95 % CI, 4.4 E+5-2.8 E+35; p = 0.007), and Pelomonas spp. (OR, 3.3 E+21; 95 % CI, 3.0 E+8-3.5 E+34; p = 0.001), along with decreased Staphylococcus spp. (OR 0.00; 95 % CI, 0.00-0.06; p = 0.003), were independent predictors of CCA occurrence.
CONCLUSION: This study reveals that intratumoral microbiota help distinguish PLC subtypes and are associated with recurrence, identifying Aquabacterium as a potential marker for HCC recurrence and microbiome-based management.
Additional Links: PMID-41318317
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PubMed:
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@article {pmid41318317,
year = {2025},
author = {Liu, WC and Kuo, HY and Tsai, HW and Lin, YJ and Ruan, JW and Lee, CC and Sun, HY and Wu, IC and Chang, TT},
title = {Intratumoral microbiome composition and its role in tumor recurrence in primary liver cancer.},
journal = {Journal of the Formosan Medical Association = Taiwan yi zhi},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jfma.2025.11.031},
pmid = {41318317},
issn = {0929-6646},
abstract = {BACKGROUND: The human microbiome is increasingly recognized as a factor in cancer development, though its role in primary liver cancer (PLC) remains unclear. This retrospective cohort study examines tissue-specific microbiota differences between hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), and explores their association with tumor recurrence in PLC.
METHODS: Clinical data from 116 patients (85 HCC and 31 age-matched CCA) were analyzed. Fresh frozen samples underwent RNAscope™ ISH assay for microbial RNA detection, while the MiSeq platform targeted 16 S ribosomal RNA. Microbiome functional pathways were explored with Tax4Fun2, and predictors of recurrence were identified through logistic regression analysis.
RESULTS: Microbial RNA was detected within liver sinusoids, the basal lamina of intrahepatic bile ducts, and hepatocyte cytosol. 16 S ribosomal RNA analysis revealed differences in microbiome composition, including a distinct Firmicutes/Bacteroidetes ratio between CCA and HCC patients. Specific functional pathways were differentially enriched between the two groups. LEfSe and logistic regression analyses identified Aquabacterium spp. as a potential marker for HCC recurrence (OR, 14.77; 95 % CI, 1.07-203.94; p = 0.044). Increased abundances of Brevundimonas spp. (OR, 3.1 E+17; 95 % CI, 4.3 E+3-2.2 E+31; p = 0.013), Novosphingobium spp. (OR, 3.5 E+20; 95 % CI, 4.4 E+5-2.8 E+35; p = 0.007), and Pelomonas spp. (OR, 3.3 E+21; 95 % CI, 3.0 E+8-3.5 E+34; p = 0.001), along with decreased Staphylococcus spp. (OR 0.00; 95 % CI, 0.00-0.06; p = 0.003), were independent predictors of CCA occurrence.
CONCLUSION: This study reveals that intratumoral microbiota help distinguish PLC subtypes and are associated with recurrence, identifying Aquabacterium as a potential marker for HCC recurrence and microbiome-based management.},
}
RevDate: 2025-11-29
Oral Immunotherapy Induces Shift in lncRNA Expression Modulating Allergen-Specific Immune Responses.
Allergy [Epub ahead of print].
BACKGROUND: Previously, we reported the success of egg oral immunotherapy (OIT) in liberating most participants from dietary restrictions. The diminishing symptoms and declining inflammation were accompanied by differential expression of genes in peripheral blood mononuclear cells (PBMCs) of 50 egg-allergic children following 8 months of OIT.
METHODS: Here, we explore the impact of OIT on long non-coding RNA (lncRNA) expression and its downstream effects on allergen-specific immune response with the help of PBMC transcriptome, co-expression gene module identification, pathway enrichment analyses and in vitro stimulation in both PBMC and THP1 cells.
RESULTS: We observed 17 lncRNAs which correlated positively with genes involved in IL-13, IL-4, and IL-10 signaling pathways. The same set of lncRNAs correlated negatively with genes playing a role in neutrophil degranulation, phagosome formation, and pyroptosis signaling. The expression of one of the most important lncRNAs, LOC644727, was found to align with CXCL8 expression in egg extract-stimulated PBMCs and LPS-stimulated THP1-derived macrophages.
CONCLUSIONS: Our results highlight the involvement of lncRNA in the regulation of gene expression during OIT. LOC644727 may serve as a potential marker for inflammatory responses and it may offer a therapeutic target for future desensitization protocols.
Additional Links: PMID-41316695
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PubMed:
Citation:
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@article {pmid41316695,
year = {2025},
author = {Liong, O and Palosuo, K and Hinkkanen, V and Fortino, V and Mäkelä, MJ and Karisola, P},
title = {Oral Immunotherapy Induces Shift in lncRNA Expression Modulating Allergen-Specific Immune Responses.},
journal = {Allergy},
volume = {},
number = {},
pages = {},
doi = {10.1111/all.70173},
pmid = {41316695},
issn = {1398-9995},
support = {190150//Pediatric Research Foundation/ ; //Finnish Society of Allergology and Immunology/ ; TYH2019313//Helsinki University Hospital Research Fund/ ; TYH2020322//Helsinki University Hospital Research Fund/ ; //Allergy Research Foundation/ ; //Helsingin Yliopisto/ ; 338325//Academy of Finland/ ; //Finnish Cultural Foundation/ ; //Magnus Ehrnrooth Foundation/ ; //Sigrid Jusélius Foundation/ ; },
abstract = {BACKGROUND: Previously, we reported the success of egg oral immunotherapy (OIT) in liberating most participants from dietary restrictions. The diminishing symptoms and declining inflammation were accompanied by differential expression of genes in peripheral blood mononuclear cells (PBMCs) of 50 egg-allergic children following 8 months of OIT.
METHODS: Here, we explore the impact of OIT on long non-coding RNA (lncRNA) expression and its downstream effects on allergen-specific immune response with the help of PBMC transcriptome, co-expression gene module identification, pathway enrichment analyses and in vitro stimulation in both PBMC and THP1 cells.
RESULTS: We observed 17 lncRNAs which correlated positively with genes involved in IL-13, IL-4, and IL-10 signaling pathways. The same set of lncRNAs correlated negatively with genes playing a role in neutrophil degranulation, phagosome formation, and pyroptosis signaling. The expression of one of the most important lncRNAs, LOC644727, was found to align with CXCL8 expression in egg extract-stimulated PBMCs and LPS-stimulated THP1-derived macrophages.
CONCLUSIONS: Our results highlight the involvement of lncRNA in the regulation of gene expression during OIT. LOC644727 may serve as a potential marker for inflammatory responses and it may offer a therapeutic target for future desensitization protocols.},
}
RevDate: 2025-11-29
Ambient temperature affects the composition of the vaginal microbiome, and temperature-sensitive vaginal microbes influence assisted reproductive technology outcomes.
Microbiome pii:10.1186/s40168-025-02212-9 [Epub ahead of print].
OBJECTIVE: To investigate the influence of environmental factors on the composition and structure of the vaginal microbiome and to explore the interaction among environmental factors, vaginal microbiome, and outcomes of assisted reproductive technology (ART).
METHODS: Adonis test was utilized to evaluate the impact of 33 host/environmental variables on vaginal microbiome. Distributed lag nonlinear model analysis (DLNM), Mfuzz analysis, and linear mixed effect model were employed to establish the correlations between ambient temperature and vaginal microbes.
RESULTS: Ambient temperature was one of the most important environmental factors associated with vaginal microbiome. As the temperature increased, succession of vaginal microbes showed four patterns of abundance variation. Furthermore, a group of vaginal microbes showed a preference for certain temperatures, and these microbes' varying interactions partly drove the shift of microbial networks at different temperatures. The community assembly process of vaginal microbiome deviated from neutral model and exposure to ambient temperature did not affect the role of stochastic processes in shaping vaginal microbial community. Notably, vaginal microbiome prior to embryo transfer was significantly associated with preterm birth. Preterm women exhibited higher abundance of Lactobacillus iners and lower abundance of Lactobacillus crispatus.
CONCLUSIONS: Ambient temperature change can affect the structure and composition of the vaginal microbiome and correlate with the abundance of certain vaginal microbes. Temperature-sensitive vaginal bacteria may affect the risk of future preterm births. Video Abstract.
Additional Links: PMID-41316495
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PubMed:
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@article {pmid41316495,
year = {2025},
author = {Liu, Z and Yu, W and Sun, T and Li, M and Li, X and Qin, L and Liu, X and Bian, Y and Zhao, S and Zhao, Q and Zhao, H and Feng, Q},
title = {Ambient temperature affects the composition of the vaginal microbiome, and temperature-sensitive vaginal microbes influence assisted reproductive technology outcomes.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02212-9},
pmid = {41316495},
issn = {2049-2618},
support = {2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 2021YFC2700400//National Key Research and Development Program of China/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 31988101//the Basic Science Center Program of NSFC/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; 32370916//the National Natural Science Foundation of China/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; ZR2023YQ061//the Natural Science Foundation of Shandong Province for Excellent Youth Scholars/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2021-I2M-5-001//CAMS Innovation Fund for Medical Sciences/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; 2020ZLYS02//Shandong Provincial Key Research and Development Program/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; Q2022144//the Program for Chang Jiang Scholars/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; ts20190988//the Taishan Scholars Program of Shandong Province/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; 2023QNTD004//the Fundamental Research Funds of Shandong University/ ; },
abstract = {OBJECTIVE: To investigate the influence of environmental factors on the composition and structure of the vaginal microbiome and to explore the interaction among environmental factors, vaginal microbiome, and outcomes of assisted reproductive technology (ART).
METHODS: Adonis test was utilized to evaluate the impact of 33 host/environmental variables on vaginal microbiome. Distributed lag nonlinear model analysis (DLNM), Mfuzz analysis, and linear mixed effect model were employed to establish the correlations between ambient temperature and vaginal microbes.
RESULTS: Ambient temperature was one of the most important environmental factors associated with vaginal microbiome. As the temperature increased, succession of vaginal microbes showed four patterns of abundance variation. Furthermore, a group of vaginal microbes showed a preference for certain temperatures, and these microbes' varying interactions partly drove the shift of microbial networks at different temperatures. The community assembly process of vaginal microbiome deviated from neutral model and exposure to ambient temperature did not affect the role of stochastic processes in shaping vaginal microbial community. Notably, vaginal microbiome prior to embryo transfer was significantly associated with preterm birth. Preterm women exhibited higher abundance of Lactobacillus iners and lower abundance of Lactobacillus crispatus.
CONCLUSIONS: Ambient temperature change can affect the structure and composition of the vaginal microbiome and correlate with the abundance of certain vaginal microbes. Temperature-sensitive vaginal bacteria may affect the risk of future preterm births. Video Abstract.},
}
RevDate: 2025-11-28
CmpDate: 2025-11-29
MicroMap: a network visualisation resource for human microbiome metabolism.
NPJ biofilms and microbiomes, 11(1):222.
The human microbiome critically influences metabolism and thereby our health. Constraint-based reconstruction and analysis (COBRA) is a proven framework for generating mechanism-derived hypotheses along the nutrition-host-microbiome-disease axis. However, no large-scale microbiome metabolism visualisation has been available. Therefore, we created the MicroMap, a manually curated network visualisation, which captures the metabolism of over a quarter million microbial genome-scale metabolic reconstructions. The MicroMap contains 5064 unique reactions and 3499 unique metabolites, including for 98 drugs. Users can intuitively explore microbiome metabolism, inspect metabolic capabilities, and visualise computational modelling results. Further, the MicroMap may serve as an educational tool to help diversify the computational modelling community. We generated 257,429 visualisations, covering all our current microbiome reconstructions, to visually compare metabolic capabilities between microbes. The MicroMap integrates with the Virtual Metabolic Human (VMH, www.vmh.life), the COBRA Toolbox (https://opencobra.github.io), and is freely accessible at the MicroMap dataverse (https://dataverse.harvard.edu/dataverse/micromap), along with all the generated reconstruction visualisations.
Additional Links: PMID-41315289
PubMed:
Citation:
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@article {pmid41315289,
year = {2025},
author = {Thinnes, CC and Waschkowitz, R and Courtney, E and Culligan, E and Fahy, K and Ferrazza, RAM and Ferris, C and Lagali, A and Lane, R and Maye, C and Murphy, O and Noone, D and Ryan, S and Bet, M and Corr, MC and Cummins, H and Hackett, D and Healy, E and Kulczycka, N and Lang, N and Madden, L and McHugh, L and Pyne, I and Varley, C and Harkin, N and Meade, R and O'Donnell, G and Nap, B and Martinelli, F and Heinken, A and Thiele, I},
title = {MicroMap: a network visualisation resource for human microbiome metabolism.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {222},
pmid = {41315289},
issn = {2055-5008},
support = {757922/ERC_/European Research Council/International ; 859890//H2020 Marie Skłodowska-Curie Actions/ ; 1RF1AG058942/NH/NIH HHS/United States ; 12/RC/2273-P2/SFI_/Science Foundation Ireland/Ireland ; },
mesh = {Humans ; *Microbiota ; *Metabolic Networks and Pathways ; *Software ; *Computational Biology/methods ; *Bacteria/metabolism/genetics/classification ; Computer Simulation ; },
abstract = {The human microbiome critically influences metabolism and thereby our health. Constraint-based reconstruction and analysis (COBRA) is a proven framework for generating mechanism-derived hypotheses along the nutrition-host-microbiome-disease axis. However, no large-scale microbiome metabolism visualisation has been available. Therefore, we created the MicroMap, a manually curated network visualisation, which captures the metabolism of over a quarter million microbial genome-scale metabolic reconstructions. The MicroMap contains 5064 unique reactions and 3499 unique metabolites, including for 98 drugs. Users can intuitively explore microbiome metabolism, inspect metabolic capabilities, and visualise computational modelling results. Further, the MicroMap may serve as an educational tool to help diversify the computational modelling community. We generated 257,429 visualisations, covering all our current microbiome reconstructions, to visually compare metabolic capabilities between microbes. The MicroMap integrates with the Virtual Metabolic Human (VMH, www.vmh.life), the COBRA Toolbox (https://opencobra.github.io), and is freely accessible at the MicroMap dataverse (https://dataverse.harvard.edu/dataverse/micromap), along with all the generated reconstruction visualisations.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota
*Metabolic Networks and Pathways
*Software
*Computational Biology/methods
*Bacteria/metabolism/genetics/classification
Computer Simulation
RevDate: 2025-11-28
Comparative volatilomics identifies ubiquitous sulfur compounds inhibiting the fungal pathogen Rasamsonia argillacea.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: Members of the phylum Actinomycetota, particularly Streptomyces species, are prolific producers of bioactive metabolites, and bioprospecting in unique environments may uncover novel species producing previously undescribed antifungal compounds. In previous work, Streptomyces strains isolated from cave moonmilk deposits completely inhibited the growth of Rasamsonia argillacea, an emerging fungal pathogen associated with chronic granulomatous disease (CGD) and cystic fibrosis (CF). Cross-streak and bipartite Petri dish assays revealed that R. argillacea inhibition occurred specifically when bacteria were cultivated on Mueller-Hinton agar (MHA) and was mediated by volatile compounds rather than diffusible metabolites. This antifungal effect was not strain specific, as it was reproduced by phylogenetically diverse bacteria grown on MHA, suggesting the involvement of ubiquitous volatile molecules. Similar inhibitory effects were observed on MHA against other fungi and yeasts relevant to CGD and CF, supporting the hypothesis that these volatiles are broadly toxic rather than species-specific. To identify candidate ubiquitous antifungal VCs, we conducted comparative volatilomics of two phylogenetically distant bacterial strains that consistently inhibited fungal growth. Among the 143 VCs detected, only dimethyl trisulfide (DMTS) and dimethyl disulfide (DMDS) showed consistent presence in both bacterial volatilomes, with significantly increased production under conditions that promoted fungal inhibition. Exposure assays with pure compounds confirmed that both DMDS and DMTS strongly inhibited R. argillacea growth, with DMTS exhibiting greater potency. Our findings position these ubiquitous sulfur compounds as valuable models for exploring novel agents against human pathogens.
IMPORTANCE: Our findings suggest that antifungal activity against human pathogens may arise from common metabolic pathways shared across diverse microbes rather than from unique biosynthetic systems. Because dimethyl disulfide and dimethyl trisulfide can also be generated through microbial and dietary sulfur metabolism, it is plausible that the human microbiome may produce similar volatiles depending on diet composition, particularly following consumption of sulfur-rich foods. This study, therefore, underscores the critical influence of culture conditions on revealing bioactive volatile production and opens intriguing perspectives on the ecological and physiological roles of ubiquitous microbial metabolites in regulating fungal colonization and microbiome-host interactions.
Additional Links: PMID-41313023
Publisher:
PubMed:
Citation:
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@article {pmid41313023,
year = {2025},
author = {Adam, D and Bensaada, D and Stulanovic, N and Focant, J-F and Stefanuto, P-H and Rigali, S},
title = {Comparative volatilomics identifies ubiquitous sulfur compounds inhibiting the fungal pathogen Rasamsonia argillacea.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0266625},
doi = {10.1128/spectrum.02666-25},
pmid = {41313023},
issn = {2165-0497},
abstract = {UNLABELLED: Members of the phylum Actinomycetota, particularly Streptomyces species, are prolific producers of bioactive metabolites, and bioprospecting in unique environments may uncover novel species producing previously undescribed antifungal compounds. In previous work, Streptomyces strains isolated from cave moonmilk deposits completely inhibited the growth of Rasamsonia argillacea, an emerging fungal pathogen associated with chronic granulomatous disease (CGD) and cystic fibrosis (CF). Cross-streak and bipartite Petri dish assays revealed that R. argillacea inhibition occurred specifically when bacteria were cultivated on Mueller-Hinton agar (MHA) and was mediated by volatile compounds rather than diffusible metabolites. This antifungal effect was not strain specific, as it was reproduced by phylogenetically diverse bacteria grown on MHA, suggesting the involvement of ubiquitous volatile molecules. Similar inhibitory effects were observed on MHA against other fungi and yeasts relevant to CGD and CF, supporting the hypothesis that these volatiles are broadly toxic rather than species-specific. To identify candidate ubiquitous antifungal VCs, we conducted comparative volatilomics of two phylogenetically distant bacterial strains that consistently inhibited fungal growth. Among the 143 VCs detected, only dimethyl trisulfide (DMTS) and dimethyl disulfide (DMDS) showed consistent presence in both bacterial volatilomes, with significantly increased production under conditions that promoted fungal inhibition. Exposure assays with pure compounds confirmed that both DMDS and DMTS strongly inhibited R. argillacea growth, with DMTS exhibiting greater potency. Our findings position these ubiquitous sulfur compounds as valuable models for exploring novel agents against human pathogens.
IMPORTANCE: Our findings suggest that antifungal activity against human pathogens may arise from common metabolic pathways shared across diverse microbes rather than from unique biosynthetic systems. Because dimethyl disulfide and dimethyl trisulfide can also be generated through microbial and dietary sulfur metabolism, it is plausible that the human microbiome may produce similar volatiles depending on diet composition, particularly following consumption of sulfur-rich foods. This study, therefore, underscores the critical influence of culture conditions on revealing bioactive volatile production and opens intriguing perspectives on the ecological and physiological roles of ubiquitous microbial metabolites in regulating fungal colonization and microbiome-host interactions.},
}
RevDate: 2025-11-28
CmpDate: 2025-11-28
Molecular Cloning and Functional Analysis of Holin and Endolysin From Escherichia Phage UE-M6 as Potential Antibacterial Agents.
MicrobiologyOpen, 14(6):e70150.
The rise of antibiotic-resistant bacteria has intensified the search for alternative antibacterial strategies. Bacteriophage (phage) therapy is gaining attention as a promising approach, utilizing phage-derived proteins such as holins and endolysins to combat bacterial infections. In this study, the endolysin (UE-lysin) and holin (UE-holin) genes from Escherichia phage UE-M6 were characterized, and their antimicrobial activity was evaluated. In silico analysis revealed that UE-lysin has a modular architecture, with the N-terminal enzymatic activity domain that contains an N-acetylmuramidase of the glycoside hydrolase family GH108, and the C-terminal cell wall-binding domain that contains the peptidoglycan binding family PG_binding_3 domain. UE-holin was predicted to belong to class II holins, featuring two transmembrane helices. Furthermore, the genes encoding the UE-lysin and UE-holin were cloned and their expression optimized in Escherichia coli BL21 (DE3). The purified recombinant UE-lysin (27 kDa) and UE-holin (15 kDa) exhibited antibacterial activity against the E. coli host strain PSU-5266 (UE-17). The addition of the outer membrane permeabilizer ethylenediaminetetraacetic acid further enhanced their activity. Notably, the combined application of UE-holin and UE-lysin demonstrated greater antibacterial efficacy than either enzyme alone, highlighting a synergistic effect. Furthermore, UE-lysin and UE-holin exhibited high lytic activity against E. coli, Bacillus, and Staphylococcus aureus strains, underscoring their potential as candidates for treating both Gram-negative and Gram-positive bacterial infections.
Additional Links: PMID-41311358
Publisher:
PubMed:
Citation:
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@article {pmid41311358,
year = {2025},
author = {Niaz, H and Skurnik, M and Adnan, F},
title = {Molecular Cloning and Functional Analysis of Holin and Endolysin From Escherichia Phage UE-M6 as Potential Antibacterial Agents.},
journal = {MicrobiologyOpen},
volume = {14},
number = {6},
pages = {e70150},
doi = {10.1002/mbo3.70150},
pmid = {41311358},
issn = {2045-8827},
support = {//We gratefully acknowledge the Higher Education Commission (HEC) of Pakistan for the award of the International Research Support Initiative Program (IRSIP) for the University of Helsinki, Finland./ ; },
mesh = {*Endopeptidases/genetics/pharmacology/metabolism/chemistry ; *Anti-Bacterial Agents/pharmacology/metabolism ; Escherichia coli/virology/drug effects ; Cloning, Molecular ; *Viral Proteins/genetics/pharmacology/metabolism ; *Coliphages/genetics/enzymology ; Microbial Sensitivity Tests ; Recombinant Proteins/pharmacology/genetics/metabolism/isolation & purification ; *Bacteriophages/genetics ; Staphylococcus aureus/drug effects ; },
abstract = {The rise of antibiotic-resistant bacteria has intensified the search for alternative antibacterial strategies. Bacteriophage (phage) therapy is gaining attention as a promising approach, utilizing phage-derived proteins such as holins and endolysins to combat bacterial infections. In this study, the endolysin (UE-lysin) and holin (UE-holin) genes from Escherichia phage UE-M6 were characterized, and their antimicrobial activity was evaluated. In silico analysis revealed that UE-lysin has a modular architecture, with the N-terminal enzymatic activity domain that contains an N-acetylmuramidase of the glycoside hydrolase family GH108, and the C-terminal cell wall-binding domain that contains the peptidoglycan binding family PG_binding_3 domain. UE-holin was predicted to belong to class II holins, featuring two transmembrane helices. Furthermore, the genes encoding the UE-lysin and UE-holin were cloned and their expression optimized in Escherichia coli BL21 (DE3). The purified recombinant UE-lysin (27 kDa) and UE-holin (15 kDa) exhibited antibacterial activity against the E. coli host strain PSU-5266 (UE-17). The addition of the outer membrane permeabilizer ethylenediaminetetraacetic acid further enhanced their activity. Notably, the combined application of UE-holin and UE-lysin demonstrated greater antibacterial efficacy than either enzyme alone, highlighting a synergistic effect. Furthermore, UE-lysin and UE-holin exhibited high lytic activity against E. coli, Bacillus, and Staphylococcus aureus strains, underscoring their potential as candidates for treating both Gram-negative and Gram-positive bacterial infections.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
*Endopeptidases/genetics/pharmacology/metabolism/chemistry
*Anti-Bacterial Agents/pharmacology/metabolism
Escherichia coli/virology/drug effects
Cloning, Molecular
*Viral Proteins/genetics/pharmacology/metabolism
*Coliphages/genetics/enzymology
Microbial Sensitivity Tests
Recombinant Proteins/pharmacology/genetics/metabolism/isolation & purification
*Bacteriophages/genetics
Staphylococcus aureus/drug effects
RevDate: 2025-11-27
CmpDate: 2025-11-27
Joint Bacterial Traces in the Gut and Oral Cavity of Obesity Patients Provide Evidence for Saliva as a Rich Microbial Biomarker Source.
Nutrients, 17(22): pii:nu17223527.
Background: The human microbiome holds promise for identifying biomarkers and therapeutic targets. In obesity, interactions between oral and gut communities are increasingly implicated and end in organ injury. Methods: From the IMAGINE study, we analyzed 418 shotgun metagenomes from three specimen types (dental plaque (n = 143; 65 non-obese, 78 obese), saliva (n = 166; 75 non-obese, 91 obese), and stool (n = 109; 57 non-obese, 52 obese)) to compare site-specific microbial shifts between obese (BMI > 30 kg/m[2]) and non-obese individuals. Differential abundance was assessed with ANCOM-BC; effect sizes were summarized as Cohen's d. Results: Across all samples, we detected 240 bacterial species in plaque, 229 in saliva, and 231 in stool, with 46 species present across all three sites. Absolute effect sizes were significantly larger in plaque (mean |d| = 0.26) and saliva (0.25) than in stool (0.21; p = 9 × 10[-3]). Several taxa showed an opposite directionality between oral and gut sites, including Streptococcus salivarius and Bifidobacterium longum, indicating site-specific associations. Notably, Actinomyces sp. and Streptococcus sp. exhibited promising effect sizes as diagnostic markers. Conclusions: The oral and gut microbiomes capture complementary obesity-related signals, with stronger shifts observed in oral sites. We suggest that integrating oral and gut profiling could enhance diagnostic and therapeutic strategies in obesity.
Additional Links: PMID-41305578
Publisher:
PubMed:
Citation:
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@article {pmid41305578,
year = {2025},
author = {Rehner, J and Gund, M and Becker, SL and Hannig, M and Rupf, S and Schattenberg, JM and Keller, A and The Imagine Consortium, and Molano, LG and Keller, V},
title = {Joint Bacterial Traces in the Gut and Oral Cavity of Obesity Patients Provide Evidence for Saliva as a Rich Microbial Biomarker Source.},
journal = {Nutrients},
volume = {17},
number = {22},
pages = {},
doi = {10.3390/nu17223527},
pmid = {41305578},
issn = {2072-6643},
support = {469073465//DFG/ ; },
mesh = {Humans ; *Saliva/microbiology ; *Obesity/microbiology ; *Gastrointestinal Microbiome ; Feces/microbiology ; *Mouth/microbiology ; Male ; Female ; Biomarkers/analysis ; Middle Aged ; Adult ; Dental Plaque/microbiology ; *Bacteria/isolation & purification/classification/genetics ; Metagenome ; },
abstract = {Background: The human microbiome holds promise for identifying biomarkers and therapeutic targets. In obesity, interactions between oral and gut communities are increasingly implicated and end in organ injury. Methods: From the IMAGINE study, we analyzed 418 shotgun metagenomes from three specimen types (dental plaque (n = 143; 65 non-obese, 78 obese), saliva (n = 166; 75 non-obese, 91 obese), and stool (n = 109; 57 non-obese, 52 obese)) to compare site-specific microbial shifts between obese (BMI > 30 kg/m[2]) and non-obese individuals. Differential abundance was assessed with ANCOM-BC; effect sizes were summarized as Cohen's d. Results: Across all samples, we detected 240 bacterial species in plaque, 229 in saliva, and 231 in stool, with 46 species present across all three sites. Absolute effect sizes were significantly larger in plaque (mean |d| = 0.26) and saliva (0.25) than in stool (0.21; p = 9 × 10[-3]). Several taxa showed an opposite directionality between oral and gut sites, including Streptococcus salivarius and Bifidobacterium longum, indicating site-specific associations. Notably, Actinomyces sp. and Streptococcus sp. exhibited promising effect sizes as diagnostic markers. Conclusions: The oral and gut microbiomes capture complementary obesity-related signals, with stronger shifts observed in oral sites. We suggest that integrating oral and gut profiling could enhance diagnostic and therapeutic strategies in obesity.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Saliva/microbiology
*Obesity/microbiology
*Gastrointestinal Microbiome
Feces/microbiology
*Mouth/microbiology
Male
Female
Biomarkers/analysis
Middle Aged
Adult
Dental Plaque/microbiology
*Bacteria/isolation & purification/classification/genetics
Metagenome
RevDate: 2025-11-27
CmpDate: 2025-11-27
The Human Archaeome: Commensals, Opportunists, or Emerging Pathogens?.
Pathogens (Basel, Switzerland), 14(11): pii:pathogens14111111.
Archaea, one of the three domains of life, are increasingly recognized as consistent, though often underappreciated, members of the human microbiome, yet their roles in health and disease remain poorly understood. Unlike bacteria, no archaeal species have been conclusively identified as primary mammalian pathogens, but their widespread presence across diverse body sites suggests potential indirect contributions to host physiology and pathology. Current evidence is synthesized on archaeal diversity and habitat specificity across multiple human-associated sites, encompassing the gastrointestinal, aerodigestive, and urogenital tracts as well as the skin. Methanogens dominate the lower gastrointestinal tract (LGT), where they influence fermentation dynamics and methane production, while members of the class Nitrososphaeria are prevalent on the skin and upper aerodigestive tract (UAT), reflecting ecological specialization. Variability in archaeal composition across niches highlights possible links to disease processes: methanogens have been associated with irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), obesity, and colorectal cancer (CRC); Methanobrevibacter oralis is enriched in periodontal disease; and archaea have been detected in the lungs of cystic fibrosis patients. Although archaea lack canonical bacterial virulence factors, they may contribute indirectly through metabolic cross-feeding, immune modulation, synergy in polymicrobial infections, and alteration of host-microbiome network dynamics. This review explores the emerging concept of the human "archaeome", evaluates current evidence for archaeal involvement in disease, and highlights emerging technologies, such as bacteria-MERFISH and multi-omics profiling, that enable translational applications including microbiome diagnostics, therapeutic targeting, and microbiome engineering.
Additional Links: PMID-41305349
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PubMed:
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@article {pmid41305349,
year = {2025},
author = {Ruden, DM},
title = {The Human Archaeome: Commensals, Opportunists, or Emerging Pathogens?.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/pathogens14111111},
pmid = {41305349},
issn = {2076-0817},
support = {5P42ES030991-07/NH/NIH HHS/United States ; 5P30ES036084-06/NH/NIH HHS/United States ; },
mesh = {Humans ; *Archaea/physiology/pathogenicity/classification ; *Microbiota ; *Symbiosis ; },
abstract = {Archaea, one of the three domains of life, are increasingly recognized as consistent, though often underappreciated, members of the human microbiome, yet their roles in health and disease remain poorly understood. Unlike bacteria, no archaeal species have been conclusively identified as primary mammalian pathogens, but their widespread presence across diverse body sites suggests potential indirect contributions to host physiology and pathology. Current evidence is synthesized on archaeal diversity and habitat specificity across multiple human-associated sites, encompassing the gastrointestinal, aerodigestive, and urogenital tracts as well as the skin. Methanogens dominate the lower gastrointestinal tract (LGT), where they influence fermentation dynamics and methane production, while members of the class Nitrososphaeria are prevalent on the skin and upper aerodigestive tract (UAT), reflecting ecological specialization. Variability in archaeal composition across niches highlights possible links to disease processes: methanogens have been associated with irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), obesity, and colorectal cancer (CRC); Methanobrevibacter oralis is enriched in periodontal disease; and archaea have been detected in the lungs of cystic fibrosis patients. Although archaea lack canonical bacterial virulence factors, they may contribute indirectly through metabolic cross-feeding, immune modulation, synergy in polymicrobial infections, and alteration of host-microbiome network dynamics. This review explores the emerging concept of the human "archaeome", evaluates current evidence for archaeal involvement in disease, and highlights emerging technologies, such as bacteria-MERFISH and multi-omics profiling, that enable translational applications including microbiome diagnostics, therapeutic targeting, and microbiome engineering.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Archaea/physiology/pathogenicity/classification
*Microbiota
*Symbiosis
RevDate: 2025-11-27
CmpDate: 2025-11-27
Characterization and Genomic Analysis of a New Bacteriophage Klebsiella pneumoniae CTF-1 from Turkey.
Antibiotics (Basel, Switzerland), 14(11): pii:antibiotics14111153.
Background/Objectives:Klebsiella pneumoniae is a clinically important pathogen that causes respiratory tract infections, pneumonia, wound infections, urinary tract infections, and sepsis. It is on the World Health Organization (WHO) priority pathogen list as it causes antimicrobial-resistant infections. The aim of this study was to isolate bacteriophages against pan-resistant K. pneumoniae isolated from clinical wound infections. Results: One of the isolated phages, CTF-1, possesses a linear double-stranded DNA genome that is 40,841 base pairs (bp) long and contains 44 predicted genes. Functional assignments were made for 31 of the predicted gene products, which are associated with genome replication, phage packaging, structural proteins, and host lysis, leaving 13 annotated as hypothetical proteins. Based on sequencing analysis, phage CTF-1 is a new member of the genus Przondovirus within the order Autographivirales. Phage CTF-1 was effective against 22 of 25 (88%) pan-resistant K. pneumoniae isolates. The latent period and lytic cycle of the phage were approximately 40 min, with a burst size of about 92 PFU/mL. Conclusions: Our findings suggest that Klebsiella phage CTF-1 is an excellent candidate for phage therapy due to its high lytic activity against pan-resistant K. pneumoniae strains and lack of genes encoding antibiotic resistance, toxins, virulence factors, or integrases.
Additional Links: PMID-41301648
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PubMed:
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@article {pmid41301648,
year = {2025},
author = {Kurt, KC and Tokuç, E and Kurt, H and Akın, DN and Sait, A and Aydın, S and Skurnik, M and Bahar Tokman, H},
title = {Characterization and Genomic Analysis of a New Bacteriophage Klebsiella pneumoniae CTF-1 from Turkey.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/antibiotics14111153},
pmid = {41301648},
issn = {2079-6382},
support = {34517//IUC-BAP/ ; },
abstract = {Background/Objectives:Klebsiella pneumoniae is a clinically important pathogen that causes respiratory tract infections, pneumonia, wound infections, urinary tract infections, and sepsis. It is on the World Health Organization (WHO) priority pathogen list as it causes antimicrobial-resistant infections. The aim of this study was to isolate bacteriophages against pan-resistant K. pneumoniae isolated from clinical wound infections. Results: One of the isolated phages, CTF-1, possesses a linear double-stranded DNA genome that is 40,841 base pairs (bp) long and contains 44 predicted genes. Functional assignments were made for 31 of the predicted gene products, which are associated with genome replication, phage packaging, structural proteins, and host lysis, leaving 13 annotated as hypothetical proteins. Based on sequencing analysis, phage CTF-1 is a new member of the genus Przondovirus within the order Autographivirales. Phage CTF-1 was effective against 22 of 25 (88%) pan-resistant K. pneumoniae isolates. The latent period and lytic cycle of the phage were approximately 40 min, with a burst size of about 92 PFU/mL. Conclusions: Our findings suggest that Klebsiella phage CTF-1 is an excellent candidate for phage therapy due to its high lytic activity against pan-resistant K. pneumoniae strains and lack of genes encoding antibiotic resistance, toxins, virulence factors, or integrases.},
}
RevDate: 2025-11-27
CmpDate: 2025-11-27
The Synaptic and Intrinsic Cellular Mechanisms of Persistent Firing in Neurogliaform Cells.
Biomolecules, 15(11): pii:biom15111603.
While persistent firing in glutamatergic neurons has been well-characterized, the intrinsic and synaptic mechanisms driving this phenomenon in neurogliaform cells (NGFCs), a subtype of GABAergic interneurons, remain unclear. This study investigates the mechanisms underlying persistent firing in hippocampal NGFCs. Whole-cell current-clamp recordings were performed on acute brain slices from C57BL/6J mice to examine the electrophysiological properties of NGFCs in the hippocampal stratum lacunosum-moleculare (SLM). Pharmacological interventions, including T-type calcium channel blocker ML218 and 5-hydroxytryptamine (5-HT) receptor antagonist olanzapine, were used to dissect the mechanisms of persistent firing. Biocytin labeling and confocal microscopy were employed to confirm neuronal morphology and location. The study revealed that persistent firing in NGFCs is induced by a long-lasting delayed afterdepolarization (L-ADP), which depends on T-type calcium channels (intrinsic mechanism) and is modulated by 5-HT receptors (synaptic mechanism). Persistent firing was observed in 62.96% of SLM neurons and was abolished by ML218 or olanzapine. The findings bridge a gap in understanding how inhibitory interneurons contribute to memory processes. The dual-mechanism framework (T-type channels and 5-HT receptors) aligns with prior work on glutamatergic systems but highlights unique features of GABAergic persistent firing. These insights advance the understanding of inhibitory circuit dynamics and their potential role in cognitive functions, paving the way for further research into interneuron-specific memory encoding.
Additional Links: PMID-41301521
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@article {pmid41301521,
year = {2025},
author = {Chen, S and Chen, X and Zhou, J and Wang, J and Li, K and Xie, W and Long, C and Wu, G},
title = {The Synaptic and Intrinsic Cellular Mechanisms of Persistent Firing in Neurogliaform Cells.},
journal = {Biomolecules},
volume = {15},
number = {11},
pages = {},
doi = {10.3390/biom15111603},
pmid = {41301521},
issn = {2218-273X},
support = {32371065 and 31671059//National Natural Science Foundation of China/ ; 2023A1515010899//Natural Science Foundation of the Guangdong Province/ ; },
mesh = {Animals ; Mice ; Mice, Inbred C57BL ; *Hippocampus/cytology/physiology/metabolism ; *Synapses/physiology/metabolism ; *Action Potentials/drug effects ; Male ; Calcium Channels, T-Type/metabolism ; *Interneurons/physiology/metabolism/drug effects ; Receptors, Serotonin/metabolism ; Olanzapine/pharmacology ; Synaptic Transmission ; Patch-Clamp Techniques ; *Neuroglia/physiology/metabolism ; },
abstract = {While persistent firing in glutamatergic neurons has been well-characterized, the intrinsic and synaptic mechanisms driving this phenomenon in neurogliaform cells (NGFCs), a subtype of GABAergic interneurons, remain unclear. This study investigates the mechanisms underlying persistent firing in hippocampal NGFCs. Whole-cell current-clamp recordings were performed on acute brain slices from C57BL/6J mice to examine the electrophysiological properties of NGFCs in the hippocampal stratum lacunosum-moleculare (SLM). Pharmacological interventions, including T-type calcium channel blocker ML218 and 5-hydroxytryptamine (5-HT) receptor antagonist olanzapine, were used to dissect the mechanisms of persistent firing. Biocytin labeling and confocal microscopy were employed to confirm neuronal morphology and location. The study revealed that persistent firing in NGFCs is induced by a long-lasting delayed afterdepolarization (L-ADP), which depends on T-type calcium channels (intrinsic mechanism) and is modulated by 5-HT receptors (synaptic mechanism). Persistent firing was observed in 62.96% of SLM neurons and was abolished by ML218 or olanzapine. The findings bridge a gap in understanding how inhibitory interneurons contribute to memory processes. The dual-mechanism framework (T-type channels and 5-HT receptors) aligns with prior work on glutamatergic systems but highlights unique features of GABAergic persistent firing. These insights advance the understanding of inhibitory circuit dynamics and their potential role in cognitive functions, paving the way for further research into interneuron-specific memory encoding.},
}
MeSH Terms:
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Animals
Mice
Mice, Inbred C57BL
*Hippocampus/cytology/physiology/metabolism
*Synapses/physiology/metabolism
*Action Potentials/drug effects
Male
Calcium Channels, T-Type/metabolism
*Interneurons/physiology/metabolism/drug effects
Receptors, Serotonin/metabolism
Olanzapine/pharmacology
Synaptic Transmission
Patch-Clamp Techniques
*Neuroglia/physiology/metabolism
RevDate: 2025-11-27
CmpDate: 2025-11-27
Melatonin Improves Intestinal Barrier Impairment in a Mouse Model of Autism Spectrum Disorder.
Biology, 14(11): pii:biology14111594.
Autism spectrum disorder (ASD) is a neurodevelopmental condition mainly characterized by social impairments and repetitive behaviors. An altered intestinal barrier morphology and increased transmucosal leaks have also been implicated in ASD; in fact, comorbidities such as gastrointestinal problems (leaky gut) have frequently been reported in these patients. The regulation of tight junctions (TJs) is essential in maintaining intestinal barrier morphology and in regulating the delicate balance of trafficking between the intestinal lumen and the submucosa. To date, there are no definitive treatments for ASD comorbidities; however, melatonin (MLT) represents a well-validated and tolerated treatment for sleep disorders in ASD patients. The potential beneficial effects of MLT on this disorder have been and continue to be better investigated. In this context, the present study examines the effects of oral MLT administration (10 mg/kg/day for 16 weeks) on the intestinal barrier in BTBR T + Itpr3tf/J (BTBR) mice, a validated ASD model. Morphological analyses of the ileum of these animals reveal modified villus height (Vh), crypt depth (Cd), and Vh-Cd ratios; an inflammatory state; and a decrease in Paneth cells. Moreover, these mice showed altered TJ expression compared to the control animals (C57BL6/J mice). Notably, MLT normalizes morphological indices and TJ expression, consistent with an improved gut barrier morphology. These data collectively suggest that orally administered MLT can promote the remodeling of the intestinal barrier; thus, we can suppose that MLT reduces gastrointestinal barrier leaks. The overall safety and economy of MLT use suggest that this indolamine could be efficacious as an adjuvant therapy to reduce the condition known as leaky gut.
Additional Links: PMID-41300382
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PubMed:
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@article {pmid41300382,
year = {2025},
author = {Sulas, F and Favero, G and Bonini, SA and Lonati, C and Pinto, D and Memo, M and Rinaldi, F and Rezzani, R},
title = {Melatonin Improves Intestinal Barrier Impairment in a Mouse Model of Autism Spectrum Disorder.},
journal = {Biology},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/biology14111594},
pmid = {41300382},
issn = {2079-7737},
support = {ex 60% grants//University of Brescia-Italy/ ; Donation//FLAMMA S.p.A.-Italy/ ; Donation.//Franchini Acciai S.p.A.-Italy/ ; },
abstract = {Autism spectrum disorder (ASD) is a neurodevelopmental condition mainly characterized by social impairments and repetitive behaviors. An altered intestinal barrier morphology and increased transmucosal leaks have also been implicated in ASD; in fact, comorbidities such as gastrointestinal problems (leaky gut) have frequently been reported in these patients. The regulation of tight junctions (TJs) is essential in maintaining intestinal barrier morphology and in regulating the delicate balance of trafficking between the intestinal lumen and the submucosa. To date, there are no definitive treatments for ASD comorbidities; however, melatonin (MLT) represents a well-validated and tolerated treatment for sleep disorders in ASD patients. The potential beneficial effects of MLT on this disorder have been and continue to be better investigated. In this context, the present study examines the effects of oral MLT administration (10 mg/kg/day for 16 weeks) on the intestinal barrier in BTBR T + Itpr3tf/J (BTBR) mice, a validated ASD model. Morphological analyses of the ileum of these animals reveal modified villus height (Vh), crypt depth (Cd), and Vh-Cd ratios; an inflammatory state; and a decrease in Paneth cells. Moreover, these mice showed altered TJ expression compared to the control animals (C57BL6/J mice). Notably, MLT normalizes morphological indices and TJ expression, consistent with an improved gut barrier morphology. These data collectively suggest that orally administered MLT can promote the remodeling of the intestinal barrier; thus, we can suppose that MLT reduces gastrointestinal barrier leaks. The overall safety and economy of MLT use suggest that this indolamine could be efficacious as an adjuvant therapy to reduce the condition known as leaky gut.},
}
RevDate: 2025-11-26
Laser-assisted microbial culturomics.
Nature communications pii:10.1038/s41467-025-66804-7 [Epub ahead of print].
Even though metagenomics have revolutionized the characterization of the human microbiome, detailed mechanistic studies are impracticable, as there is a dearth of robust culture collections. We now describe the development and use of a laser-assisted culturomics platform, incorporating the elements of a bioprinter, the culture conditions, the methods to characterize the microorganisms and a biobank. With laser-assisted bioprinting, the microorganisms can be rapidly and precisely transferred from clinical biofilms to highly organized arrays of microbial colonies, which are suitable for co-culturing and molecular analyses. The presented technique has propagated 99 of 100 microbial species and recovered 79% of abundant species from dental plaque in accordance with full 16S rRNA gene profiling of 691,199 sequences. Microscopy, spectroscopy and enzyme assays have been used to guide isolations. Processing of oral biofilms from four individuals has yielded 249 representative isolates, from 14 classes and 124 species in total. Functional profiling with bioprinting has indicated commensals which could potentially contribute to disease development. Isolates from peri-implantitis cover 85.4% of the transcriptionally active clinical biofilms at genus level. Taken together, this work provides the basis for generating on-demand culture collections and biofilms for research and clinical use.
Additional Links: PMID-41298564
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PubMed:
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@article {pmid41298564,
year = {2025},
author = {Qu, T and Koch, L and Mukherjee, R and Tu, Y and Seidel, AL and Püttmann, LD and Winkel, A and Yang, I and Grischke, J and Liu, D and Wolkers, WF and Kittler, S and Chichkov, B and Stiesch, M and Szafrański, SP},
title = {Laser-assisted microbial culturomics.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-025-66804-7},
pmid = {41298564},
issn = {2041-1723},
support = {German Cluster of Excellence Ex62/2 Rebirth//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; German Cluster of Excellence Ex62/2 Rebirth//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; SFB/TRR 298 SIIRI - Project-ID 426335750//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; EXC 2155 - project number 390874280//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; Laser-Tissue-Perfude, 101054009//EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council)/ ; },
abstract = {Even though metagenomics have revolutionized the characterization of the human microbiome, detailed mechanistic studies are impracticable, as there is a dearth of robust culture collections. We now describe the development and use of a laser-assisted culturomics platform, incorporating the elements of a bioprinter, the culture conditions, the methods to characterize the microorganisms and a biobank. With laser-assisted bioprinting, the microorganisms can be rapidly and precisely transferred from clinical biofilms to highly organized arrays of microbial colonies, which are suitable for co-culturing and molecular analyses. The presented technique has propagated 99 of 100 microbial species and recovered 79% of abundant species from dental plaque in accordance with full 16S rRNA gene profiling of 691,199 sequences. Microscopy, spectroscopy and enzyme assays have been used to guide isolations. Processing of oral biofilms from four individuals has yielded 249 representative isolates, from 14 classes and 124 species in total. Functional profiling with bioprinting has indicated commensals which could potentially contribute to disease development. Isolates from peri-implantitis cover 85.4% of the transcriptionally active clinical biofilms at genus level. Taken together, this work provides the basis for generating on-demand culture collections and biofilms for research and clinical use.},
}
RevDate: 2025-11-26
The Role of the Gut Non-Bacterial Microbiome (Virome, Mycobiome, Archaeome) and its Impact on Obesity.
Molecular metabolism pii:S2212-8778(25)00196-6 [Epub ahead of print].
The epidemic of obesity and metabolic syndrome is a major public health concern internationally. There is increasing knowledge and research in areas of appetite regulation and drivers of obesity but there is still a gap on how the interactomes are altered in a metabolically dysregulated human body. The human microbiome has been implicated in the pathogenesis of obesity. While the association of gut bacteriome dysbiosis is well described in obesity and metabolic syndrome, there is a lack of an integrative understanding about the roles of the non-bacterial microbiome (virome, mycobiome, and archaeome) in the pathogenesis and protection of obesity and metabolic syndrome. Accumulating studies have revealed that the non-bacterial microbes in the gut, including viruses/ phages, fungi, and archaea, are profoundly altered in obesity, and impact host adiposity and physiology in nuanced manners. In this review, we aim to provide a comprehensive view on the role and the mechanisms of the gut virome, mycobiome, and archaeome in obesity. These insights will shed light on the translational value as well as the future research directions for harnessing the gut non-bacterial microbial entities in the therapeutics and prevention of metabolic diseases.
Additional Links: PMID-41297880
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PubMed:
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@article {pmid41297880,
year = {2025},
author = {Chue, KM and Wong, SH and Zuo, T and Ali, Y},
title = {The Role of the Gut Non-Bacterial Microbiome (Virome, Mycobiome, Archaeome) and its Impact on Obesity.},
journal = {Molecular metabolism},
volume = {},
number = {},
pages = {102289},
doi = {10.1016/j.molmet.2025.102289},
pmid = {41297880},
issn = {2212-8778},
abstract = {The epidemic of obesity and metabolic syndrome is a major public health concern internationally. There is increasing knowledge and research in areas of appetite regulation and drivers of obesity but there is still a gap on how the interactomes are altered in a metabolically dysregulated human body. The human microbiome has been implicated in the pathogenesis of obesity. While the association of gut bacteriome dysbiosis is well described in obesity and metabolic syndrome, there is a lack of an integrative understanding about the roles of the non-bacterial microbiome (virome, mycobiome, and archaeome) in the pathogenesis and protection of obesity and metabolic syndrome. Accumulating studies have revealed that the non-bacterial microbes in the gut, including viruses/ phages, fungi, and archaea, are profoundly altered in obesity, and impact host adiposity and physiology in nuanced manners. In this review, we aim to provide a comprehensive view on the role and the mechanisms of the gut virome, mycobiome, and archaeome in obesity. These insights will shed light on the translational value as well as the future research directions for harnessing the gut non-bacterial microbial entities in the therapeutics and prevention of metabolic diseases.},
}
RevDate: 2025-11-26
CmpDate: 2025-11-26
Harnessing Probiotics to Combat Candidiasis: Mechanisms, Evidence, and Future Directions.
Journal of fungi (Basel, Switzerland), 11(11): pii:jof11110779.
Candida species are common commensals within the human microbiome but can transition opportunistically to pathogenic states when host-microbe homeostasis is disrupted. Their ability to adhere to mucosa and implanted medical devices, form thick biofilms, and invade epithelial tissues makes candidiasis particularly harmful in immunocompromised and elderly populations. This review examines the reported antifungal activity of common probiotic genera such as Lactobacillus, Bacillus, Bifidobacterium, and Saccharomyces across the oral cavity, gastrointestinal tract, and vaginal tract. The probiotic mechanisms of action, such as competitive exclusion, secretion of antifungal metabolites, and immunomodulation, are explored in detail, and research methodologies are scrutinised to assess the robustness of current evidence. This review compiles evidence from a variety of studies and clinical trials showing certain probiotic strains and formulations have the ability to significantly decrease Candida colonisation and reduce candidiasis symptom prevalence. Although outcomes vary greatly between probiotic strains tested, species of Candida targeted, and specific site of infection, it is clear that selected probiotic species and their secreted substances can have prominent anti-Candida effects and promote tangible clinical improvements. Future directions for the field of probiotic study are suggested, including the roles of prebiotics, postbiotics, and synbiotic formulations to enhance probiotic efficacy against candidiasis.
Additional Links: PMID-41295160
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PubMed:
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@article {pmid41295160,
year = {2025},
author = {Wright, E and Valand, N and Venkatraman Girija, U},
title = {Harnessing Probiotics to Combat Candidiasis: Mechanisms, Evidence, and Future Directions.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {11},
number = {11},
pages = {},
doi = {10.3390/jof11110779},
pmid = {41295160},
issn = {2309-608X},
abstract = {Candida species are common commensals within the human microbiome but can transition opportunistically to pathogenic states when host-microbe homeostasis is disrupted. Their ability to adhere to mucosa and implanted medical devices, form thick biofilms, and invade epithelial tissues makes candidiasis particularly harmful in immunocompromised and elderly populations. This review examines the reported antifungal activity of common probiotic genera such as Lactobacillus, Bacillus, Bifidobacterium, and Saccharomyces across the oral cavity, gastrointestinal tract, and vaginal tract. The probiotic mechanisms of action, such as competitive exclusion, secretion of antifungal metabolites, and immunomodulation, are explored in detail, and research methodologies are scrutinised to assess the robustness of current evidence. This review compiles evidence from a variety of studies and clinical trials showing certain probiotic strains and formulations have the ability to significantly decrease Candida colonisation and reduce candidiasis symptom prevalence. Although outcomes vary greatly between probiotic strains tested, species of Candida targeted, and specific site of infection, it is clear that selected probiotic species and their secreted substances can have prominent anti-Candida effects and promote tangible clinical improvements. Future directions for the field of probiotic study are suggested, including the roles of prebiotics, postbiotics, and synbiotic formulations to enhance probiotic efficacy against candidiasis.},
}
RevDate: 2025-11-26
CmpDate: 2025-11-26
Advancing Yeast Identification Using High-Throughput DNA Barcode Data From a Curated Culture Collection.
Molecular ecology resources, 26(1):e70082.
Yeast identification is essential in fields ranging from microbiology and biotechnology to food science and medicine. While DNA barcoding has become the standard for identifying cultured strains, environmental DNA (eDNA) metabarcoding has revolutionised microbial community profiling, providing deeper insights into yeast communities across diverse ecosystems. A major challenge in DNA (meta)barcoding remains the limited availability of high-quality reference sequences, which are critical for accurate species identification and comprehensive taxonomic profiling of both environmental and clinical samples. To address this gap, the Westerdijk Fungal Biodiversity Institute (WI) launched a DNA barcoding initiative in 2006 to generate high-quality, often type-derived ITS and LSU barcodes for all ~100,000 fungal strains preserved in the CBS culture collection, including approximately 15,000 yeasts. Building on the yeast barcode dataset released in 2016, we now present an expanded set of 2856 ITS and 3815 LSU sequences, representing 911 and 1137 yeast species, respectively. Notably, 27%-29% of these sequences are derived from ex-type cultures. Using both newly generated and previously published barcodes, we assess the taxonomic resolution of commonly used yeast metabarcoding markers (ITS, ITS1, ITS2 and LSU) and propose marker-specific similarity cutoffs for different yeast taxonomic groups. These results provide actionable guidance for marker selection and improve the interpretation of metabarcoding data. We further demonstrate the impact of well-curated reference databases with up-to-date taxonomy by reanalyzing Human Microbiome Project data, revealing how diet and environment shape the gut mycobiota.
Additional Links: PMID-41294086
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@article {pmid41294086,
year = {2026},
author = {Vu, D and de Vries, M and van den Ende, BG and Houbraken, J and Nilsson, RH and Brankovics, B and Hernández-Restrepo, M and Groenewald, JZ and Crous, PW and Hagen, F and Meyer, W and Verkley, GJM and Groenewald, M},
title = {Advancing Yeast Identification Using High-Throughput DNA Barcode Data From a Curated Culture Collection.},
journal = {Molecular ecology resources},
volume = {26},
number = {1},
pages = {e70082},
doi = {10.1111/1755-0998.70082},
pmid = {41294086},
issn = {1755-0998},
mesh = {*DNA Barcoding, Taxonomic/methods ; *Yeasts/classification/genetics/isolation & purification ; DNA, Fungal/genetics/chemistry ; High-Throughput Nucleotide Sequencing/methods ; DNA, Ribosomal Spacer/genetics/chemistry ; Sequence Analysis, DNA ; },
abstract = {Yeast identification is essential in fields ranging from microbiology and biotechnology to food science and medicine. While DNA barcoding has become the standard for identifying cultured strains, environmental DNA (eDNA) metabarcoding has revolutionised microbial community profiling, providing deeper insights into yeast communities across diverse ecosystems. A major challenge in DNA (meta)barcoding remains the limited availability of high-quality reference sequences, which are critical for accurate species identification and comprehensive taxonomic profiling of both environmental and clinical samples. To address this gap, the Westerdijk Fungal Biodiversity Institute (WI) launched a DNA barcoding initiative in 2006 to generate high-quality, often type-derived ITS and LSU barcodes for all ~100,000 fungal strains preserved in the CBS culture collection, including approximately 15,000 yeasts. Building on the yeast barcode dataset released in 2016, we now present an expanded set of 2856 ITS and 3815 LSU sequences, representing 911 and 1137 yeast species, respectively. Notably, 27%-29% of these sequences are derived from ex-type cultures. Using both newly generated and previously published barcodes, we assess the taxonomic resolution of commonly used yeast metabarcoding markers (ITS, ITS1, ITS2 and LSU) and propose marker-specific similarity cutoffs for different yeast taxonomic groups. These results provide actionable guidance for marker selection and improve the interpretation of metabarcoding data. We further demonstrate the impact of well-curated reference databases with up-to-date taxonomy by reanalyzing Human Microbiome Project data, revealing how diet and environment shape the gut mycobiota.},
}
MeSH Terms:
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*DNA Barcoding, Taxonomic/methods
*Yeasts/classification/genetics/isolation & purification
DNA, Fungal/genetics/chemistry
High-Throughput Nucleotide Sequencing/methods
DNA, Ribosomal Spacer/genetics/chemistry
Sequence Analysis, DNA
RevDate: 2025-11-25
Polyclonal origins of human premalignant colorectal lesions.
Nature pii:10.1038/s41586-025-09930-y [Epub ahead of print].
Cancer is generally thought to be caused by expansion of a single mutant cell[1]. However, analyses of early colorectal cancer lesions suggest that tumors may instead originate from multiple, genetically distinct cell populations[2,3]. Detecting polyclonal tumor initiation is challenging in patients, as it requires profiling early-stage lesions before clonal sweeps obscure diversity. To investigate this, we analyzed normal colorectal mucosa, benign and dysplastic premalignant polyps, and malignant adenocarcinomas (123 samples) from six individuals with familial adenomatous polyposis (FAP). Individuals with FAP have a germline heterozygous APC mutation, predisposing them to colorectal cancer and numerous premalignant polyps by early adulthood[4]. Whole-genome and/or whole-exome sequencing revealed that many premalignant polyps-40% with benign histology and 28% with dysplasia-were composed of multiple genetic lineages that diverged early, consistent with polyclonal origins. This conclusion was reinforced by whole-genome sequencing of single crypts from multiple polyps in additional patients which showed limited sharing of mutations among crypts within the same lesion. In some cases, multiple distinct APC mutations co-existed in different lineages of a single polyp, consistent with polyclonality. These findings reshape our understanding of early neoplastic events, demonstrating that tumor initiation can arise from the convergence of diverse mutant clones. They also suggest that cell-intrinsic growth advantages alone may not fully explain tumor initiation, highlighting the importance of microenvironmental and tissue-level factors in early cancer evolution.
Additional Links: PMID-41291291
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@article {pmid41291291,
year = {2025},
author = {Van Egeren, D and Schenck, RO and Khan, A and Horning, AM and Mo, S and Weiß, CL and Esplin, ED and Becker, WR and Wu, S and Hanson, C and Barapour, N and Jiang, L and Contrepois, K and Lee, H and Nevins, SA and Guha, TK and Zhang, H and He, Z and Ma, Z and Monte, E and Karathanos, TV and Laquindanum, R and Mills, MA and Chaib, H and Chiu, R and Jian, R and Chan, J and Ellenberger, M and Bahmani, B and Michael, B and Weimer, AK and Esplin, DG and Lancaster, S and Shen, J and Ladabaum, U and Longacre, TA and Kundaje, A and Greenleaf, WJ and Hu, Z and Ford, JM and Snyder, MP and Curtis, C},
title = {Polyclonal origins of human premalignant colorectal lesions.},
journal = {Nature},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41586-025-09930-y},
pmid = {41291291},
issn = {1476-4687},
abstract = {Cancer is generally thought to be caused by expansion of a single mutant cell[1]. However, analyses of early colorectal cancer lesions suggest that tumors may instead originate from multiple, genetically distinct cell populations[2,3]. Detecting polyclonal tumor initiation is challenging in patients, as it requires profiling early-stage lesions before clonal sweeps obscure diversity. To investigate this, we analyzed normal colorectal mucosa, benign and dysplastic premalignant polyps, and malignant adenocarcinomas (123 samples) from six individuals with familial adenomatous polyposis (FAP). Individuals with FAP have a germline heterozygous APC mutation, predisposing them to colorectal cancer and numerous premalignant polyps by early adulthood[4]. Whole-genome and/or whole-exome sequencing revealed that many premalignant polyps-40% with benign histology and 28% with dysplasia-were composed of multiple genetic lineages that diverged early, consistent with polyclonal origins. This conclusion was reinforced by whole-genome sequencing of single crypts from multiple polyps in additional patients which showed limited sharing of mutations among crypts within the same lesion. In some cases, multiple distinct APC mutations co-existed in different lineages of a single polyp, consistent with polyclonality. These findings reshape our understanding of early neoplastic events, demonstrating that tumor initiation can arise from the convergence of diverse mutant clones. They also suggest that cell-intrinsic growth advantages alone may not fully explain tumor initiation, highlighting the importance of microenvironmental and tissue-level factors in early cancer evolution.},
}
RevDate: 2025-11-25
Microbial variations in the multibody sites of the pancreatic ductal adenocarcinoma patients.
International journal of surgery (London, England) pii:01279778-990000000-03846 [Epub ahead of print].
OBJECTIVES: We aimed to investigate microbial characteristics across multibody sites of pancreatic ductal adenocarcinoma (PDAC) and identify novel microbial markers for PDAC.
METHOD: We conducted 16S ribosomal RNA (rRNA) amplicon sequencing on saliva, duodenal fluid, and pancreatic tissue obtained via endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) from 63 PDAC patients and 22 benign controls.
RESULTS: From controls to PDAC patients, the contribution of salivary and duodenal microbes to the assembly of pancreatic microbes increased. In PDAC patients and controls, duodenal microbes contributed more significantly to the pancreatic microbial assembly than salivary microbes. Prevotella dentalis, Peptoanaerobacter stomatis, Slackia exigua, etc. were enriched, whereas Loigolactobacillus coryniformis, Akkermansia muciniphila, Faecalibacterium prausnitzii, etc., were reduced in pancreatic tissue, duodenal fluid, and saliva of PDAC patients (P < 0.05). We developed microbial classifiers for discriminating PDAC based on the differential species shared among the three sites with the areas under the curves (AUCs) of 0.946, 0.991, and 0.971 in pancreatic tissue, duodenal fluid, and saliva, respectively. Faecalibacterium prausnitzii in duodenal fluid, Prevotella dentalis and Slackia exigua in saliva, and Anaeroglobus geminatus and Propionibacterium acidifaciens across all three sites were "driver" microbes contributing to the variations from controls to PDAC patients.
CONCLUSIONS: Salivary and duodenal microbes were significant contributors to the pancreatic microbial composition associated with PDAC. Novel microbial markers with high discriminative power were identified, underscoring their potential for PDAC detection.
Additional Links: PMID-41287874
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PubMed:
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@article {pmid41287874,
year = {2025},
author = {Zhu, Y and Zhi, M and Liang, X and Li, L and Dong, M and Zhang, G and Wang, L and Wang, P and Zhong, N and Feng, Q and Li, Z},
title = {Microbial variations in the multibody sites of the pancreatic ductal adenocarcinoma patients.},
journal = {International journal of surgery (London, England)},
volume = {},
number = {},
pages = {},
doi = {10.1097/JS9.0000000000003799},
pmid = {41287874},
issn = {1743-9159},
abstract = {OBJECTIVES: We aimed to investigate microbial characteristics across multibody sites of pancreatic ductal adenocarcinoma (PDAC) and identify novel microbial markers for PDAC.
METHOD: We conducted 16S ribosomal RNA (rRNA) amplicon sequencing on saliva, duodenal fluid, and pancreatic tissue obtained via endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) from 63 PDAC patients and 22 benign controls.
RESULTS: From controls to PDAC patients, the contribution of salivary and duodenal microbes to the assembly of pancreatic microbes increased. In PDAC patients and controls, duodenal microbes contributed more significantly to the pancreatic microbial assembly than salivary microbes. Prevotella dentalis, Peptoanaerobacter stomatis, Slackia exigua, etc. were enriched, whereas Loigolactobacillus coryniformis, Akkermansia muciniphila, Faecalibacterium prausnitzii, etc., were reduced in pancreatic tissue, duodenal fluid, and saliva of PDAC patients (P < 0.05). We developed microbial classifiers for discriminating PDAC based on the differential species shared among the three sites with the areas under the curves (AUCs) of 0.946, 0.991, and 0.971 in pancreatic tissue, duodenal fluid, and saliva, respectively. Faecalibacterium prausnitzii in duodenal fluid, Prevotella dentalis and Slackia exigua in saliva, and Anaeroglobus geminatus and Propionibacterium acidifaciens across all three sites were "driver" microbes contributing to the variations from controls to PDAC patients.
CONCLUSIONS: Salivary and duodenal microbes were significant contributors to the pancreatic microbial composition associated with PDAC. Novel microbial markers with high discriminative power were identified, underscoring their potential for PDAC detection.},
}
RevDate: 2025-11-24
Phylo-Spec: a phylogeny-fusion deep learning model advances microbiome status identification.
mSystems [Epub ahead of print].
The human microbiome is crucial for health regulation and disease progression, presenting a valuable opportunity for health state classification. Traditional microbiome-based classification relies on pre-trained machine learning (ML) or deep learning (DL) models, which typically focus on microbial distribution patterns, neglecting the underlying relationships between microbes. As a result, model performance can be significantly affected by data sparsity, misclassified features, or incomplete microbial profiles. To overcome these challenges, we introduce Phylo-Spec, a phylogeny-driven deep learning algorithm that integrates multi-aspect microbial information for improved status recognition. Phylo-Spec fuses convolutional features of microbes within a phylogenetic hierarchy via a bottom-up iteration and significantly alleviates the challenges due to sparse data and inaccurate profiling. Additionally, the model dynamically assigns unclassified species to virtual nodes on the phylogenetic tree based on higher-level taxonomy, minimizing interferences from unclassified species. Phylo-Spec also captures the feature importance via an information gain-based mechanism through the phylogenetic structure propagation, enhancing the interpretability of classification decisions. Phylo-Spec demonstrated superior efficacy in microbiome status classification across two in silico synthetic data sets that simulate the aforementioned cases, outperforming existing ML and DL methods. Validation with real-world metagenomic and amplicon data further confirmed the model's performance in multiple status classification, establishing a powerful framework for microbiome-based health state identification and microbe-disease association. The source code is available at https://github.com/qdu-bioinfo/Phylo-Spec.IMPORTANCEThe human microbiome profoundly influences health and disease, but current computational tools often overlook the evolutionary relationships among microbes, leading to incomplete or inaccurate interpretations of complex microbial data. Phylo-Spec provides a new way to understand the microbiome by combining microbial abundance, taxonomy, and phylogeny within a unified deep learning framework. This model not only improves the accuracy of health status classification but also highlights key microbial contributors linked to disease. By capturing both microbial diversity and evolutionary context, Phylo-Spec bridges the gap between bioinformatics and biological insight, offering a powerful and interpretable approach for advancing microbiome-based diagnostics and precision medicine.
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@article {pmid41283667,
year = {2025},
author = {Zhang, J and Meng, F and Sun, Y and Xu, W and Wu, S and Su, X},
title = {Phylo-Spec: a phylogeny-fusion deep learning model advances microbiome status identification.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0145325},
doi = {10.1128/msystems.01453-25},
pmid = {41283667},
issn = {2379-5077},
abstract = {The human microbiome is crucial for health regulation and disease progression, presenting a valuable opportunity for health state classification. Traditional microbiome-based classification relies on pre-trained machine learning (ML) or deep learning (DL) models, which typically focus on microbial distribution patterns, neglecting the underlying relationships between microbes. As a result, model performance can be significantly affected by data sparsity, misclassified features, or incomplete microbial profiles. To overcome these challenges, we introduce Phylo-Spec, a phylogeny-driven deep learning algorithm that integrates multi-aspect microbial information for improved status recognition. Phylo-Spec fuses convolutional features of microbes within a phylogenetic hierarchy via a bottom-up iteration and significantly alleviates the challenges due to sparse data and inaccurate profiling. Additionally, the model dynamically assigns unclassified species to virtual nodes on the phylogenetic tree based on higher-level taxonomy, minimizing interferences from unclassified species. Phylo-Spec also captures the feature importance via an information gain-based mechanism through the phylogenetic structure propagation, enhancing the interpretability of classification decisions. Phylo-Spec demonstrated superior efficacy in microbiome status classification across two in silico synthetic data sets that simulate the aforementioned cases, outperforming existing ML and DL methods. Validation with real-world metagenomic and amplicon data further confirmed the model's performance in multiple status classification, establishing a powerful framework for microbiome-based health state identification and microbe-disease association. The source code is available at https://github.com/qdu-bioinfo/Phylo-Spec.IMPORTANCEThe human microbiome profoundly influences health and disease, but current computational tools often overlook the evolutionary relationships among microbes, leading to incomplete or inaccurate interpretations of complex microbial data. Phylo-Spec provides a new way to understand the microbiome by combining microbial abundance, taxonomy, and phylogeny within a unified deep learning framework. This model not only improves the accuracy of health status classification but also highlights key microbial contributors linked to disease. By capturing both microbial diversity and evolutionary context, Phylo-Spec bridges the gap between bioinformatics and biological insight, offering a powerful and interpretable approach for advancing microbiome-based diagnostics and precision medicine.},
}
RevDate: 2025-11-24
CmpDate: 2025-11-24
The Impact of Serum on a Complex Synthetic Community Model of the Subgingival Microbiome.
bioRxiv : the preprint server for biology pii:2025.10.07.681017.
Despite rapid advances in characterizing the human microbiome, the ecological pressures shaping its transitions from healthy to diseased states remain poorly resolved. This is particularly true for periodontitis, a slow-progressing chronic inflammatory disease associated with well-defined shifts in the subgingival microbiome. Here, we report the development of a complex synthetic community model of the subgingival microbiome, designed for systematic interrogation of ecological factors that drive community restructuring. The model includes 22 prevalent and abundant subgingival species maintained in mucin-rich medium under microaerophilic, continuous culture conditions, in a chemostat. Using this system, we interrogated the impact of serum, as a surrogate for the inflammatory exudate, on community structure and function. Through integrated 16S rRNA gene sequencing, metatranscriptomics, and metabolomics, we found that serum was not required for a community with a periodontitis-like configuration to establish, but its presence intensified features of dysbiosis. Serum increased total biomass, promoted polymicrobial aggregate formation, promoted nitrogen and protein metabolism thereby modifying the environmental pH towards alkalinity, and introduced nitrosative stress. Serum also modified the community metatranscriptome in ways that paralleled microbiome activities in human periodontitis. Serum, however, decreased community diversity by disproportionally conferring a competitive advantage to the pathogen Porphyromonas gingivalis . This synthetic community model has revealed serum as a key nutritional pressure that modulates subgingival microbiome ecology and may perpetuate dysbiosis.
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@article {pmid41279900,
year = {2025},
author = {Li, L and Smardz, M and Soh, D and Marsh, PD and Hoare, A and Diaz, PI},
title = {The Impact of Serum on a Complex Synthetic Community Model of the Subgingival Microbiome.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.10.07.681017},
pmid = {41279900},
issn = {2692-8205},
abstract = {Despite rapid advances in characterizing the human microbiome, the ecological pressures shaping its transitions from healthy to diseased states remain poorly resolved. This is particularly true for periodontitis, a slow-progressing chronic inflammatory disease associated with well-defined shifts in the subgingival microbiome. Here, we report the development of a complex synthetic community model of the subgingival microbiome, designed for systematic interrogation of ecological factors that drive community restructuring. The model includes 22 prevalent and abundant subgingival species maintained in mucin-rich medium under microaerophilic, continuous culture conditions, in a chemostat. Using this system, we interrogated the impact of serum, as a surrogate for the inflammatory exudate, on community structure and function. Through integrated 16S rRNA gene sequencing, metatranscriptomics, and metabolomics, we found that serum was not required for a community with a periodontitis-like configuration to establish, but its presence intensified features of dysbiosis. Serum increased total biomass, promoted polymicrobial aggregate formation, promoted nitrogen and protein metabolism thereby modifying the environmental pH towards alkalinity, and introduced nitrosative stress. Serum also modified the community metatranscriptome in ways that paralleled microbiome activities in human periodontitis. Serum, however, decreased community diversity by disproportionally conferring a competitive advantage to the pathogen Porphyromonas gingivalis . This synthetic community model has revealed serum as a key nutritional pressure that modulates subgingival microbiome ecology and may perpetuate dysbiosis.},
}
RevDate: 2025-11-22
MiMeDB 2.0: the Human Microbial Metabolome Database for 2026.
Nucleic acids research pii:8340166 [Epub ahead of print].
The Microbial Metabolome Database (MiMeDB) (https://mimedb.org) is a comprehensive, freely accessible resource linking human-associated microbes to the metabolites they produce, along with their connections to human health, disease, and diet. Since the release of MiMeDB 1.0 in 2023, the database has been substantially expanded and redesigned. Major updates include the systematic addition of millions of newly annotated genes and pathways, thousands of new metabolites, significantly expanded pathway and reaction coverage, along with broader representation of eukaryotic gut microbes. MiMeDB 2.0 now contains >12.9 million annotated microbial genes, over 23.1 million microbial pathways, 29 295 metabolites, 21 829 metabolic reactions, 3725 microbial species and strains, and 514 076 new experimental and predicted nuclear magnetic resonance and mass spectrometry spectra of microbial metabolites. New features, such as detailed microbial descriptions, metabolite origin tags, refined search filters, and species-specific reaction queries, have been added to enhance usability. Likewise, redesigned network and genome viewers have been implemented to support more comprehensive, intuitive, and integrated visualization of complex, multi-omic relationships. The significant addition of more metabolite spectral data and improved spectral search capabilities further strengthen metabolite identification and discovery. Together, these improvements make MiMeDB 2.0 one of the most comprehensive and user-friendly platforms for investigating the human microbiome at a molecular level and exploring the roles of microbes and microbial metabolites in human health, diet, and disease.
Additional Links: PMID-41273085
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@article {pmid41273085,
year = {2025},
author = {Kruger, R and Oler, E and Saha, S and Poelzer, J and Han, S and Punsalan, MP and Green, B and Bushra, F and Kyes, M and Disu, F and Wakoli, J and Woudstra, R and Tejol, E and Fakutan, O and Wang, F and Lee, BL and Sajed, T and Tian, S and Torres-Calzada, C and Berjanskii, M and MacKay, S and Karu, N and Kadurrah-Daouk, R and Wishart, DS},
title = {MiMeDB 2.0: the Human Microbial Metabolome Database for 2026.},
journal = {Nucleic acids research},
volume = {},
number = {},
pages = {},
doi = {10.1093/nar/gkaf1272},
pmid = {41273085},
issn = {1362-4962},
support = {//NIH/ ; AG063744/AG/NIA NIH HHS/United States/AG/NIA NIH HHS/United States ; CFI MSIF 42495//Canada Foundation for Innovation/ ; CRC TIER1 100628//Canada Research Chairs/ ; //Genome Alberta, a division of Genome Canada/ ; ALLRP 597259-24//Natural Sciences and Engineering Research Council of Canada/ ; UBC F23-05862 WFF//Weston Family Foundation/ ; 2007-2024-1003//Social Sciences and Humanities Research Council of Canada/ ; //Genome Alberta/ ; },
abstract = {The Microbial Metabolome Database (MiMeDB) (https://mimedb.org) is a comprehensive, freely accessible resource linking human-associated microbes to the metabolites they produce, along with their connections to human health, disease, and diet. Since the release of MiMeDB 1.0 in 2023, the database has been substantially expanded and redesigned. Major updates include the systematic addition of millions of newly annotated genes and pathways, thousands of new metabolites, significantly expanded pathway and reaction coverage, along with broader representation of eukaryotic gut microbes. MiMeDB 2.0 now contains >12.9 million annotated microbial genes, over 23.1 million microbial pathways, 29 295 metabolites, 21 829 metabolic reactions, 3725 microbial species and strains, and 514 076 new experimental and predicted nuclear magnetic resonance and mass spectrometry spectra of microbial metabolites. New features, such as detailed microbial descriptions, metabolite origin tags, refined search filters, and species-specific reaction queries, have been added to enhance usability. Likewise, redesigned network and genome viewers have been implemented to support more comprehensive, intuitive, and integrated visualization of complex, multi-omic relationships. The significant addition of more metabolite spectral data and improved spectral search capabilities further strengthen metabolite identification and discovery. Together, these improvements make MiMeDB 2.0 one of the most comprehensive and user-friendly platforms for investigating the human microbiome at a molecular level and exploring the roles of microbes and microbial metabolites in human health, diet, and disease.},
}
RevDate: 2025-11-21
Microbiota Metabolism and Immune Regulation: From Mechanisms to Immunotherapeutic Applications in Cancer.
Seminars in cancer biology pii:S1044-579X(25)00160-9 [Epub ahead of print].
The human microbiome plays a pivotal role in shaping immune responses by producing bioactive metabolites such as bile acids (BAs) and short-chain fatty acids (SCFAs). These microbial metabolites influence a broad range of cell types, including innate and adaptive immune cells and non-immune cells. Emerging evidence suggests that microbiome metabolism is a crucial factor affecting the success of cancer immunotherapy. Promising therapeutic approaches, such as the use of probiotics, engineered bacteria, metabolite supplementation, and bile acid sequestrants, are being explored to enhance immunotherapeutic outcomes. This review critically evaluates current insights into how microbiome-derived metabolites modulate cellular functions, with a particular focus on immune cells within the tumor microenvironment, and highlights their potential to improve the efficacy of cancer immunotherapy.
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@article {pmid41270950,
year = {2025},
author = {Yuan, S and Bremmer, A and Yang, X and Hu, Q},
title = {Microbiota Metabolism and Immune Regulation: From Mechanisms to Immunotherapeutic Applications in Cancer.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.11.023},
pmid = {41270950},
issn = {1096-3650},
abstract = {The human microbiome plays a pivotal role in shaping immune responses by producing bioactive metabolites such as bile acids (BAs) and short-chain fatty acids (SCFAs). These microbial metabolites influence a broad range of cell types, including innate and adaptive immune cells and non-immune cells. Emerging evidence suggests that microbiome metabolism is a crucial factor affecting the success of cancer immunotherapy. Promising therapeutic approaches, such as the use of probiotics, engineered bacteria, metabolite supplementation, and bile acid sequestrants, are being explored to enhance immunotherapeutic outcomes. This review critically evaluates current insights into how microbiome-derived metabolites modulate cellular functions, with a particular focus on immune cells within the tumor microenvironment, and highlights their potential to improve the efficacy of cancer immunotherapy.},
}
RevDate: 2025-11-21
Environmental exposure augments the abundance and transferability of antibiotic resistance genes in the respiratory tract.
Cell reports pii:S2211-1247(25)01288-4 [Epub ahead of print].
Exposure to environmental pollutants has been linked to increased antibiotic resistance, a critical global health challenge. The respiratory microbiome constitutes a key reservoir of antibiotic resistance genes (ARGs). Here, we constructed a respiratory ARG catalog from sputum metagenomes of 1,128 individuals. We demonstrate that exposures, particularly to cigarette smoke and biofuels, are associated with increased abundance and enhanced mobility of respiratory ARGs. These resistome alterations correlate inversely with lung function, with elevated mobile ARG abundance detectable even in individuals with mild airflow limitation within normal spirometry. Specific ARGs, including opmD and tet(K), interact with smoking in relation to lung function impairment. Murine experiments recapitulate these findings, showing exposure-induced increases in homologous ARGs that confer heightened phenotypic resistance in cultured respiratory bacteria. Our results elucidate a pathway through which environmental pollutants augment the respiratory resistome, suggesting the need for actions to mitigate the antimicrobial resistance burden by addressing environmental pollution.
Additional Links: PMID-41270740
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@article {pmid41270740,
year = {2025},
author = {Yi, X and Cai, H and Liu, H and Xu, S and Meng, R and Rao, J and Wu, M and Yang, L and Shi, Y and Zhang, J and Zhu, T and Yang, Y and Wen, P and Qin, Y and Song, W and Li, JT and Shu, W and Dai, J and Sun, J and Lin, L and Guan, WJ and Brightling, CE and Zheng, XY and Wang, Z},
title = {Environmental exposure augments the abundance and transferability of antibiotic resistance genes in the respiratory tract.},
journal = {Cell reports},
volume = {},
number = {},
pages = {116517},
doi = {10.1016/j.celrep.2025.116517},
pmid = {41270740},
issn = {2211-1247},
abstract = {Exposure to environmental pollutants has been linked to increased antibiotic resistance, a critical global health challenge. The respiratory microbiome constitutes a key reservoir of antibiotic resistance genes (ARGs). Here, we constructed a respiratory ARG catalog from sputum metagenomes of 1,128 individuals. We demonstrate that exposures, particularly to cigarette smoke and biofuels, are associated with increased abundance and enhanced mobility of respiratory ARGs. These resistome alterations correlate inversely with lung function, with elevated mobile ARG abundance detectable even in individuals with mild airflow limitation within normal spirometry. Specific ARGs, including opmD and tet(K), interact with smoking in relation to lung function impairment. Murine experiments recapitulate these findings, showing exposure-induced increases in homologous ARGs that confer heightened phenotypic resistance in cultured respiratory bacteria. Our results elucidate a pathway through which environmental pollutants augment the respiratory resistome, suggesting the need for actions to mitigate the antimicrobial resistance burden by addressing environmental pollution.},
}
RevDate: 2025-11-20
Calculating fast differential genome coverages among metagenomic sources using micov.
Communications biology, 8(1):1624.
Breadth of coverage, the proportion of a reference genome covered by at least one sequencing read, is critical for interpreting metagenomic data, informing analyses from genome assembly to taxonomic profiling. However, existing tools typically summarize coverage breadth at the whole-genome or aggregate-sample level, missing informative variation along genomes and between sample groups. Here we introduce MIcrobiome COVerage (micov), a tool that computes and compares per-sample breadth of coverage across many genomes and samples. micov offers two key advances: (1) rapid cumulative coverage breadth calculations specific to each sample type, and (2) detection of differential coverage breadth along genomes. Applying micov to three metagenomic datasets, we show that it identifies a genomic region in Prevotella copri that explains variation in community composition independent of host country of origin, uncovers dietary association with a partially annotated region in an uncharacterized Lachnospiraceae genome, enabling hypothesis generation for genes of unknown function, and improves sensitivity in low-biomass settings by detecting a single genomic copy of enteropathogenic Escherichia coli (EPEC) in wastewater and distinguishing Mediterraneibacter gnavus across specimen types.
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@article {pmid41266796,
year = {2025},
author = {Weng, Y and Guccione, C and McDonald, D and Oles, R and Devkota, S and Kopylova, E and Sepich-Poore, GD and Salido, RA and Din, MO and Song, SJ and Curtius, K and Chu, H and Bartko, A and Hasty, J and Knight, R},
title = {Calculating fast differential genome coverages among metagenomic sources using micov.},
journal = {Communications biology},
volume = {8},
number = {1},
pages = {1624},
pmid = {41266796},
issn = {2399-3642},
abstract = {Breadth of coverage, the proportion of a reference genome covered by at least one sequencing read, is critical for interpreting metagenomic data, informing analyses from genome assembly to taxonomic profiling. However, existing tools typically summarize coverage breadth at the whole-genome or aggregate-sample level, missing informative variation along genomes and between sample groups. Here we introduce MIcrobiome COVerage (micov), a tool that computes and compares per-sample breadth of coverage across many genomes and samples. micov offers two key advances: (1) rapid cumulative coverage breadth calculations specific to each sample type, and (2) detection of differential coverage breadth along genomes. Applying micov to three metagenomic datasets, we show that it identifies a genomic region in Prevotella copri that explains variation in community composition independent of host country of origin, uncovers dietary association with a partially annotated region in an uncharacterized Lachnospiraceae genome, enabling hypothesis generation for genes of unknown function, and improves sensitivity in low-biomass settings by detecting a single genomic copy of enteropathogenic Escherichia coli (EPEC) in wastewater and distinguishing Mediterraneibacter gnavus across specimen types.},
}
RevDate: 2025-11-18
The role of the human microbiome in prostate cancer: a systematic review from diagnosis to treatment.
Prostate cancer and prostatic diseases [Epub ahead of print].
BACKGROUND: Prostate cancer (PC) heterogeneity and treatment resistance remain major clinical challenges, with emerging evidence implicating the microbiome as a key modulator of disease pathogenesis. While microbial dysbiosis has been linked to PC diagnosis, progression, and therapeutic outcomes, the mechanisms underlying these associations are poorly understood. This review synthesizes current evidence on the diagnostic, prognostic, and therapeutic potential of the microbiome in PC.
METHODS: A systematic search of PubMed, Embase, and Cochrane Central Register of Controlled Trials (through April 2024) was conducted following PRISMA guidelines (PROSPERO: CRD42024534899). Controlled and observational studies investigating microbial roles in PC diagnosis (e.g., ISUP grading group), prognosis, or treatment response were included. Data extraction and quality assessment used the QUIPS tool. From 810 screened records, 42 studies met inclusion criteria.
RESULTS: Distinct microbial profiles differentiated PC from controls, with Mycoplasma genitalium and Staphylococcus spp. enriched in prostate tumors (3.1- and 2.7-fold, respectively) and correlated with inflammation (IL-6: r = 0.38, p = 0.002). Urinary microbiota showed diagnostic potential (sensitivity: 58-82%), though sampling methods influenced variability. Prognostically, Betaproteobacteria gut enrichment predicted earlier castration-resistant progression (5.2 months; HR 1.8, 95% CI 1.3-2.5), while ADT-induced dysbiosis (e.g., Klebsiella overgrowth) accelerated resistance (2.1-fold risk). Therapies altered microbial ecology: radiotherapy depleted Bacteroides (linked to proctitis; OR 3.1), and immunotherapy responders harbored higher Akkermansia muciniphila. Microbial androgen synthesis and endotoxin production emerged as resistance mechanisms.
CONCLUSIONS: The microbiome influences PC detection, aggressiveness, and treatment efficacy through direct (tissue-resident) and indirect (gut-derived) mechanisms. Standardized profiling and microbiome-modulating strategies (e.g., probiotics during ADT) may personalize management. Prospective trials are needed to validate causality and translate microbial biomarkers into clinical practice.
Additional Links: PMID-41254344
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@article {pmid41254344,
year = {2025},
author = {Distante, A and Garino, D and Cerrato, C and Perez-Ardavin, J and Flores, FQ and Lopetuso, L and Mir, MC},
title = {The role of the human microbiome in prostate cancer: a systematic review from diagnosis to treatment.},
journal = {Prostate cancer and prostatic diseases},
volume = {},
number = {},
pages = {},
pmid = {41254344},
issn = {1476-5608},
abstract = {BACKGROUND: Prostate cancer (PC) heterogeneity and treatment resistance remain major clinical challenges, with emerging evidence implicating the microbiome as a key modulator of disease pathogenesis. While microbial dysbiosis has been linked to PC diagnosis, progression, and therapeutic outcomes, the mechanisms underlying these associations are poorly understood. This review synthesizes current evidence on the diagnostic, prognostic, and therapeutic potential of the microbiome in PC.
METHODS: A systematic search of PubMed, Embase, and Cochrane Central Register of Controlled Trials (through April 2024) was conducted following PRISMA guidelines (PROSPERO: CRD42024534899). Controlled and observational studies investigating microbial roles in PC diagnosis (e.g., ISUP grading group), prognosis, or treatment response were included. Data extraction and quality assessment used the QUIPS tool. From 810 screened records, 42 studies met inclusion criteria.
RESULTS: Distinct microbial profiles differentiated PC from controls, with Mycoplasma genitalium and Staphylococcus spp. enriched in prostate tumors (3.1- and 2.7-fold, respectively) and correlated with inflammation (IL-6: r = 0.38, p = 0.002). Urinary microbiota showed diagnostic potential (sensitivity: 58-82%), though sampling methods influenced variability. Prognostically, Betaproteobacteria gut enrichment predicted earlier castration-resistant progression (5.2 months; HR 1.8, 95% CI 1.3-2.5), while ADT-induced dysbiosis (e.g., Klebsiella overgrowth) accelerated resistance (2.1-fold risk). Therapies altered microbial ecology: radiotherapy depleted Bacteroides (linked to proctitis; OR 3.1), and immunotherapy responders harbored higher Akkermansia muciniphila. Microbial androgen synthesis and endotoxin production emerged as resistance mechanisms.
CONCLUSIONS: The microbiome influences PC detection, aggressiveness, and treatment efficacy through direct (tissue-resident) and indirect (gut-derived) mechanisms. Standardized profiling and microbiome-modulating strategies (e.g., probiotics during ADT) may personalize management. Prospective trials are needed to validate causality and translate microbial biomarkers into clinical practice.},
}
RevDate: 2025-11-17
MNetClass: a control-free microbial network clustering framework for identifying central subcommunities across ecological niches.
mSystems [Epub ahead of print].
Investigating microbiome subnetworks and identifying central microbes in specific ecological niches is a critical issue in human microbiome studies. Traditional methods typically require control samples, limiting the ability to study microbiomes at distinct body sites without matched controls. Moreover, some clustering methods are not well-suited for microbial data and fail to identify central subcommunities across ecological niches after clustering. In this study, we present MNetClass, a novel microbial network clustering analysis framework. It utilizes a random walk algorithm and a rank-sum ratio-entropy weight evaluation model to classify key subnetworks and identify central microbes at any body site, without the need for control samples. We demonstrate its capabilities on both simulated and real microbiome data sets. Simulation results indicate that MNetClass outperforms current unsupervised microbial clustering methods. In applied case studies, the analysis of microbiome data from five distinct oral sites revealed site-specific microbial communities. Furthermore, MNetClass demonstrated superior predictive performance on cross-cohort Autism Spectrum Disorder data and identified age-related microbial communities across different oral sites, underscoring its broad applicability in microbiome research.IMPORTANCEMNetClass provides a valuable tool for microbiome network analysis, enabling the identification of key microbial subcommunities across diverse ecological niches. Implemented as an R package (https://github.com/YihuaWWW/MNetClass), it offers broad accessibility for researchers. Here, we systematically benchmarked MNetClass against existing microbial clustering methods on synthetic data using various performance metrics, demonstrating its superior efficacy. Notably, MNetClass operates without the need for control groups and effectively identifies central microbes, highlighting its potential as a robust framework for advancing microbiome research.
Additional Links: PMID-41247142
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@article {pmid41247142,
year = {2025},
author = {Wang, Y and Hou, Q and Wei, F and Liu, B and Feng, Q},
title = {MNetClass: a control-free microbial network clustering framework for identifying central subcommunities across ecological niches.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0098925},
doi = {10.1128/msystems.00989-25},
pmid = {41247142},
issn = {2379-5077},
abstract = {Investigating microbiome subnetworks and identifying central microbes in specific ecological niches is a critical issue in human microbiome studies. Traditional methods typically require control samples, limiting the ability to study microbiomes at distinct body sites without matched controls. Moreover, some clustering methods are not well-suited for microbial data and fail to identify central subcommunities across ecological niches after clustering. In this study, we present MNetClass, a novel microbial network clustering analysis framework. It utilizes a random walk algorithm and a rank-sum ratio-entropy weight evaluation model to classify key subnetworks and identify central microbes at any body site, without the need for control samples. We demonstrate its capabilities on both simulated and real microbiome data sets. Simulation results indicate that MNetClass outperforms current unsupervised microbial clustering methods. In applied case studies, the analysis of microbiome data from five distinct oral sites revealed site-specific microbial communities. Furthermore, MNetClass demonstrated superior predictive performance on cross-cohort Autism Spectrum Disorder data and identified age-related microbial communities across different oral sites, underscoring its broad applicability in microbiome research.IMPORTANCEMNetClass provides a valuable tool for microbiome network analysis, enabling the identification of key microbial subcommunities across diverse ecological niches. Implemented as an R package (https://github.com/YihuaWWW/MNetClass), it offers broad accessibility for researchers. Here, we systematically benchmarked MNetClass against existing microbial clustering methods on synthetic data using various performance metrics, demonstrating its superior efficacy. Notably, MNetClass operates without the need for control groups and effectively identifies central microbes, highlighting its potential as a robust framework for advancing microbiome research.},
}
RevDate: 2025-11-17
CmpDate: 2025-11-17
Benchmarking single cell transcriptome matching methods for incremental growth of reference atlases.
bioRxiv : the preprint server for biology.
BACKGROUND: The advancement of single cell technologies has driven significant progress in constructing a multiscale, pan-organ Human Reference Atlas (HRA) for healthy human cells, though challenges remain in harmonizing cell types and unifying nomenclature. Multiple machine learning and artificial intelligence methods, including pre-trained and fine-tuned models on large-scale atlas data, are publicly available for the single cell community users to computationally annotate and match their cell clusters to the reference atlas.
RESULTS: This study benchmarks four computational tools for cell type annotation and matching - Azimuth, CellTypist, scArches, and FR-Match - using two lung atlas datasets, the Human Lung Cell Atlas (HLCA) and the LungMAP single-cell reference (CellRef). Despite achieving high overall performance while comparing algorithmic cell type annotations to expert annotated data, variations in accuracy were observed, especially in annotating rare cell types, underlining the need for improved consistency across cell type prediction methods. The benchmarked methods were used to cross-compare and incrementally integrate 61 cell types from HLCA and 48 cell types from CellRef, resulting in a meta-atlas of 41 matched cell types, 20 HLCA-specific cell types, and 7 CellRef-specific cell types.
CONCLUSION: This study reveals complementing strengths of the benchmarked methods and presents a framework for incremental growth of the cell type inventory in the reference atlases, leading to 68 unique cell types in the meta-atlas across CellRef and HLCA. The benchmarking analysis contributes to improving the coverage and quality of HRA construction by assessing the reliability and performance of cell type annotation approaches for single cell transcriptomics datasets.
Additional Links: PMID-40568082
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@article {pmid40568082,
year = {2025},
author = {Hu, J and Peng, B and Pankajam, AV and Xu, B and Deshpande, VA and Bueckle, A and Herr, BW and Börner, K and Dupont, C and Scheuermann, RH and Zhang, Y},
title = {Benchmarking single cell transcriptome matching methods for incremental growth of reference atlases.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {40568082},
issn = {2692-8205},
support = {OT2 OD026671/OD/NIH HHS/United States ; OT2 OD033756/OD/NIH HHS/United States ; R03 OD036499/OD/NIH HHS/United States ; },
abstract = {BACKGROUND: The advancement of single cell technologies has driven significant progress in constructing a multiscale, pan-organ Human Reference Atlas (HRA) for healthy human cells, though challenges remain in harmonizing cell types and unifying nomenclature. Multiple machine learning and artificial intelligence methods, including pre-trained and fine-tuned models on large-scale atlas data, are publicly available for the single cell community users to computationally annotate and match their cell clusters to the reference atlas.
RESULTS: This study benchmarks four computational tools for cell type annotation and matching - Azimuth, CellTypist, scArches, and FR-Match - using two lung atlas datasets, the Human Lung Cell Atlas (HLCA) and the LungMAP single-cell reference (CellRef). Despite achieving high overall performance while comparing algorithmic cell type annotations to expert annotated data, variations in accuracy were observed, especially in annotating rare cell types, underlining the need for improved consistency across cell type prediction methods. The benchmarked methods were used to cross-compare and incrementally integrate 61 cell types from HLCA and 48 cell types from CellRef, resulting in a meta-atlas of 41 matched cell types, 20 HLCA-specific cell types, and 7 CellRef-specific cell types.
CONCLUSION: This study reveals complementing strengths of the benchmarked methods and presents a framework for incremental growth of the cell type inventory in the reference atlases, leading to 68 unique cell types in the meta-atlas across CellRef and HLCA. The benchmarking analysis contributes to improving the coverage and quality of HRA construction by assessing the reliability and performance of cell type annotation approaches for single cell transcriptomics datasets.},
}
RevDate: 2025-11-13
CmpDate: 2025-11-14
The silent microbial shift: climate change amplifies pathogen evolution, microbiome dysbiosis, and antimicrobial resistance.
Tropical diseases, travel medicine and vaccines, 11(1):43.
Climate change is a primary driver of new infectious diseases. It affects pathogen evolution, vector ecology, and human susceptibility. Rising temperatures, changed rainfall patterns, and extreme weather events contributed to the spread of vector-borne, food-borne, and water-borne diseases. Furthermore, climate stressors promote antimicrobial resistance (AMR) and disrupt the human microbiome. This increases susceptibility to infections and chronic diseases. This review explores the complex relationships between climate change, microbial ecosystems, and public health focusing on how microbial dysbiosis and environmental changes interact to influence disease dynamics. We also highlight long-term solutions, such as One Health approaches, probiotics, and AI-powered early warning systems, as strategies for reducing future risks. Addressing these challenges requires global collaboration, climate-resilient health systems, and proactive actions to mitigate the health consequences of a rapidly changing environment.
Additional Links: PMID-41233921
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@article {pmid41233921,
year = {2025},
author = {Naga, NG and Taha, RM and Hamed, EA and Nawar, EA and Jaheen, HO and Mobarak, AA and Radwan, YM and Faramawy, AG and Arayes, MA},
title = {The silent microbial shift: climate change amplifies pathogen evolution, microbiome dysbiosis, and antimicrobial resistance.},
journal = {Tropical diseases, travel medicine and vaccines},
volume = {11},
number = {1},
pages = {43},
pmid = {41233921},
issn = {2055-0936},
abstract = {Climate change is a primary driver of new infectious diseases. It affects pathogen evolution, vector ecology, and human susceptibility. Rising temperatures, changed rainfall patterns, and extreme weather events contributed to the spread of vector-borne, food-borne, and water-borne diseases. Furthermore, climate stressors promote antimicrobial resistance (AMR) and disrupt the human microbiome. This increases susceptibility to infections and chronic diseases. This review explores the complex relationships between climate change, microbial ecosystems, and public health focusing on how microbial dysbiosis and environmental changes interact to influence disease dynamics. We also highlight long-term solutions, such as One Health approaches, probiotics, and AI-powered early warning systems, as strategies for reducing future risks. Addressing these challenges requires global collaboration, climate-resilient health systems, and proactive actions to mitigate the health consequences of a rapidly changing environment.},
}
RevDate: 2025-11-14
From microbiome to metabolism: Bridging a two-decade translational gap.
Cell metabolism pii:S1550-4131(25)00445-0 [Epub ahead of print].
The mapping of the human genome sparked high expectations for biomedical breakthroughs, yet attention has since shifted toward the human microbiome as a key player in health and disease. Pioneering studies revealed striking inter-individual variability and numerous associations between gut microbiota and a wide range of conditions (i.e., obesity, diabetes, cardiovascular and inflammatory bowel diseases, autism, allergies, neurodegenerative diseases, and cancers). However, the field has faced a deluge of correlative "dysbiosis" studies with limited causal evidence. Although animal models have provided crucial mechanistic insights, translating these findings to humans has proven challenging. Interventions such as fecal microbiota transplantation, prebiotics, probiotics, and postbiotics often yield inconsistent or modest effects in clinical trials. This gap highlights the need for precision, functional profiling, and integration of multi-omics , for instance, through artificial intelligence. In this perspective, we discuss what microbiome research offers as a transformative shift and how we conceptualize disease, favoring systems biology and personalized interventions over reductionist approaches.
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@article {pmid41237775,
year = {2025},
author = {Van Hul, M and Cani, PD},
title = {From microbiome to metabolism: Bridging a two-decade translational gap.},
journal = {Cell metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmet.2025.10.011},
pmid = {41237775},
issn = {1932-7420},
abstract = {The mapping of the human genome sparked high expectations for biomedical breakthroughs, yet attention has since shifted toward the human microbiome as a key player in health and disease. Pioneering studies revealed striking inter-individual variability and numerous associations between gut microbiota and a wide range of conditions (i.e., obesity, diabetes, cardiovascular and inflammatory bowel diseases, autism, allergies, neurodegenerative diseases, and cancers). However, the field has faced a deluge of correlative "dysbiosis" studies with limited causal evidence. Although animal models have provided crucial mechanistic insights, translating these findings to humans has proven challenging. Interventions such as fecal microbiota transplantation, prebiotics, probiotics, and postbiotics often yield inconsistent or modest effects in clinical trials. This gap highlights the need for precision, functional profiling, and integration of multi-omics , for instance, through artificial intelligence. In this perspective, we discuss what microbiome research offers as a transformative shift and how we conceptualize disease, favoring systems biology and personalized interventions over reductionist approaches.},
}
RevDate: 2025-11-14
Serum metabolites link immune-microbiota interaction in children and young adults from Russian Karelia and Finnish Karelia with contrasting lifestyle and environment.
Environment international, 205:109911 pii:S0160-4120(25)00662-2 [Epub ahead of print].
BACKGROUND: Environmental exposureregulates the immune, circulatory, and nervous systems, thereby affecting health. We investigated the associations between serum metabolite profiles, skin microbiota, and immune-related gene expression of peripheral blood mononuclear cells in children and young adults from Russian Karelia (RUS) and Finnish Karelia (FIN), two regions with contrasting environmental exposures and lifestyles.
METHODS: Serum metabolites (n = 278) from 15 to 20-year-old participants from RUS (n = 162) and FIN (n = 116) were profiled. Using integrative analysis, a subset of metabolomics was combined with skin microbiota (n = 143) and blood transcriptomics (n = 144) to characterize environment-linked metabolic and immune signatures.
RESULTS: Serum metabolite profiles differed significantly between the RUS and FIN subjects, reflecting divergent metabolic states. Citrulline and glutamate/glutamine metabolism were prominent in the RUS subjects while tryptophan catabolism was enhanced in the FIN subjects. Transcriptomic network analysis identified co-expression modules associated with metabolites, skin microbial taxa and key immune traits. A strongly RUS-associated module was dominated by epigenetic long non-coding RNAs and associated positively with anti-inflammatory metabolites such as circulating short-chain fatty acids (SCFAs) and betaine - both present at reduced levels in the FIN subjects. In contrast, FIN-associated modules were linked to inflammatory metabolites such as xanthurenic acid and L-cystine, as well as gene pathways involved in interferon (anti-viral) signaling and neutrophil responses. Across all omics layers, RUS subjects exhibited a more tightly integrated molecular network, with stronger correlations between circulating metabolites, microbial taxa and immune-related gene regulation.
CONCLUSIONS: Multi-omics integration revealed a more coordinated and responsive immune-metabolic network in RUS youth, potentially shaped by environmental exposures typical of their living context. In contrast, the FIN cohort exhibited metabolic patterns more closely linked to inflammatory gene expression.
Additional Links: PMID-41237539
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@article {pmid41237539,
year = {2025},
author = {Karisola, P and Sinkko, H and Nieminen, A and Laatikainen, T and Yang, Y and Paalanen, L and Jousilahti, P and Vartiainen, E and Mäkelä, MJ and Fyhrquist, N and Haahtela, T and Alenius, H},
title = {Serum metabolites link immune-microbiota interaction in children and young adults from Russian Karelia and Finnish Karelia with contrasting lifestyle and environment.},
journal = {Environment international},
volume = {205},
number = {},
pages = {109911},
doi = {10.1016/j.envint.2025.109911},
pmid = {41237539},
issn = {1873-6750},
abstract = {BACKGROUND: Environmental exposureregulates the immune, circulatory, and nervous systems, thereby affecting health. We investigated the associations between serum metabolite profiles, skin microbiota, and immune-related gene expression of peripheral blood mononuclear cells in children and young adults from Russian Karelia (RUS) and Finnish Karelia (FIN), two regions with contrasting environmental exposures and lifestyles.
METHODS: Serum metabolites (n = 278) from 15 to 20-year-old participants from RUS (n = 162) and FIN (n = 116) were profiled. Using integrative analysis, a subset of metabolomics was combined with skin microbiota (n = 143) and blood transcriptomics (n = 144) to characterize environment-linked metabolic and immune signatures.
RESULTS: Serum metabolite profiles differed significantly between the RUS and FIN subjects, reflecting divergent metabolic states. Citrulline and glutamate/glutamine metabolism were prominent in the RUS subjects while tryptophan catabolism was enhanced in the FIN subjects. Transcriptomic network analysis identified co-expression modules associated with metabolites, skin microbial taxa and key immune traits. A strongly RUS-associated module was dominated by epigenetic long non-coding RNAs and associated positively with anti-inflammatory metabolites such as circulating short-chain fatty acids (SCFAs) and betaine - both present at reduced levels in the FIN subjects. In contrast, FIN-associated modules were linked to inflammatory metabolites such as xanthurenic acid and L-cystine, as well as gene pathways involved in interferon (anti-viral) signaling and neutrophil responses. Across all omics layers, RUS subjects exhibited a more tightly integrated molecular network, with stronger correlations between circulating metabolites, microbial taxa and immune-related gene regulation.
CONCLUSIONS: Multi-omics integration revealed a more coordinated and responsive immune-metabolic network in RUS youth, potentially shaped by environmental exposures typical of their living context. In contrast, the FIN cohort exhibited metabolic patterns more closely linked to inflammatory gene expression.},
}
RevDate: 2025-11-14
Characterization of Gut Microbiota of Honey Bees in Korea.
Polish journal of microbiology pii:pjm-2025-025 [Epub ahead of print].
Korea's unique climate and agricultural environment suggest that the gut microbiome of honey bees may possess distinctive compositions influenced by regional factors. With the decline in honey bee populations and rising health challenges, understanding the role of gut microbiomes is essential for enhancing honey bee health and their resilience to environmental stressors. To explore caste-specific gut microbiota and identify microbial signatures associated with honey bee health, this study examined the gut microbial composition of worker bees, queen bees, and drones of Apis mellifera using 16S rRNA gene amplicon sequencing. Analysis of beta diversity and species richness demonstrated significant differences between worker bees and both drones and queens, with no significant differences identified between drones and queens. Notably, Lactobacillus dominated all groups, comprising 98.6% of the drones, 95.4% of the queens, and 68.3% of the workers. Additionally, Bombella was prominent in queens (4%), whereas Gilliamella (23%) and Frischella (4.7%) were notably enriched in workers. Drones and queens exhibited similar gut microbiome profiles, while workers displayed distinctly different compositions. These findings underscore the variation in gut microbiota composition and potential functional roles across honey bee castes. Such microbial distinctions may reflect caste-specific roles and physiological demands within the colony. Future research should investigate the physiological roles of gut microbiota and their contributions to environmental resilience, paving the way for microbiome-based strategies to promote honey bee health. This study lays a crucial scientific foundation for conserving the honey bee ecosystem and promoting sustainable agriculture.
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@article {pmid41236809,
year = {2025},
author = {Shuvo, MSH and Kim, S and Jo, S and Rahim, MA and Barman, I and Hossain, MS and Jeong, Y and Jeong, H and Kim, S and Seo, H and Song, HY},
title = {Characterization of Gut Microbiota of Honey Bees in Korea.},
journal = {Polish journal of microbiology},
volume = {},
number = {},
pages = {},
doi = {10.33073/pjm-2025-025},
pmid = {41236809},
issn = {2544-4646},
abstract = {Korea's unique climate and agricultural environment suggest that the gut microbiome of honey bees may possess distinctive compositions influenced by regional factors. With the decline in honey bee populations and rising health challenges, understanding the role of gut microbiomes is essential for enhancing honey bee health and their resilience to environmental stressors. To explore caste-specific gut microbiota and identify microbial signatures associated with honey bee health, this study examined the gut microbial composition of worker bees, queen bees, and drones of Apis mellifera using 16S rRNA gene amplicon sequencing. Analysis of beta diversity and species richness demonstrated significant differences between worker bees and both drones and queens, with no significant differences identified between drones and queens. Notably, Lactobacillus dominated all groups, comprising 98.6% of the drones, 95.4% of the queens, and 68.3% of the workers. Additionally, Bombella was prominent in queens (4%), whereas Gilliamella (23%) and Frischella (4.7%) were notably enriched in workers. Drones and queens exhibited similar gut microbiome profiles, while workers displayed distinctly different compositions. These findings underscore the variation in gut microbiota composition and potential functional roles across honey bee castes. Such microbial distinctions may reflect caste-specific roles and physiological demands within the colony. Future research should investigate the physiological roles of gut microbiota and their contributions to environmental resilience, paving the way for microbiome-based strategies to promote honey bee health. This study lays a crucial scientific foundation for conserving the honey bee ecosystem and promoting sustainable agriculture.},
}
RevDate: 2025-11-14
Impact of female sexual dysfunction on assisted reproductive technology outcome.
The journal of sexual medicine pii:8323203 [Epub ahead of print].
BACKGROUND: Despite its high prevalence in infertile women and known impact on natural conception, the specific influence of female sexual dysfunction (FSD) on assisted reproductive technology (ART) outcomes, which bypass intercourse, remains unclear.
AIM: To investigate the association between female sexual function and ART outcomes, including live birth.
METHODS: In this prospective cohort study, 300 women undergoing their first ART cycle completed the Female Sexual Function Index (FSFI) prior to treatment. Multivariable regression models were used to assess the association between FSFI measures (FSD status, total score, and domain scores) and ART outcomes, adjusting for key clinical confounders.
OUTCOMES: The primary outcome was live birth rate following in vitro fertilization or intracytoplasmic sperm injection treatment, with secondary outcomes including biochemical pregnancy, clinical pregnancy rate, ovarian response, and embryology parameters.
RESULTS: Participants with FSD (n = 200) exhibited significantly lower biochemical pregnancy rates (55.5% vs. 82%, P < .01), clinical pregnancy rates (51% vs. 78%, P < .01), and live birth rates (36.5% vs. 54%, P < .01) compared to those without (n = 100). After adjusting for confounders, female sexual function, as measured by FSFI, held independent predictive value for these critical pregnancy outcomes. Furthermore, when analyzed as a continuous variable, higher total FSFI scores positively correlated with indicators of improved parameters of embryo development and increased pregnancy success rates. Notably, all six FSFI domains also demonstrated significant positive associations with key ART outcomes. Compared to the standard 26.55 threshold, a data-driven FSFI threshold of 20.70 showed higher Youden index values for predicting ART outcomes.
CLINICAL IMPLICATIONS: Evaluating FSD should be considered part of routine infertility treatment, as addressing it may offer a novel strategy to improve ART outcomes.
STRENGTHS & LIMITATIONS: Key strengths are the prospective cohort design establishing temporality and use of a validated FSFI scale. However, as an observational study, it cannot establish causality; other limitations include the single-center design, potential unmeasured confounders, and the subjective nature of self-reported FSFI scores.
CONCLUSION: Lower female sexual function is significantly associated with poorer outcomes following ART, including substantially reduced live birth rates.
Additional Links: PMID-41236171
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@article {pmid41236171,
year = {2025},
author = {Shi, H and Li, L and Liu, Z and Zhao, X and Wang, Y and Yang, X and Chen, P},
title = {Impact of female sexual dysfunction on assisted reproductive technology outcome.},
journal = {The journal of sexual medicine},
volume = {},
number = {},
pages = {},
doi = {10.1093/jsxmed/qdaf317},
pmid = {41236171},
issn = {1743-6109},
support = {2023A1515012940//Natural Science Foundation of Guangdong Province/ ; 2023WST04//Sixth Affiliated Hospital of Sun Yat-sen University/ ; GZC20233216//Postdoctoral Fellowship Program of CPSF/ ; },
abstract = {BACKGROUND: Despite its high prevalence in infertile women and known impact on natural conception, the specific influence of female sexual dysfunction (FSD) on assisted reproductive technology (ART) outcomes, which bypass intercourse, remains unclear.
AIM: To investigate the association between female sexual function and ART outcomes, including live birth.
METHODS: In this prospective cohort study, 300 women undergoing their first ART cycle completed the Female Sexual Function Index (FSFI) prior to treatment. Multivariable regression models were used to assess the association between FSFI measures (FSD status, total score, and domain scores) and ART outcomes, adjusting for key clinical confounders.
OUTCOMES: The primary outcome was live birth rate following in vitro fertilization or intracytoplasmic sperm injection treatment, with secondary outcomes including biochemical pregnancy, clinical pregnancy rate, ovarian response, and embryology parameters.
RESULTS: Participants with FSD (n = 200) exhibited significantly lower biochemical pregnancy rates (55.5% vs. 82%, P < .01), clinical pregnancy rates (51% vs. 78%, P < .01), and live birth rates (36.5% vs. 54%, P < .01) compared to those without (n = 100). After adjusting for confounders, female sexual function, as measured by FSFI, held independent predictive value for these critical pregnancy outcomes. Furthermore, when analyzed as a continuous variable, higher total FSFI scores positively correlated with indicators of improved parameters of embryo development and increased pregnancy success rates. Notably, all six FSFI domains also demonstrated significant positive associations with key ART outcomes. Compared to the standard 26.55 threshold, a data-driven FSFI threshold of 20.70 showed higher Youden index values for predicting ART outcomes.
CLINICAL IMPLICATIONS: Evaluating FSD should be considered part of routine infertility treatment, as addressing it may offer a novel strategy to improve ART outcomes.
STRENGTHS & LIMITATIONS: Key strengths are the prospective cohort design establishing temporality and use of a validated FSFI scale. However, as an observational study, it cannot establish causality; other limitations include the single-center design, potential unmeasured confounders, and the subjective nature of self-reported FSFI scores.
CONCLUSION: Lower female sexual function is significantly associated with poorer outcomes following ART, including substantially reduced live birth rates.},
}
RevDate: 2025-11-13
Mutanobactin D from the Human Microbiome: Chemistry, Biology, and Molecular Dynamics Studies.
Journal of the American Chemical Society [Epub ahead of print].
Mutanobactin D is an interkingdom communicator derived from the human oral microbiome. The lipopeptide prevents yeast-to-hyphae morphogenesis in Candida albicans, notably without fungicidal or fungistatic activity. The mode of action and structure-activity relationship of mutanobactin D are unknown and prompt an interdisciplinary program of study. Stereoselective synthesis of designed mutanobactin D analogs reveals that the C26 configuration is crucial for bioactivity associated with inhibition of pathogenesis, or yeast-to-hyphae transition, in C. albicans. To shed light on this finding, we employ molecular dynamics (MD) simulations of mutanobactin D and selected analogs in increasingly complex environments: Monophasic (water or CHCl3), interfacial (water/CHCl3), and explicit lipid membrane (phosphatidylcholine) models. Monophasic MD simulations do not distinguish between bioactive and inactive compounds. In contrast, at a polar/apolar interphase, a dominant, stable conformation emerges for mutanobactin D and bioactive analogs. Explicit lipid membrane simulations reinforce these results and further reveal the formation of a continuous, structured water cushion, which is not found for inactive analogs. Our studies collectively reveal how the stereodefined attachment of the lipid in the C26-C28 motif governs activity against C. albicans and provide a framework for understanding the membrane behavior of mutanobactin D, which may be coupled to its role in the human oral microbiome. The approach described herein, consisting of synthesis and evaluation of designed analogs complemented by MD simulations, provides a blueprint for the study of bioactive natural products in various contexts, including the human microbiome.
Additional Links: PMID-41231122
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@article {pmid41231122,
year = {2025},
author = {Brandl, P and Lüthy, L and Pultar, F and Hansen, ME and Jelmini, N and Faris, J and Yasmin, SO and Kamenik, AS and Arnold, R and Ebert, MO and Wolfrum, S and Lokey, RS and Riniker, S and Carreira, EM},
title = {Mutanobactin D from the Human Microbiome: Chemistry, Biology, and Molecular Dynamics Studies.},
journal = {Journal of the American Chemical Society},
volume = {},
number = {},
pages = {},
doi = {10.1021/jacs.5c08850},
pmid = {41231122},
issn = {1520-5126},
abstract = {Mutanobactin D is an interkingdom communicator derived from the human oral microbiome. The lipopeptide prevents yeast-to-hyphae morphogenesis in Candida albicans, notably without fungicidal or fungistatic activity. The mode of action and structure-activity relationship of mutanobactin D are unknown and prompt an interdisciplinary program of study. Stereoselective synthesis of designed mutanobactin D analogs reveals that the C26 configuration is crucial for bioactivity associated with inhibition of pathogenesis, or yeast-to-hyphae transition, in C. albicans. To shed light on this finding, we employ molecular dynamics (MD) simulations of mutanobactin D and selected analogs in increasingly complex environments: Monophasic (water or CHCl3), interfacial (water/CHCl3), and explicit lipid membrane (phosphatidylcholine) models. Monophasic MD simulations do not distinguish between bioactive and inactive compounds. In contrast, at a polar/apolar interphase, a dominant, stable conformation emerges for mutanobactin D and bioactive analogs. Explicit lipid membrane simulations reinforce these results and further reveal the formation of a continuous, structured water cushion, which is not found for inactive analogs. Our studies collectively reveal how the stereodefined attachment of the lipid in the C26-C28 motif governs activity against C. albicans and provide a framework for understanding the membrane behavior of mutanobactin D, which may be coupled to its role in the human oral microbiome. The approach described herein, consisting of synthesis and evaluation of designed analogs complemented by MD simulations, provides a blueprint for the study of bioactive natural products in various contexts, including the human microbiome.},
}
RevDate: 2025-11-13
Succinate-driven virulence enhancement in hypervirulent Klebsiella pneumoniae via DcuSR two-component system.
Microbiology spectrum [Epub ahead of print].
UNLABELLED: Hypervirulent Klebsiella pneumoniae (hvKP) primarily colonizes the mammalian gastrointestinal tract, and it is prone to causing invasive infections under specific conditions. To establish infection, hvKP must compete with the resident gut microbiota for essential nutrients. This study focuses on the C4-dicarboxylate (C4-DC) succinate, which has been reported to accumulate in the gut under specific pathological conditions. We demonstrate that hvKP utilizes succinate as a signaling molecule to enhance virulence gene expression. Specifically, extracellular succinate activates type VI secretion system gene expression via the DcuSR two-component system (TCS), thereby increasing cytotoxicity toward intestinal epithelial cells and enhancing competitiveness against commensal Escherichia coli. Additionally, succinate facilitates the expression of type III fimbriae via the DcuSR TCS, promoting hvKP adherence to intestinal epithelial cells. Beyond its signaling role, succinate functions as a metabolic substrate and contributes to adenosine 5'-triphosphate (ATP) synthesis, potentially through C4-dicarboxylic acid transporters DctA or DcuB to boost energy synthesis. This study focuses on elucidating the impact of succinate in regulating hvKP virulence, with particular attention to the potential role of the DcuSR TCS in hvKP pathogenesis.
IMPORTANCE: Succinate, a C4-DC, is produced by the host and the gut microbiota and can accumulate in the intestinal environment under various pathological conditions, such as diabetes and inflammatory bowel disease. It acts as a pivotal regulator of virulence traits and metabolic pathways in Enterobacteriaceae. Our findings highlight the significant impact of succinate on hvKP pathogenesis: (i) functioning through the DcuSR TCS to activate virulence programs and (ii) serving as a metabolic substrate that fuels bioenergetic adaptation through ATP synthesis.
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@article {pmid41230977,
year = {2025},
author = {Zhong, G and Yang, X and Deng, R and Zeng, J and Pu, J and Shen, C and Zhao, S and Yang, T and Liu, H and Luo, M and Li, S and Chen, C and Huang, B},
title = {Succinate-driven virulence enhancement in hypervirulent Klebsiella pneumoniae via DcuSR two-component system.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0145325},
doi = {10.1128/spectrum.01453-25},
pmid = {41230977},
issn = {2165-0497},
abstract = {UNLABELLED: Hypervirulent Klebsiella pneumoniae (hvKP) primarily colonizes the mammalian gastrointestinal tract, and it is prone to causing invasive infections under specific conditions. To establish infection, hvKP must compete with the resident gut microbiota for essential nutrients. This study focuses on the C4-dicarboxylate (C4-DC) succinate, which has been reported to accumulate in the gut under specific pathological conditions. We demonstrate that hvKP utilizes succinate as a signaling molecule to enhance virulence gene expression. Specifically, extracellular succinate activates type VI secretion system gene expression via the DcuSR two-component system (TCS), thereby increasing cytotoxicity toward intestinal epithelial cells and enhancing competitiveness against commensal Escherichia coli. Additionally, succinate facilitates the expression of type III fimbriae via the DcuSR TCS, promoting hvKP adherence to intestinal epithelial cells. Beyond its signaling role, succinate functions as a metabolic substrate and contributes to adenosine 5'-triphosphate (ATP) synthesis, potentially through C4-dicarboxylic acid transporters DctA or DcuB to boost energy synthesis. This study focuses on elucidating the impact of succinate in regulating hvKP virulence, with particular attention to the potential role of the DcuSR TCS in hvKP pathogenesis.
IMPORTANCE: Succinate, a C4-DC, is produced by the host and the gut microbiota and can accumulate in the intestinal environment under various pathological conditions, such as diabetes and inflammatory bowel disease. It acts as a pivotal regulator of virulence traits and metabolic pathways in Enterobacteriaceae. Our findings highlight the significant impact of succinate on hvKP pathogenesis: (i) functioning through the DcuSR TCS to activate virulence programs and (ii) serving as a metabolic substrate that fuels bioenergetic adaptation through ATP synthesis.},
}
RevDate: 2025-11-12
CmpDate: 2025-11-12
Persistent human-associated microbial signatures in burial soils from the 17th and 18th century New York African burial ground.
ISME communications, 5(1):ycaf181.
Understanding the long-term persistence of human-associated microbial signatures in burial soils offers a untapped insights into historical human health, decomposition, and ecological transformation. This study investigates whether centuries-old burial soils retain distinguishable microbial evidence of human decomposition using 16S rRNA gene sequencing on 81 samples from the New York African Burial Ground (NYABG), a 17th and 18th century cemetery for free and enslaved Africans. Comparative analyses against six control soils from nearby urban parks were conducted using QIIME2, ALDEx2, and ANCOM. Burial soils exhibited significantly greater alpha diversity (Faith's PD, Shannon, observed ASVs; P < .01) and distinct beta diversity patterns (Bray-Curtis, UniFrac; PERMANOVA P = .001). Enrichment of Firmicutes, Actinobacteriota, and gut-associated genera such as Bacillus and Ruminococcus characterized burial soils, whereas oligotrophic taxa dominated controls. Tentative identifications of human-associated pathogenic genera (e.g. Fusobacterium periodonticum, Prevotella pleuritidis) were observed exclusively in burial soils, suggesting their origin from the interred individuals but requiring further validation. These findings demonstrate that soil microbiomes reflect host-associated microbial communities long after decomposition, providing a scalable, nondestructive approach for reconstructing ancient microbial communities and host-associated health signatures. This work establishes the NYABG burial soil microbiome as a valuable model for microbial archaeology and introduces a replicable framework for integrating environmental microbiology, bioarchaeology, and historical epidemiology through the lens of postmortem microbial ecology.
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@article {pmid41221507,
year = {2025},
author = {Clinton, CK and Jackson, FLC},
title = {Persistent human-associated microbial signatures in burial soils from the 17th and 18th century New York African burial ground.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf181},
pmid = {41221507},
issn = {2730-6151},
abstract = {Understanding the long-term persistence of human-associated microbial signatures in burial soils offers a untapped insights into historical human health, decomposition, and ecological transformation. This study investigates whether centuries-old burial soils retain distinguishable microbial evidence of human decomposition using 16S rRNA gene sequencing on 81 samples from the New York African Burial Ground (NYABG), a 17th and 18th century cemetery for free and enslaved Africans. Comparative analyses against six control soils from nearby urban parks were conducted using QIIME2, ALDEx2, and ANCOM. Burial soils exhibited significantly greater alpha diversity (Faith's PD, Shannon, observed ASVs; P < .01) and distinct beta diversity patterns (Bray-Curtis, UniFrac; PERMANOVA P = .001). Enrichment of Firmicutes, Actinobacteriota, and gut-associated genera such as Bacillus and Ruminococcus characterized burial soils, whereas oligotrophic taxa dominated controls. Tentative identifications of human-associated pathogenic genera (e.g. Fusobacterium periodonticum, Prevotella pleuritidis) were observed exclusively in burial soils, suggesting their origin from the interred individuals but requiring further validation. These findings demonstrate that soil microbiomes reflect host-associated microbial communities long after decomposition, providing a scalable, nondestructive approach for reconstructing ancient microbial communities and host-associated health signatures. This work establishes the NYABG burial soil microbiome as a valuable model for microbial archaeology and introduces a replicable framework for integrating environmental microbiology, bioarchaeology, and historical epidemiology through the lens of postmortem microbial ecology.},
}
RevDate: 2025-11-11
Colonizing the clinic: tracking bacterial succession and longitudinal dynamics in five new hospital departments over an entire year.
Microbiology spectrum [Epub ahead of print].
The development of hospital-associated microbial communities over time remains poorly characterized, particularly in terms of how microbial populations dynamically respond to changes in building function, the integration of molecular and cultivation-based data, and the early identification of intervention points for flexible, adaptive microbial control strategies. In this longitudinal study, we investigated microbiome dynamics across five newly built departments at the University Hospital of Graz, Austria, over one year. Surface samples were collected at seven time points: before and after hospital operation started. Alpha and beta diversity analyses revealed a distinct two-phase microbial transition, marked by an initial disruption followed by a gradual homogenization of microbial communities. The strongest driver of community change was the arrival of patients, which led to a significant shift in both diversity and taxonomic composition. While early time points were dominated by environmental taxa such as Acinetobacter and Pseudomonas, human-associated genera like Staphylococcus and Corynebacterium became more prevalent over time, particularly on frequently touched surfaces. Department-specific and surface-specific microbial signatures were observed, with outpatient and transplant departments showing more variability than surgical and intensive care units (ICUs). Propidium monoazide treatment indicated that Pseudomonas and Acinetobacter may persist as viable community members, whereas Staphylococcus and Corynebacterium likely reflect frequent human deposition. Cultivation data supported these findings, showing episodic contamination primarily linked to human contact. Phenotypic predictions revealed a decline in aerobic, Gram-negative, and potentially pathogenic bacteria over time, although these trends were less pronounced in the ICU. Together, our findings reveal a longitudinal homogenization of hospital microbiomes driven by human activity and highlight key taxa and surfaces that warrant targeted monitoring to improve hygiene protocols and infection control strategies.IMPORTANCEThis study provides crucial insights into how hospital environments transform microbially after new departments open, a process poorly understood until now. We reveal a two-phase microbial shift, starting with environmental bacteria like Acinetobacter and Pseudomonas before the hospital opens, then rapidly transitioning to human-associated microbes such as Staphylococcus and Corynebacterium once patients and staff arrive. Our findings highlight that human activity is the strongest driver of these changes, especially on frequently touched surfaces. This work is vital for developing targeted and adaptive hygiene concepts, improving infection control, and ultimately making hospital environments safer for patients and staff by focusing on specific surfaces and microbial groups that warrant continuous monitoring.
Additional Links: PMID-41217181
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@article {pmid41217181,
year = {2025},
author = {Weinberger, V and Neumann, C and Kumpitsch, C and Duller, S and Shinde, T and Mantaj, P and Schmidberger, L and Zurabishvili, T and Halmer, I and Cecovini, M and Vrbancic, S and Pepper, K and Schmon, E and Wenninger, J and Kamolz, L-P and Sendlhofer, G and Koskinen, K and Moissl-Eichinger, C and Mahnert, A},
title = {Colonizing the clinic: tracking bacterial succession and longitudinal dynamics in five new hospital departments over an entire year.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0217825},
doi = {10.1128/spectrum.02178-25},
pmid = {41217181},
issn = {2165-0497},
abstract = {The development of hospital-associated microbial communities over time remains poorly characterized, particularly in terms of how microbial populations dynamically respond to changes in building function, the integration of molecular and cultivation-based data, and the early identification of intervention points for flexible, adaptive microbial control strategies. In this longitudinal study, we investigated microbiome dynamics across five newly built departments at the University Hospital of Graz, Austria, over one year. Surface samples were collected at seven time points: before and after hospital operation started. Alpha and beta diversity analyses revealed a distinct two-phase microbial transition, marked by an initial disruption followed by a gradual homogenization of microbial communities. The strongest driver of community change was the arrival of patients, which led to a significant shift in both diversity and taxonomic composition. While early time points were dominated by environmental taxa such as Acinetobacter and Pseudomonas, human-associated genera like Staphylococcus and Corynebacterium became more prevalent over time, particularly on frequently touched surfaces. Department-specific and surface-specific microbial signatures were observed, with outpatient and transplant departments showing more variability than surgical and intensive care units (ICUs). Propidium monoazide treatment indicated that Pseudomonas and Acinetobacter may persist as viable community members, whereas Staphylococcus and Corynebacterium likely reflect frequent human deposition. Cultivation data supported these findings, showing episodic contamination primarily linked to human contact. Phenotypic predictions revealed a decline in aerobic, Gram-negative, and potentially pathogenic bacteria over time, although these trends were less pronounced in the ICU. Together, our findings reveal a longitudinal homogenization of hospital microbiomes driven by human activity and highlight key taxa and surfaces that warrant targeted monitoring to improve hygiene protocols and infection control strategies.IMPORTANCEThis study provides crucial insights into how hospital environments transform microbially after new departments open, a process poorly understood until now. We reveal a two-phase microbial shift, starting with environmental bacteria like Acinetobacter and Pseudomonas before the hospital opens, then rapidly transitioning to human-associated microbes such as Staphylococcus and Corynebacterium once patients and staff arrive. Our findings highlight that human activity is the strongest driver of these changes, especially on frequently touched surfaces. This work is vital for developing targeted and adaptive hygiene concepts, improving infection control, and ultimately making hospital environments safer for patients and staff by focusing on specific surfaces and microbial groups that warrant continuous monitoring.},
}
RevDate: 2025-11-10
Health Reversion Effects of Autoprobiotics on Serum and Urine Metabolomes in Patients With Metabolic Syndrome: A Pilot Study.
Molecular nutrition & food research [Epub ahead of print].
The effectiveness of oral administration of autoprobiotic (nonpathogenic, indigenous) Enterococcus faecium or Enterococcus hirae for 20 days in patients with metabolic syndrome (MetS), characterized by obesity and impaired carbohydrate and lipid metabolism, was investigated. The dynamics of changes in anthropometric, biochemical parameters, and metabolism were monitored 14 and 28 days after the end of therapy. Clinical and laboratory changes after using autoprobiotics indicate a decrease in the severity of MetS. In the reversed-phase high-performance liquid chromatography-mass spectrometry analysis of blood serum metabolome, a significant decrease in the levels of all identified long-chain acylcarnitines - palmitoyl-L-carnitine (C16:0), stearoyl-L-carnitine (C18:0), and oleoyl-L-carnitine (C25), trimethylamine-N-oxide, and homocysteine 14 and 28 days after the end of therapy, and, conversely, a significant increase in L-histidine levels. The targeted gas-liquid chromatography showed an increase in the concentrations of hippuric, glycolic, methylmalonic acids, and 5-oxoproline at the same time. The effectiveness of therapy is confirmed by changes in serum and urinary metabolism, primarily aimed at correcting these and reducing signs characteristic of patients with obesity and impaired energy metabolism. The revealed positive changes in the concentration of individual serum and urine metabolites allow for their further use in a targeted study to predict the severity of MetS and the effectiveness of its therapy.
Additional Links: PMID-41211619
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PubMed:
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@article {pmid41211619,
year = {2025},
author = {Ermolenko, E and Sitkin, S and Alferova, L and Ilyushonok, S and Beltyukov, P and Babakov, V and Novikova, N and Gladyshev, N and Berdichevskiy, G and Demchenko, E and Suvorov, A},
title = {Health Reversion Effects of Autoprobiotics on Serum and Urine Metabolomes in Patients With Metabolic Syndrome: A Pilot Study.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e70273},
doi = {10.1002/mnfr.70273},
pmid = {41211619},
issn = {1613-4133},
abstract = {The effectiveness of oral administration of autoprobiotic (nonpathogenic, indigenous) Enterococcus faecium or Enterococcus hirae for 20 days in patients with metabolic syndrome (MetS), characterized by obesity and impaired carbohydrate and lipid metabolism, was investigated. The dynamics of changes in anthropometric, biochemical parameters, and metabolism were monitored 14 and 28 days after the end of therapy. Clinical and laboratory changes after using autoprobiotics indicate a decrease in the severity of MetS. In the reversed-phase high-performance liquid chromatography-mass spectrometry analysis of blood serum metabolome, a significant decrease in the levels of all identified long-chain acylcarnitines - palmitoyl-L-carnitine (C16:0), stearoyl-L-carnitine (C18:0), and oleoyl-L-carnitine (C25), trimethylamine-N-oxide, and homocysteine 14 and 28 days after the end of therapy, and, conversely, a significant increase in L-histidine levels. The targeted gas-liquid chromatography showed an increase in the concentrations of hippuric, glycolic, methylmalonic acids, and 5-oxoproline at the same time. The effectiveness of therapy is confirmed by changes in serum and urinary metabolism, primarily aimed at correcting these and reducing signs characteristic of patients with obesity and impaired energy metabolism. The revealed positive changes in the concentration of individual serum and urine metabolites allow for their further use in a targeted study to predict the severity of MetS and the effectiveness of its therapy.},
}
RevDate: 2025-11-10
How intense is high-intensity interval training? Biomarker responses and associations with training load and fitness.
iScience, 28(11):113738.
High-intensity interval training (HIIT) enhances physical performance but requires close monitoring to avoid illnesses/injuries. We monitored physiological responses at rest during and up to 14 days following a 7-day HIIT intervention to identify chronic physiological changes and to explore correlations between blood biomarkers (blood count, cytokines, creatine kinase [CK], urea, ferritin, and transferrin), training load, cardiorespiratory fitness (VO2max), and muscle soreness. Thirty participants were randomly allocated to either HIIT shock cycle (10× HIIT in 7 days) (1) with or (2) without additional low-intensity training after each HIIT session or (3) control group. Repeated HIIT resulted in a chronic decrease of hemoglobin, hematocrit, red blood cells, CK, interleukin [IL]-2, -4, -9, -17A, -17F, tumor necrosis factor alpha (TNF-α), and ferritin. CK showed highest positive correlation with training load and muscle soreness, while VO2max correlated with cytokines IL-5, -6, -10, -17F, -22. The present study revealed reliable biomarkers reflecting training load and VO2max, suitable for personalized monitoring of health and recovery and performance optimization.
Additional Links: PMID-41210964
PubMed:
Citation:
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@article {pmid41210964,
year = {2025},
author = {Haller, N and Widauer, HL and Strepp, T and Nunes, N and Blumkaitis, JC and Wenger, M and Stöggl, T and Aglas, L},
title = {How intense is high-intensity interval training? Biomarker responses and associations with training load and fitness.},
journal = {iScience},
volume = {28},
number = {11},
pages = {113738},
pmid = {41210964},
issn = {2589-0042},
abstract = {High-intensity interval training (HIIT) enhances physical performance but requires close monitoring to avoid illnesses/injuries. We monitored physiological responses at rest during and up to 14 days following a 7-day HIIT intervention to identify chronic physiological changes and to explore correlations between blood biomarkers (blood count, cytokines, creatine kinase [CK], urea, ferritin, and transferrin), training load, cardiorespiratory fitness (VO2max), and muscle soreness. Thirty participants were randomly allocated to either HIIT shock cycle (10× HIIT in 7 days) (1) with or (2) without additional low-intensity training after each HIIT session or (3) control group. Repeated HIIT resulted in a chronic decrease of hemoglobin, hematocrit, red blood cells, CK, interleukin [IL]-2, -4, -9, -17A, -17F, tumor necrosis factor alpha (TNF-α), and ferritin. CK showed highest positive correlation with training load and muscle soreness, while VO2max correlated with cytokines IL-5, -6, -10, -17F, -22. The present study revealed reliable biomarkers reflecting training load and VO2max, suitable for personalized monitoring of health and recovery and performance optimization.},
}
RevDate: 2025-11-09
HLRMDB: a comprehensive database of the human microbiome with metagenomic assembly, taxonomic classification, and functional annotation by analysis of long-read and hybrid sequencing data.
Nucleic acids research pii:8317319 [Epub ahead of print].
The human microbiome harbours an immense diversity of uncultivated microbes; short-read metagenomic sequencing has elucidated much of this diversity, but fragment repeats and mobile elements constrain strain-level resolution. Fortunately, long-read metagenomic sequencing can generate reads spanning tens of kilobases with single-molecule accuracies exceeding 99%, enabling near-complete genome and gene cluster recovery in a cultivation-independent manner. However, systematic resources that aggregate and standardise long-read outputs remain limited. Here, we present HLRMDB (http://www.inbirg.com/hlrmdb/), a comprehensive database of human microbiome datasets derived from long-read and hybrid metagenomic sequencing. We curated 1672 publicly available metagenomes (1291 long reads; 381 hybrids) spanning 38 studies, 39 sampling contexts and 42 host health states. A uniform assembly and binning pipeline reconstructed >98 Gb of contigs and yielded 18 721 metagenome-assembled genomes (MAGs). These MAGs span 21 phyla and 1323 bacterial species, with 6339 classified as near-complete and 5609 as medium-quality. HLRMDB integrates these genome-resolved data with extensive gene-centric functional profiles and antimicrobial resistance annotations. An interactive web interface supports flexible access to both sample-level and genome-level results, with multiple visualisations linking raw reads to assembled genomes. Overall, HLRMDB offers a harmonised, long-read-oriented repository that supports reproducible, strain-resolved comparative genomics and context-sensitive ecological investigations of the human microbiome.
Additional Links: PMID-41207298
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PubMed:
Citation:
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@article {pmid41207298,
year = {2025},
author = {Zhai, Z and Che, X and Shen, W and Zhang, Z and Li, Y and Pan, J},
title = {HLRMDB: a comprehensive database of the human microbiome with metagenomic assembly, taxonomic classification, and functional annotation by analysis of long-read and hybrid sequencing data.},
journal = {Nucleic acids research},
volume = {},
number = {},
pages = {},
doi = {10.1093/nar/gkaf1152},
pmid = {41207298},
issn = {1362-4962},
support = {32470699//National Natural Science Foundation of China/ ; //Chongqing Medical University/ ; },
abstract = {The human microbiome harbours an immense diversity of uncultivated microbes; short-read metagenomic sequencing has elucidated much of this diversity, but fragment repeats and mobile elements constrain strain-level resolution. Fortunately, long-read metagenomic sequencing can generate reads spanning tens of kilobases with single-molecule accuracies exceeding 99%, enabling near-complete genome and gene cluster recovery in a cultivation-independent manner. However, systematic resources that aggregate and standardise long-read outputs remain limited. Here, we present HLRMDB (http://www.inbirg.com/hlrmdb/), a comprehensive database of human microbiome datasets derived from long-read and hybrid metagenomic sequencing. We curated 1672 publicly available metagenomes (1291 long reads; 381 hybrids) spanning 38 studies, 39 sampling contexts and 42 host health states. A uniform assembly and binning pipeline reconstructed >98 Gb of contigs and yielded 18 721 metagenome-assembled genomes (MAGs). These MAGs span 21 phyla and 1323 bacterial species, with 6339 classified as near-complete and 5609 as medium-quality. HLRMDB integrates these genome-resolved data with extensive gene-centric functional profiles and antimicrobial resistance annotations. An interactive web interface supports flexible access to both sample-level and genome-level results, with multiple visualisations linking raw reads to assembled genomes. Overall, HLRMDB offers a harmonised, long-read-oriented repository that supports reproducible, strain-resolved comparative genomics and context-sensitive ecological investigations of the human microbiome.},
}
RevDate: 2025-11-08
Corrigendum to "Long-term neutralization capacity of vaccine and breakthrough infection induced SARS-CoV-2 specific antibodies against omicron subvariants BA.2, XBB.1.5, and JN.1" [Vaccine 68 (2025) 127894].
Additional Links: PMID-41205405
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PubMed:
Citation:
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@article {pmid41205405,
year = {2025},
author = {Reinholm, A and Khan, H and Laakso, T and Maljanen, S and Jalkanen, P and Gunell, M and Kallonen, T and Österlund, P and Ritvos, O and Nousiainen, A and Häkkinen, HK and Pakkanen, SH and Välimaa, H and Kantele, A and Lempainen, J and Julkunen, I and Kolehmainen, P and Kakkola, L},
title = {Corrigendum to "Long-term neutralization capacity of vaccine and breakthrough infection induced SARS-CoV-2 specific antibodies against omicron subvariants BA.2, XBB.1.5, and JN.1" [Vaccine 68 (2025) 127894].},
journal = {Vaccine},
volume = {68},
number = {},
pages = {127939},
doi = {10.1016/j.vaccine.2025.127939},
pmid = {41205405},
issn = {1873-2518},
}
RevDate: 2025-11-08
The hidden players: The mycobiome of pancreatic ductal adenocarcinoma tumors.
Microbiological research, 303:128392 pii:S0944-5013(25)00351-9 [Epub ahead of print].
The microorganisms that inhabit the human body are known to play a role in human health and disease. Continuing to elucidate their specific role in disease progression is, however, necessary. The imbalance of these microorganisms-known as dysbiosis-has been linked to a myriad of intestinal diseases, and more recently to cancer. Despite making up less than 0.1 % of the human microbiome, dysbiosis of the fungal component of the microbiome-the mycobiome-has been found to contribute to the tumorigenesis and progression of certain types of tumors, pancreatic ductal adenocarcinoma (PDAC) included. The quantity and composition of the mycobiome was found to differ between healthy pancreatic tissue, the gut mycobiome of PDAC patients and PDAC tissue. Moreover, in a murine model of PDAC, it was shown that fungal ablation had a protective effect on tumor growth, and that specific fungal species, such as Malassezia globosa, contribute to tumor growth as well as to the inflammatory environment observed in PDAC tumors which promotes tumor progression. Research shows that fungal presence contributes to shaping the immune microenvironment through the activation of the complement system and/or by eliciting a type 2 immune response. Despite these preliminary findings, given the novelty of the field and of the bioinformatics pipelines used to analyze sequencing data, standardized approaches are still under development, thus leading to disagreement on the reliability of these results. The purpose of this review is to provide an up-to-date overview of the current research regarding the contribution of the fungal mycobiome in PDAC tumor progression and the overall tumor microenvironment (TME) of PDAC tumors.
Additional Links: PMID-41205302
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@article {pmid41205302,
year = {2025},
author = {Camille, E and Sébastien, B and Virginie, B},
title = {The hidden players: The mycobiome of pancreatic ductal adenocarcinoma tumors.},
journal = {Microbiological research},
volume = {303},
number = {},
pages = {128392},
doi = {10.1016/j.micres.2025.128392},
pmid = {41205302},
issn = {1618-0623},
abstract = {The microorganisms that inhabit the human body are known to play a role in human health and disease. Continuing to elucidate their specific role in disease progression is, however, necessary. The imbalance of these microorganisms-known as dysbiosis-has been linked to a myriad of intestinal diseases, and more recently to cancer. Despite making up less than 0.1 % of the human microbiome, dysbiosis of the fungal component of the microbiome-the mycobiome-has been found to contribute to the tumorigenesis and progression of certain types of tumors, pancreatic ductal adenocarcinoma (PDAC) included. The quantity and composition of the mycobiome was found to differ between healthy pancreatic tissue, the gut mycobiome of PDAC patients and PDAC tissue. Moreover, in a murine model of PDAC, it was shown that fungal ablation had a protective effect on tumor growth, and that specific fungal species, such as Malassezia globosa, contribute to tumor growth as well as to the inflammatory environment observed in PDAC tumors which promotes tumor progression. Research shows that fungal presence contributes to shaping the immune microenvironment through the activation of the complement system and/or by eliciting a type 2 immune response. Despite these preliminary findings, given the novelty of the field and of the bioinformatics pipelines used to analyze sequencing data, standardized approaches are still under development, thus leading to disagreement on the reliability of these results. The purpose of this review is to provide an up-to-date overview of the current research regarding the contribution of the fungal mycobiome in PDAC tumor progression and the overall tumor microenvironment (TME) of PDAC tumors.},
}
RevDate: 2025-11-07
CmpDate: 2025-11-07
Two of a kind, one with MS: Gut microbes tip the balance.
Science immunology, 10(113):eaed4910.
An MS twin study links ileal Lachnospiraceae to spontaneous CNS autoimmunity in mice receiving a human microbiome transplant.
Additional Links: PMID-41202150
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@article {pmid41202150,
year = {2025},
author = {Champagne-Jorgensen, K and Gommerman, JL},
title = {Two of a kind, one with MS: Gut microbes tip the balance.},
journal = {Science immunology},
volume = {10},
number = {113},
pages = {eaed4910},
doi = {10.1126/sciimmunol.aed4910},
pmid = {41202150},
issn = {2470-9468},
mesh = {*Gastrointestinal Microbiome/immunology ; Humans ; Animals ; *Multiple Sclerosis/immunology/microbiology ; Mice ; Fecal Microbiota Transplantation ; },
abstract = {An MS twin study links ileal Lachnospiraceae to spontaneous CNS autoimmunity in mice receiving a human microbiome transplant.},
}
MeSH Terms:
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*Gastrointestinal Microbiome/immunology
Humans
Animals
*Multiple Sclerosis/immunology/microbiology
Mice
Fecal Microbiota Transplantation
RevDate: 2025-11-06
Microbial Metabolites for Cancer Immunotherapy: Current Evidence and Future Directions.
Seminars in cancer biology pii:S1044-579X(25)00127-0 [Epub ahead of print].
Immune checkpoint blockade (ICB) therapy has transformed cancer treatment by activating the body's immune defenses to combat malignancies, offering substantial therapeutic outcomes for patients with advanced cancers. However, its efficacy varies considerably across different tumor types and individual patients. Recent studies have identified the human microbiome as a pivotal regulator of host homeostasis and systemic immunity and also found that it is essential for regulating immunotherapy's efficacy. Beyond direct microbial-host interactions, microbiota-derived immunomodulatory products, including metabolites, extracellular vesicles, and polysaccharides, have been shown to profoundly influence tumorigenesis, disease progression, and therapeutic responses. These microbial-derived immunomodulatory products can reshape the tumor microenvironment (TME) and modulate tumor immunity. Notably, emerging therapeutic strategies targeting or utilizing microbial immunomodulators have demonstrated promising efficacy in both preclinical and clinical models. This review provides a comprehensive overview of current research on microbiota-derived immunomodulatory products in cancer immunotherapy, highlighting their mechanistic roles and potential as innovative adjuncts in future tumor treatment strategies.
Additional Links: PMID-41197755
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PubMed:
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@article {pmid41197755,
year = {2025},
author = {Wang, XX and Liang, JJ and Duan, X and Chen, G},
title = {Microbial Metabolites for Cancer Immunotherapy: Current Evidence and Future Directions.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.10.005},
pmid = {41197755},
issn = {1096-3650},
abstract = {Immune checkpoint blockade (ICB) therapy has transformed cancer treatment by activating the body's immune defenses to combat malignancies, offering substantial therapeutic outcomes for patients with advanced cancers. However, its efficacy varies considerably across different tumor types and individual patients. Recent studies have identified the human microbiome as a pivotal regulator of host homeostasis and systemic immunity and also found that it is essential for regulating immunotherapy's efficacy. Beyond direct microbial-host interactions, microbiota-derived immunomodulatory products, including metabolites, extracellular vesicles, and polysaccharides, have been shown to profoundly influence tumorigenesis, disease progression, and therapeutic responses. These microbial-derived immunomodulatory products can reshape the tumor microenvironment (TME) and modulate tumor immunity. Notably, emerging therapeutic strategies targeting or utilizing microbial immunomodulators have demonstrated promising efficacy in both preclinical and clinical models. This review provides a comprehensive overview of current research on microbiota-derived immunomodulatory products in cancer immunotherapy, highlighting their mechanistic roles and potential as innovative adjuncts in future tumor treatment strategies.},
}
RevDate: 2025-11-06
Microbial Modulation as a Game Changer: Boosting Immunotherapy Efficacy in Breast Cancer.
Seminars in cancer biology pii:S1044-579X(25)00136-1 [Epub ahead of print].
Breast cancer is generally regarded as an immunologically cold tumor, characterized by limited T cell infiltration and poor responsiveness to immune checkpoint inhibitors. Increasing evidence suggests that the human microbiome, including both gut and tumor-associated microbial communities, serves as a critical regulator of systemic and local antitumor immunity, with potential to convert inert tumors into immune-responsive states. Gut microbiota influence systemic immune homeostasis through metabolites such as lipids, lactic acid, and trimethylamine N-oxide, which modulate T lymphocytes, dendritic cells, leukocytes, and stromal components. Tumor-resident microbiota further shape the tumor immune microenvironment by regulating CD4[+] and CD8[+] T cells, NKT cells, Tregs, and macrophages, thereby impacting the efficacy of immune checkpoint blockade. Emerging strategies to sensitize cold breast tumors through microbiome modulation include dietary phytochemicals, bariatric surgery induced microbial shifts, probiotics and postbiotics, polyvalent microbial antigen vaccines, and nanotechnology-based platforms. Clinical challenges remain, particularly interindividual microbial heterogeneity, safety and regulatory considerations, and the need for reliable microbial and immune biomarkers. This review summarizes current advances in microbiota-immune interactions in breast cancer and discusses opportunities for microbiome-targeted strategies to enhance immunotherapy outcomes.
Additional Links: PMID-41197754
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PubMed:
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@article {pmid41197754,
year = {2025},
author = {Xia, F and Yi, Q and Xu, Z and Zhou, Z and Tang, H and Zhang, K and Yan, Y},
title = {Microbial Modulation as a Game Changer: Boosting Immunotherapy Efficacy in Breast Cancer.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.10.006},
pmid = {41197754},
issn = {1096-3650},
abstract = {Breast cancer is generally regarded as an immunologically cold tumor, characterized by limited T cell infiltration and poor responsiveness to immune checkpoint inhibitors. Increasing evidence suggests that the human microbiome, including both gut and tumor-associated microbial communities, serves as a critical regulator of systemic and local antitumor immunity, with potential to convert inert tumors into immune-responsive states. Gut microbiota influence systemic immune homeostasis through metabolites such as lipids, lactic acid, and trimethylamine N-oxide, which modulate T lymphocytes, dendritic cells, leukocytes, and stromal components. Tumor-resident microbiota further shape the tumor immune microenvironment by regulating CD4[+] and CD8[+] T cells, NKT cells, Tregs, and macrophages, thereby impacting the efficacy of immune checkpoint blockade. Emerging strategies to sensitize cold breast tumors through microbiome modulation include dietary phytochemicals, bariatric surgery induced microbial shifts, probiotics and postbiotics, polyvalent microbial antigen vaccines, and nanotechnology-based platforms. Clinical challenges remain, particularly interindividual microbial heterogeneity, safety and regulatory considerations, and the need for reliable microbial and immune biomarkers. This review summarizes current advances in microbiota-immune interactions in breast cancer and discusses opportunities for microbiome-targeted strategies to enhance immunotherapy outcomes.},
}
RevDate: 2025-11-05
Ultrasound-responsive Janus patch with mechanical anisotropy, pro-healing, and anti-adhesion properties for abdominal wall defect repair.
Journal of nanobiotechnology, 23(1):702.
Abdominal wall exhibits a complex anisotropic architecture with region-specific mechanical gradients, essential for maintaining biomechanical integrity during physiological deformations. However, most clinical patches possess isotropic structures and fail to meet the mechanical anisotropy requirements of abdominal wall. Herein, inspired by the hierarchical structure of abdominal wall, an innovative ultrasound-responsive Janus patch (JPLCL/ZnO) is designed by constructing a poly (2-methacryloyloxyethyl phosphorylcholine) (PMPC) coating on the top surface of a fibrous anisotropic patch (PLCL/ZnO) via multi-channel electrospinning and in situ photocuring technologies. By adjusting fiber orientation, our patch achieves tunable anisotropy ratios (1-14), matching the mechanical gradients of abdominal wall (1-9). The PMPC-coated side prevents tissue adhesion, while the anisotropic PLCL/ZnO side promotes directional cell growth and tissue regeneration under ultrasound stimulation. Moving toward clinical translation, we developed a large mammal defect model in pigs with abdominal wall resection. By integrating excellent mechanical anisotropy, pro-healing, anti-adhesion, and immune regulation properties, our JPLCL/ZnO patch demonstrates a significant advancement for abdominal wall defect repair.
Additional Links: PMID-41194223
PubMed:
Citation:
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@article {pmid41194223,
year = {2025},
author = {Peng, B and Ma, B and Lu, H and Chen, Z and Xiong, W and Wang, H and Cai, Z and Shi, X and Huang, R},
title = {Ultrasound-responsive Janus patch with mechanical anisotropy, pro-healing, and anti-adhesion properties for abdominal wall defect repair.},
journal = {Journal of nanobiotechnology},
volume = {23},
number = {1},
pages = {702},
pmid = {41194223},
issn = {1477-3155},
support = {2021YFC2101700//National Key Research Development Program of China/ ; 22371312//National Natural Science Foundation of China/ ; 52203112//National Natural Science Foundation of China/ ; 22271320//National Natural Science Foundation of China/ ; 2017008//Sun Yat-sen University Clinical Research 5010 Program/ ; RCBS20221008093103014//Shenzhen Science and Technology Program/ ; 23qnpy155//Fundamental Research Funds for the Central Universities, Sun Yat-sen University/ ; 23yxqntd002//Fundamental Research Funds for the Central Universities, Sun Yat-sen University/ ; FTWS2025001//the Futian Healthcare Research Project/ ; 2023B0303000025//Guangdong Major Project of Basic and Applied Basic Research/ ; 2021-M04//CIFST-Abbott Foundation of Food Nutrition and Safety/ ; },
abstract = {Abdominal wall exhibits a complex anisotropic architecture with region-specific mechanical gradients, essential for maintaining biomechanical integrity during physiological deformations. However, most clinical patches possess isotropic structures and fail to meet the mechanical anisotropy requirements of abdominal wall. Herein, inspired by the hierarchical structure of abdominal wall, an innovative ultrasound-responsive Janus patch (JPLCL/ZnO) is designed by constructing a poly (2-methacryloyloxyethyl phosphorylcholine) (PMPC) coating on the top surface of a fibrous anisotropic patch (PLCL/ZnO) via multi-channel electrospinning and in situ photocuring technologies. By adjusting fiber orientation, our patch achieves tunable anisotropy ratios (1-14), matching the mechanical gradients of abdominal wall (1-9). The PMPC-coated side prevents tissue adhesion, while the anisotropic PLCL/ZnO side promotes directional cell growth and tissue regeneration under ultrasound stimulation. Moving toward clinical translation, we developed a large mammal defect model in pigs with abdominal wall resection. By integrating excellent mechanical anisotropy, pro-healing, anti-adhesion, and immune regulation properties, our JPLCL/ZnO patch demonstrates a significant advancement for abdominal wall defect repair.},
}
RevDate: 2025-11-05
Biocompatible Nanozyme Shell-Armed Probiotic with Inflammation Targeting and Scavenging Properties Enables Effective Treatment of Colitis.
Advanced materials (Deerfield Beach, Fla.) [Epub ahead of print].
Coupling probiotics with lesion targeting and inflammation control properties without complex chemical modifications is crucial for preserving their native bioactivity, but remains challenging. Herein, metformin as a functional self-modulated alkaline reagent is incorporated to achieve the rapid and biocompatible construction of a polydopamine-based nanozyme shell (DMCe) on the surface of probiotics, thus avoiding the biological toxicity caused by traditional triggering methods. DMCe can not only serve as a robust physical barrier to protect probiotics from the invasion of digestive juices and antibiotics, but also synergistically scavenge reactive oxygen species (ROS) at colitis lesions via the intrinsic antioxidant property of catechol and the catalase-mimicking activity of cerium oxide. It is worth noting that during the process of scavenging ROS, the originally harmful ROS can be utilized by DMCe as reactive components to facilitate chemical reactions between the modified probiotics and colitis lesions, thus achieving prolonged inflammation targeting for up to 7 days. In addition, nanozyme shell-armed probiotics can improve microbial community composition and increase the levels of short-chain fatty acids. By integrating inflammation targeting, ROS scavenging, and microbiome remodeling, nanozyme shell-armed probiotics can significantly reduce inflammation levels and promote healing of the mucosal barrier in a mouse colitis model.
Additional Links: PMID-41190871
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@article {pmid41190871,
year = {2025},
author = {Liang, W and Chen, G and Zheng, B and Zhou, H and Ouyang, Y and Wang, X and He, Z and Wu, D and Lan, P and Huang, R},
title = {Biocompatible Nanozyme Shell-Armed Probiotic with Inflammation Targeting and Scavenging Properties Enables Effective Treatment of Colitis.},
journal = {Advanced materials (Deerfield Beach, Fla.)},
volume = {},
number = {},
pages = {e08532},
doi = {10.1002/adma.202508532},
pmid = {41190871},
issn = {1521-4095},
support = {2022YFA1304000//National Key Research and Development Program of China/ ; 22271320//National Natural Science Foundation of China/ ; 52372057//National Natural Science Foundation of China/ ; 2021B1212040017//Science and Technology Planning Project of Guangdong Province/ ; 2023B0303000025//Guangdong Major Project of Basic and Applied Basic Research/ ; //Fundamental Research Funds for the Central Universities/ ; 23yxqntd002//Sun Yat-sen University/ ; JCYJ20240813150654069//Shenzhen Science and Technology Program/ ; //Guangdong Basic Research Center of Excellence for Functional Molecular Engineering/ ; //National Key Clinical Discipline/ ; },
abstract = {Coupling probiotics with lesion targeting and inflammation control properties without complex chemical modifications is crucial for preserving their native bioactivity, but remains challenging. Herein, metformin as a functional self-modulated alkaline reagent is incorporated to achieve the rapid and biocompatible construction of a polydopamine-based nanozyme shell (DMCe) on the surface of probiotics, thus avoiding the biological toxicity caused by traditional triggering methods. DMCe can not only serve as a robust physical barrier to protect probiotics from the invasion of digestive juices and antibiotics, but also synergistically scavenge reactive oxygen species (ROS) at colitis lesions via the intrinsic antioxidant property of catechol and the catalase-mimicking activity of cerium oxide. It is worth noting that during the process of scavenging ROS, the originally harmful ROS can be utilized by DMCe as reactive components to facilitate chemical reactions between the modified probiotics and colitis lesions, thus achieving prolonged inflammation targeting for up to 7 days. In addition, nanozyme shell-armed probiotics can improve microbial community composition and increase the levels of short-chain fatty acids. By integrating inflammation targeting, ROS scavenging, and microbiome remodeling, nanozyme shell-armed probiotics can significantly reduce inflammation levels and promote healing of the mucosal barrier in a mouse colitis model.},
}
RevDate: 2025-11-04
Smart hybrid nanomaterials for chronic infections: microbiome-responsive and sustainable therapeutic platforms.
Journal of nanobiotechnology, 23(1):698.
UNLABELLED: Chronic wounds remain a persistent clinical challenge due to their complex pathology involving prolonged inflammation, microbial biofilms, and impaired tissue regeneration. Emerging research highlights the dynamic role of the human microbiome in modulating immune responses and influencing wound healing outcomes. Disruptions to this microbial balance, termed dysbiosis, not only exacerbate infection but also hinder therapeutic efficacy. Recent advances in smart and sustainable nanotechnology offer promising avenues to address these challenges. By integrating microbiome-sensitive mechanisms with targeted delivery systems, bio-based nanomaterials can overcome multidrug resistance, modulate inflammation, and accelerate healing. This review explores the molecular interplay between chronic infections and host immunity, highlights next-generation nanomaterials for regenerative applications, and proposes a sustainable paradigm that bridges clinical effectiveness with environmental responsibility.
GRAPHICAL ABSTRACT: [Image: see text]
Additional Links: PMID-41184906
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@article {pmid41184906,
year = {2025},
author = {Singh, H and Balusamy, SR and Sukweenadhi, J and Saravanan, M and Aruchamy, M and Mijakovic, I and Singh, P},
title = {Smart hybrid nanomaterials for chronic infections: microbiome-responsive and sustainable therapeutic platforms.},
journal = {Journal of nanobiotechnology},
volume = {23},
number = {1},
pages = {698},
pmid = {41184906},
issn = {1477-3155},
abstract = {UNLABELLED: Chronic wounds remain a persistent clinical challenge due to their complex pathology involving prolonged inflammation, microbial biofilms, and impaired tissue regeneration. Emerging research highlights the dynamic role of the human microbiome in modulating immune responses and influencing wound healing outcomes. Disruptions to this microbial balance, termed dysbiosis, not only exacerbate infection but also hinder therapeutic efficacy. Recent advances in smart and sustainable nanotechnology offer promising avenues to address these challenges. By integrating microbiome-sensitive mechanisms with targeted delivery systems, bio-based nanomaterials can overcome multidrug resistance, modulate inflammation, and accelerate healing. This review explores the molecular interplay between chronic infections and host immunity, highlights next-generation nanomaterials for regenerative applications, and proposes a sustainable paradigm that bridges clinical effectiveness with environmental responsibility.
GRAPHICAL ABSTRACT: [Image: see text]},
}
RevDate: 2025-11-04
A global survey of taxa-metabolic associations across mouse microbiome communities.
Cell host & microbe pii:S1931-3128(25)00424-X [Epub ahead of print].
Host-microbiota mutualism is rooted in the exchange of dietary and metabolic molecules. Microbial diversity broadens the metabolite pool, with each taxon contributing distinct compounds in varying proportions. In the human microbiome, high variability in consortial composition is largely compensated by similar metabolic functions across different taxa. However, the extent of compensation in lower diversity mouse models, and whether vivaria are metabolically equivalent, is unknown. We provide a searchable resource of microbiome composition variability across 51 murine vivaria and 12 wild mouse colonies worldwide, with vivarium-specific variants mapped according to predicted 3D structures for each microbial species. Our matched metabolomics data show that realized metabolic potential has relatively low variability, providing functional evidence for metabolic compensation. Additionally, variability is related to taxonomic composition rather than vivarium, revealing taxa-metabolite associations that are potentially relevant to phenotypic differences between vivaria. Collectively, this resource offers tools to strengthen microbiome studies and collaborative science.
Additional Links: PMID-41187758
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PubMed:
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@article {pmid41187758,
year = {2025},
author = {Yilmaz, B and Baertschi, I and Meier, KHU and Le Gac, C and Jordi, SBU and Black, C and Li, J and Lindholm, AK and , and König, B and Sauer, U and Stelling, J and Macpherson, AJ},
title = {A global survey of taxa-metabolic associations across mouse microbiome communities.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2025.10.010},
pmid = {41187758},
issn = {1934-6069},
abstract = {Host-microbiota mutualism is rooted in the exchange of dietary and metabolic molecules. Microbial diversity broadens the metabolite pool, with each taxon contributing distinct compounds in varying proportions. In the human microbiome, high variability in consortial composition is largely compensated by similar metabolic functions across different taxa. However, the extent of compensation in lower diversity mouse models, and whether vivaria are metabolically equivalent, is unknown. We provide a searchable resource of microbiome composition variability across 51 murine vivaria and 12 wild mouse colonies worldwide, with vivarium-specific variants mapped according to predicted 3D structures for each microbial species. Our matched metabolomics data show that realized metabolic potential has relatively low variability, providing functional evidence for metabolic compensation. Additionally, variability is related to taxonomic composition rather than vivarium, revealing taxa-metabolite associations that are potentially relevant to phenotypic differences between vivaria. Collectively, this resource offers tools to strengthen microbiome studies and collaborative science.},
}
RevDate: 2025-11-03
Microbiome alterations in healthy pregnancy and pregnancy disorders in association with autoimmune diseases.
Folia microbiologica [Epub ahead of print].
Pregnancy induces significant alterations in the maternal microbiome, which are critical for fetal development and maternal health. Gynecological diseases, along with infertility, have increased due to excessive personal care product usage, which contains endocrine-disrupting chemicals (EDCs). Mammalian immune systems develop during pregnancy and after birth owing to crucial inputs from the environment. The growing incidence of autoimmune diseases (AIMDs) emphasizes the need to understand the environmental elements that play a role in their development, with the microbiome emerging as a key player. Exposure to EDCs with oxidative stress (OS) induces microbiome disruptions to promote AIMDs and negatively impacts female reproductive health and fetuses. Because the body changes in a number of ways to provide ideal conditions for fetal growth, pregnancy is a special moment in a woman's life. All microorganisms undergo changes, and their quantity and composition vary over the three trimesters of pregnancy. Recent research suggests a connection between pregnancy issues and the microorganisms present during pregnancy. This review explores the pivotal role of the human microbiome in pregnancy health, emphasizing how microbiome dynamics influence immune development and long-term immunity in offspring. It examines the impact of environmental factors, particularly EDCs, on maternal microbiota and their association with pregnancy complications such as hypertensive disorders and autoimmune diseases. The manuscript highlights current research findings and discusses potential microbiome-targeted interventions to promote maternal and fetal well-being.
Additional Links: PMID-41182672
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@article {pmid41182672,
year = {2025},
author = {El-Demerdash, FE and Mohammed, OA and Mohamed, HH and Doghish, AS},
title = {Microbiome alterations in healthy pregnancy and pregnancy disorders in association with autoimmune diseases.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {41182672},
issn = {1874-9356},
abstract = {Pregnancy induces significant alterations in the maternal microbiome, which are critical for fetal development and maternal health. Gynecological diseases, along with infertility, have increased due to excessive personal care product usage, which contains endocrine-disrupting chemicals (EDCs). Mammalian immune systems develop during pregnancy and after birth owing to crucial inputs from the environment. The growing incidence of autoimmune diseases (AIMDs) emphasizes the need to understand the environmental elements that play a role in their development, with the microbiome emerging as a key player. Exposure to EDCs with oxidative stress (OS) induces microbiome disruptions to promote AIMDs and negatively impacts female reproductive health and fetuses. Because the body changes in a number of ways to provide ideal conditions for fetal growth, pregnancy is a special moment in a woman's life. All microorganisms undergo changes, and their quantity and composition vary over the three trimesters of pregnancy. Recent research suggests a connection between pregnancy issues and the microorganisms present during pregnancy. This review explores the pivotal role of the human microbiome in pregnancy health, emphasizing how microbiome dynamics influence immune development and long-term immunity in offspring. It examines the impact of environmental factors, particularly EDCs, on maternal microbiota and their association with pregnancy complications such as hypertensive disorders and autoimmune diseases. The manuscript highlights current research findings and discusses potential microbiome-targeted interventions to promote maternal and fetal well-being.},
}
RevDate: 2025-11-03
CmpDate: 2025-11-03
Atopic dermatitis, primary atopic disorders, and the cutaneous microbiome: current understanding of an expanding field.
Frontiers in pediatrics, 13:1670623.
Atopic dermatitis is a common inflammatory skin disease with rapidly expanding worldwide prevalence. Increasingly, cases of severe and early-onset dermatitis have been identified and found to be due to underlying monogenic mutations, leading to immune dysregulation. These conditions, called primary atopic disorders, have become an area of extensive study over the last 30 years. Simultaneously, our understanding of the human microbiome has steadily grown, and there is clear evidence that dysbiosis plays a major role in atopic dermatitis, not only in severity of disease and as a potential trigger but also offering clues for targeted treatment strategies. Unfortunately, despite our growing understanding of the cutaneous microbiome and the expanding availability of genetic testing allowing for diagnosis of primary atopic disorders, there remains very limited understanding regarding the microbiomics changes that underlie these disorders. Here we review the current research regarding atopic dermatitis in the setting of primary atopic disorders, understanding regarding primary atopic disorders and associated cutaneous dysbiosis, and identify specific gaps in knowledge.
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@article {pmid41181176,
year = {2025},
author = {Abidov, A and Bayer, DK},
title = {Atopic dermatitis, primary atopic disorders, and the cutaneous microbiome: current understanding of an expanding field.},
journal = {Frontiers in pediatrics},
volume = {13},
number = {},
pages = {1670623},
pmid = {41181176},
issn = {2296-2360},
abstract = {Atopic dermatitis is a common inflammatory skin disease with rapidly expanding worldwide prevalence. Increasingly, cases of severe and early-onset dermatitis have been identified and found to be due to underlying monogenic mutations, leading to immune dysregulation. These conditions, called primary atopic disorders, have become an area of extensive study over the last 30 years. Simultaneously, our understanding of the human microbiome has steadily grown, and there is clear evidence that dysbiosis plays a major role in atopic dermatitis, not only in severity of disease and as a potential trigger but also offering clues for targeted treatment strategies. Unfortunately, despite our growing understanding of the cutaneous microbiome and the expanding availability of genetic testing allowing for diagnosis of primary atopic disorders, there remains very limited understanding regarding the microbiomics changes that underlie these disorders. Here we review the current research regarding atopic dermatitis in the setting of primary atopic disorders, understanding regarding primary atopic disorders and associated cutaneous dysbiosis, and identify specific gaps in knowledge.},
}
RevDate: 2025-11-02
Pushing the frontier of gut microbiome health cross-kingdom and cross-organ.
Nature reviews. Gastroenterology & hepatology [Epub ahead of print].
Additional Links: PMID-41177823
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@article {pmid41177823,
year = {2025},
author = {Zuo, T},
title = {Pushing the frontier of gut microbiome health cross-kingdom and cross-organ.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {41177823},
issn = {1759-5053},
}
RevDate: 2025-11-01
Global surge of human metapneumovirus (hMPV) and its interactions with microbiome to disease severity.
Journal of infection and public health, 19(1):103024 pii:S1876-0341(25)00373-9 [Epub ahead of print].
Human metapneumovirus (hMPV) is a significant virus of the lungs that causes diversified symptoms such as mild colds to severe pneumonia in people of all ages, especially in children, the elderly, and immunosuppressed individuals. The review highlights the global escalation of hMPV and explores how the human microbiome may shape the susceptibility of infections, immune responses and disease severity. The virus can form inclusion bodies inside the host cells and increase hMPV virulence to induce severe viral infection. hMPV also exploits immune-evasion strategy that weaken the host-body's defenses. Disturbances of gut-lung-microbiota can weaken the host immunity and worsen the disease severity. Nevertheless, intestinal microbes may promote the lung health through the compounds e.g., short-chain fatty acids. Although no particular treatment exists, there is an increasing concern in microbiome-based therapeutic approaches and personalized medicine. Understanding the microbiome interaction to hMPV may develop strategies to predict, prevent, and manage the hMPV infections.
Additional Links: PMID-41175426
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@article {pmid41175426,
year = {2025},
author = {Meher, MM and Afrin, M},
title = {Global surge of human metapneumovirus (hMPV) and its interactions with microbiome to disease severity.},
journal = {Journal of infection and public health},
volume = {19},
number = {1},
pages = {103024},
doi = {10.1016/j.jiph.2025.103024},
pmid = {41175426},
issn = {1876-035X},
abstract = {Human metapneumovirus (hMPV) is a significant virus of the lungs that causes diversified symptoms such as mild colds to severe pneumonia in people of all ages, especially in children, the elderly, and immunosuppressed individuals. The review highlights the global escalation of hMPV and explores how the human microbiome may shape the susceptibility of infections, immune responses and disease severity. The virus can form inclusion bodies inside the host cells and increase hMPV virulence to induce severe viral infection. hMPV also exploits immune-evasion strategy that weaken the host-body's defenses. Disturbances of gut-lung-microbiota can weaken the host immunity and worsen the disease severity. Nevertheless, intestinal microbes may promote the lung health through the compounds e.g., short-chain fatty acids. Although no particular treatment exists, there is an increasing concern in microbiome-based therapeutic approaches and personalized medicine. Understanding the microbiome interaction to hMPV may develop strategies to predict, prevent, and manage the hMPV infections.},
}
RevDate: 2025-10-31
PRIME: a database for 16S rRNA microbiome data with phenotypic reference and comprehensive metadata.
Nucleic acids research pii:8307359 [Epub ahead of print].
PRIME (Phenotypic Reference for Integrated Microbiome Enrichment) is a curated and standardized database of human microbiome 16S rRNA amplicon sequencing data, designed to facilitate cross-study analysis, reproducibility, and phenotype-driven discovery. PRIME aggregates 53 449 samples from 111 public studies, covering 93 body sites and 101 phenotypic categories, with detailed harmonization of sample-level metadata such as disease status, demographics, body sites, sequencing protocols, and experimental design. Each sample includes taxonomic abundance profiles generated via a consistent pipeline using both SILVA (138.2) and Greengenes2 (2024.09) reference databases, with results reported at multiple taxonomic levels as observed abundances (read counts) and relative abundances (proportions). A major strength of PRIME is its extensive manual curation, which standardizes phenotypic and contextual metadata across studies, enabling precise querying and robust phenotype-based comparisons. Users can interactively explore the database through a modern web interface, filter and visualize data by metadata fields, and download customized subsets. Programmatic access is supported via RESTful APIs and R package. PRIME aims to advance microbiome data integration and is continuously updated to incorporate new studies and features. The database is freely available at https://primedb.sjtu.edu.cn.
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@article {pmid41171140,
year = {2025},
author = {Zhang, Z and Zhao, H and Wang, T},
title = {PRIME: a database for 16S rRNA microbiome data with phenotypic reference and comprehensive metadata.},
journal = {Nucleic acids research},
volume = {},
number = {},
pages = {},
doi = {10.1093/nar/gkaf1057},
pmid = {41171140},
issn = {1362-4962},
support = {12222111//National Natural Science Foundation of China/ ; 12331009//National Natural Science Foundation of China/ ; 12571306//National Natural Science Foundation of China/ ; //Fundamental Research Funds for the Central Universities/ ; //Shanghai Jiao Tong University/ ; //National Natural Science Foundation of China/ ; },
abstract = {PRIME (Phenotypic Reference for Integrated Microbiome Enrichment) is a curated and standardized database of human microbiome 16S rRNA amplicon sequencing data, designed to facilitate cross-study analysis, reproducibility, and phenotype-driven discovery. PRIME aggregates 53 449 samples from 111 public studies, covering 93 body sites and 101 phenotypic categories, with detailed harmonization of sample-level metadata such as disease status, demographics, body sites, sequencing protocols, and experimental design. Each sample includes taxonomic abundance profiles generated via a consistent pipeline using both SILVA (138.2) and Greengenes2 (2024.09) reference databases, with results reported at multiple taxonomic levels as observed abundances (read counts) and relative abundances (proportions). A major strength of PRIME is its extensive manual curation, which standardizes phenotypic and contextual metadata across studies, enabling precise querying and robust phenotype-based comparisons. Users can interactively explore the database through a modern web interface, filter and visualize data by metadata fields, and download customized subsets. Programmatic access is supported via RESTful APIs and R package. PRIME aims to advance microbiome data integration and is continuously updated to incorporate new studies and features. The database is freely available at https://primedb.sjtu.edu.cn.},
}
RevDate: 2025-10-31
Predicting age from binarized human oral microbial data combined with an ensemble of classifiers.
mSystems [Epub ahead of print].
It is well established that the composition of the human microbiome changes with age; however, limited research has explored the association between the oral microbiome and aging, as well as its potential for age prediction. In this study, we investigated the correlation between the oral microbiome and age by analyzing samples from 150 individuals across a wide age range (6-78 years). The observed species richness and Chao1 index significantly increased with age. Permutational multivariate analysis of variance (PERMANOVA), using both Bray-Curtis and Jaccard distances, identified age as a major factor influencing microbial variation. After a comprehensive comparison of four different oral microbiome data processing approaches, we then developed an ensemble model based on binarized oral microbial data, incorporating an eXtreme Gradient Boosting (XGBoost) algorithm with 32 classifiers. This ensemble model achieved a mean absolute error (MAE) of 7.20 years in the independent validation set (n = 15) and 4.33 years in the 20-59 age subgroup (n = 12), significantly outperforming traditional models. When the sample size increased to 2,550, the MAE in the independent validation set (n = 255) was reduced to 4.80 years, with the 20-59 age subgroup (n = 232) achieving an MAE of 3.76 years, highlighting its generalizability and robustness. Additionally, compared to the previously published model for age prediction based on oral microbiome, our model demonstrated significantly superior performance. These findings support the potential of integrating binarized microbial data with ensemble modeling as a promising direction for human age prediction based on the microbiome.IMPORTANCEPERMANOVA analysis with Jaccard distances revealed age as a major determinant of variation in microbial composition, highlighting the potential of binarized oral microbial data as a novel predictor for human age prediction. Furthermore, we developed an ensemble model combining an XGBoost algorithm and 32 classifiers to predict age from binarized oral microbial data. The model achieved an MAE of 7.20 years in the independent validation set (n = 15) and 4.33 years in the 20-59 age subgroup (n = 12). When applied to predict age in 2,550 samples from previous studies, the ensemble model outperformed the prior model, achieving an MAE of 4.44 years compared to the previous model's 4.94 years. These findings demonstrate that binarized oral microbial data, along with the ensemble model we developed, can effectively predict human age and provide a solid foundation for future age-related research.
Additional Links: PMID-41171074
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@article {pmid41171074,
year = {2025},
author = {Zhou, Y and Wang, Y and Xiao, B and Wang, S and Zhang, Z and Wang, X and Liu, B and Yang, Y and Wang, C and Zhou, C and Liao, M and Song, F and Luo, H},
title = {Predicting age from binarized human oral microbial data combined with an ensemble of classifiers.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0118225},
doi = {10.1128/msystems.01182-25},
pmid = {41171074},
issn = {2379-5077},
abstract = {It is well established that the composition of the human microbiome changes with age; however, limited research has explored the association between the oral microbiome and aging, as well as its potential for age prediction. In this study, we investigated the correlation between the oral microbiome and age by analyzing samples from 150 individuals across a wide age range (6-78 years). The observed species richness and Chao1 index significantly increased with age. Permutational multivariate analysis of variance (PERMANOVA), using both Bray-Curtis and Jaccard distances, identified age as a major factor influencing microbial variation. After a comprehensive comparison of four different oral microbiome data processing approaches, we then developed an ensemble model based on binarized oral microbial data, incorporating an eXtreme Gradient Boosting (XGBoost) algorithm with 32 classifiers. This ensemble model achieved a mean absolute error (MAE) of 7.20 years in the independent validation set (n = 15) and 4.33 years in the 20-59 age subgroup (n = 12), significantly outperforming traditional models. When the sample size increased to 2,550, the MAE in the independent validation set (n = 255) was reduced to 4.80 years, with the 20-59 age subgroup (n = 232) achieving an MAE of 3.76 years, highlighting its generalizability and robustness. Additionally, compared to the previously published model for age prediction based on oral microbiome, our model demonstrated significantly superior performance. These findings support the potential of integrating binarized microbial data with ensemble modeling as a promising direction for human age prediction based on the microbiome.IMPORTANCEPERMANOVA analysis with Jaccard distances revealed age as a major determinant of variation in microbial composition, highlighting the potential of binarized oral microbial data as a novel predictor for human age prediction. Furthermore, we developed an ensemble model combining an XGBoost algorithm and 32 classifiers to predict age from binarized oral microbial data. The model achieved an MAE of 7.20 years in the independent validation set (n = 15) and 4.33 years in the 20-59 age subgroup (n = 12). When applied to predict age in 2,550 samples from previous studies, the ensemble model outperformed the prior model, achieving an MAE of 4.44 years compared to the previous model's 4.94 years. These findings demonstrate that binarized oral microbial data, along with the ensemble model we developed, can effectively predict human age and provide a solid foundation for future age-related research.},
}
RevDate: 2025-10-30
Host-specific bacterial modulation of airway gene expression and alternative splicing.
mSphere [Epub ahead of print].
The human microbiome varies extensively between individuals. While there are numerous studies investigating the effects of inter-individual differences on microbiome composition, there are few studies investigating inter-individual effects on microbial modulation of the host or host-specific effects. To address this knowledge gap, we colonized human bronchial epithelial air-liquid interface tissue cultures generated from six different adults with one of three phylogenetically diverse bacteria and compared how each microbe differentially modulated host gene expression in each of the six donors. Microbial treatment had the strongest effect on transcription, followed by donor-specific effects. Gene pathways differed markedly in their donor and microbe specificity; interferon expression was highly donor-dependent, while transcription of epithelial barrier and antibacterial innate immunity genes was predominantly microbially driven. Moreover, we evaluated whether microbial regulation of alternative splicing was modulated by the donor. Strikingly, we found significant nonredundant, donor-specific regulation of alternative splicing exclusively in the gram-positive commensal microbes. These findings highlight that microbial effects on the human airway epithelium are not only species-specific but also deeply individualized, underscoring the importance of the host context in shaping microbe-induced transcriptional and splicing responses.IMPORTANCEMicrobiota are integral regulators of host gene expression, utilizing diverse mechanisms that are shaped by the interplay between microbiome composition and inter-individual differences, i.e., host-specific factors. While previous studies have characterized inter-individual variation in microbiome composition and the effects of variable microbiome composition on the host, the extent to which host-specificity itself regulates host-microbe interactions remains poorly understood. In this study, we address this gap by characterizing changes in epithelial gene expression from six different human donors following colonization with one of three phylogenetically diverse bacteria. By systematically comparing donor-specific responses, we demonstrate that host specificity is a key determinant of the host transcriptional response to microbial colonization. Importantly, we demonstrate that the effects of host specificity are not uniform, but instead are dependent on the colonizing microbe. Our findings underscore the complexity of host-microbe relationships and establish host specificity as a significant factor shaping host-microbe interactions.
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@article {pmid41165334,
year = {2025},
author = {Horvath, M and Kang, HG and Wu, T-C and Aiken, E and Castaneda, DC and Akkurt, S and Marches, F and Anczuków, O and Palucka, K and Oh, J},
title = {Host-specific bacterial modulation of airway gene expression and alternative splicing.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0057725},
doi = {10.1128/msphere.00577-25},
pmid = {41165334},
issn = {2379-5042},
abstract = {The human microbiome varies extensively between individuals. While there are numerous studies investigating the effects of inter-individual differences on microbiome composition, there are few studies investigating inter-individual effects on microbial modulation of the host or host-specific effects. To address this knowledge gap, we colonized human bronchial epithelial air-liquid interface tissue cultures generated from six different adults with one of three phylogenetically diverse bacteria and compared how each microbe differentially modulated host gene expression in each of the six donors. Microbial treatment had the strongest effect on transcription, followed by donor-specific effects. Gene pathways differed markedly in their donor and microbe specificity; interferon expression was highly donor-dependent, while transcription of epithelial barrier and antibacterial innate immunity genes was predominantly microbially driven. Moreover, we evaluated whether microbial regulation of alternative splicing was modulated by the donor. Strikingly, we found significant nonredundant, donor-specific regulation of alternative splicing exclusively in the gram-positive commensal microbes. These findings highlight that microbial effects on the human airway epithelium are not only species-specific but also deeply individualized, underscoring the importance of the host context in shaping microbe-induced transcriptional and splicing responses.IMPORTANCEMicrobiota are integral regulators of host gene expression, utilizing diverse mechanisms that are shaped by the interplay between microbiome composition and inter-individual differences, i.e., host-specific factors. While previous studies have characterized inter-individual variation in microbiome composition and the effects of variable microbiome composition on the host, the extent to which host-specificity itself regulates host-microbe interactions remains poorly understood. In this study, we address this gap by characterizing changes in epithelial gene expression from six different human donors following colonization with one of three phylogenetically diverse bacteria. By systematically comparing donor-specific responses, we demonstrate that host specificity is a key determinant of the host transcriptional response to microbial colonization. Importantly, we demonstrate that the effects of host specificity are not uniform, but instead are dependent on the colonizing microbe. Our findings underscore the complexity of host-microbe relationships and establish host specificity as a significant factor shaping host-microbe interactions.},
}
RevDate: 2025-10-30
CmpDate: 2025-10-30
Sparse Canonical Correlation Analysis for Multiple Measurements With Latent Trajectories.
Biometrical journal. Biometrische Zeitschrift, 67(6):e70090.
Canonical correlation analysis (CCA) is a widely used multivariate method in omics research for integrating high-dimensional datasets. CCA identifies hidden links by deriving linear projections of observed features that maximally correlate datasets. An important requirement of standard CCA is that observations are independent of each other. As a result, it cannot properly deal with repeated measurements. Current CCA extensions dealing with these challenges either perform CCA on summarized data or estimate correlations for each measurement. While these techniques factor in the correlation between measurements, they are suboptimal for high-dimensional analysis and exploiting this data's longitudinal qualities. We propose a novel extension of sparse CCA that incorporates time dynamics at the latent variable level through longitudinal models. This approach addresses the correlation of repeated measurements while drawing latent paths, focusing on dynamics in the correlation structures. To aid interpretability and computational efficiency, we implement an ℓ 0 $\ell _0$ penalty to enforce fixed sparsity levels. We estimate these trajectories fitting longitudinal models to the low-dimensional latent variables, leveraging the clustered structure of high-dimensional datasets, thus exploring shared longitudinal latent mechanisms. Furthermore, modeling time in the latent space significantly reduces computational burden. We validate our model's performance using simulated data and show its real-world applicability with data from the Human Microbiome Project. This application highlights the model's ability to handle high-dimensional, sparsely, and irregularly observed data. Our CCA method for repeated measurements enables efficient estimation of canonical correlations across measurements for clustered data. Compared to existing methods, ours substantially reduces computational time in high-dimensional analyses as well as provides longitudinal trajectories that yield interpretable and insightful results.
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@article {pmid41165062,
year = {2025},
author = {Senar, N and Zwinderman, AH and Hof, MH},
title = {Sparse Canonical Correlation Analysis for Multiple Measurements With Latent Trajectories.},
journal = {Biometrical journal. Biometrische Zeitschrift},
volume = {67},
number = {6},
pages = {e70090},
doi = {10.1002/bimj.70090},
pmid = {41165062},
issn = {1521-4036},
mesh = {*Biometry/methods ; Humans ; Correlation of Data ; Models, Statistical ; },
abstract = {Canonical correlation analysis (CCA) is a widely used multivariate method in omics research for integrating high-dimensional datasets. CCA identifies hidden links by deriving linear projections of observed features that maximally correlate datasets. An important requirement of standard CCA is that observations are independent of each other. As a result, it cannot properly deal with repeated measurements. Current CCA extensions dealing with these challenges either perform CCA on summarized data or estimate correlations for each measurement. While these techniques factor in the correlation between measurements, they are suboptimal for high-dimensional analysis and exploiting this data's longitudinal qualities. We propose a novel extension of sparse CCA that incorporates time dynamics at the latent variable level through longitudinal models. This approach addresses the correlation of repeated measurements while drawing latent paths, focusing on dynamics in the correlation structures. To aid interpretability and computational efficiency, we implement an ℓ 0 $\ell _0$ penalty to enforce fixed sparsity levels. We estimate these trajectories fitting longitudinal models to the low-dimensional latent variables, leveraging the clustered structure of high-dimensional datasets, thus exploring shared longitudinal latent mechanisms. Furthermore, modeling time in the latent space significantly reduces computational burden. We validate our model's performance using simulated data and show its real-world applicability with data from the Human Microbiome Project. This application highlights the model's ability to handle high-dimensional, sparsely, and irregularly observed data. Our CCA method for repeated measurements enables efficient estimation of canonical correlations across measurements for clustered data. Compared to existing methods, ours substantially reduces computational time in high-dimensional analyses as well as provides longitudinal trajectories that yield interpretable and insightful results.},
}
MeSH Terms:
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*Biometry/methods
Humans
Correlation of Data
Models, Statistical
RevDate: 2025-10-30
CmpDate: 2025-10-30
The role of gut mycobiome in responses to cancer immunotherapy.
Gut microbes, 17(1):2571433.
The gut microbiome has emerged as an important modulator of cancer progression and therapy response, yet the role of its fungal component, the gut mycobiome, remains poorly understood. In this review, we summarize current knowledge on the relationship between intestinal fungi and cancer, with a particular focus on the potential influence of the gut mycobiome on the efficacy of immune checkpoint inhibitors (ICIs). Drawing from both human studies and preclinical models, we discuss evidence linking fungal dysbiosis to altered immune responses and therapy outcomes in cancer patients. Specific fungal taxa, such as Candida and Malassezia, have been associated with changes in the tumor microenvironment and modulation of host immunity. We also review the proposed mechanisms through which fungi may impact antitumor immunity, including interactions with immune receptors and production of bioactive metabolites. Although research in this field is still in its early stages, emerging data suggest that the gut mycobiome may serve as a biomarker for immunotherapy response and a potential target for therapeutic intervention. A better understanding of host-fungus interactions in the gut could contribute to the development of personalized strategies to improve the effectiveness and safety of cancer immunotherapy.
Additional Links: PMID-41163402
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PubMed:
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@article {pmid41163402,
year = {2025},
author = {Szóstak, N and Kozłowski, P and Zuo, T and Philips, A},
title = {The role of gut mycobiome in responses to cancer immunotherapy.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2571433},
doi = {10.1080/19490976.2025.2571433},
pmid = {41163402},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Mycobiome ; *Neoplasms/therapy/immunology/microbiology ; *Immunotherapy ; Animals ; Tumor Microenvironment/immunology ; *Fungi/classification/immunology ; Dysbiosis/microbiology/immunology ; Immune Checkpoint Inhibitors/therapeutic use ; },
abstract = {The gut microbiome has emerged as an important modulator of cancer progression and therapy response, yet the role of its fungal component, the gut mycobiome, remains poorly understood. In this review, we summarize current knowledge on the relationship between intestinal fungi and cancer, with a particular focus on the potential influence of the gut mycobiome on the efficacy of immune checkpoint inhibitors (ICIs). Drawing from both human studies and preclinical models, we discuss evidence linking fungal dysbiosis to altered immune responses and therapy outcomes in cancer patients. Specific fungal taxa, such as Candida and Malassezia, have been associated with changes in the tumor microenvironment and modulation of host immunity. We also review the proposed mechanisms through which fungi may impact antitumor immunity, including interactions with immune receptors and production of bioactive metabolites. Although research in this field is still in its early stages, emerging data suggest that the gut mycobiome may serve as a biomarker for immunotherapy response and a potential target for therapeutic intervention. A better understanding of host-fungus interactions in the gut could contribute to the development of personalized strategies to improve the effectiveness and safety of cancer immunotherapy.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Gastrointestinal Microbiome/immunology
*Mycobiome
*Neoplasms/therapy/immunology/microbiology
*Immunotherapy
Animals
Tumor Microenvironment/immunology
*Fungi/classification/immunology
Dysbiosis/microbiology/immunology
Immune Checkpoint Inhibitors/therapeutic use
RevDate: 2025-10-30
CmpDate: 2025-10-30
Peculiarities of vaginal microbiota in perimenopausal and postmenopausal women with type 2 diabetes mellitus.
Annals of clinical microbiology and antimicrobials, 24(1):59.
BACKGROUND: The changes in the vaginal microbiota and potential dysbiosis adjustment strategies in diabetic patients remain inconclusive. This study was designed to investigate the impact of Type 2 diabetes mellitus (T2DM) on the ecological dynamics of the vaginal microbiota in perimenopausal and postmenopausal women, with a focus on microbial community structure and functional homeostasis.
METHODS: Vaginal secretion samples from 22 T2DM patients (DM group) and 23 healthy controls (CT group) under perimenopausal and postmenopausal conditions were analyzed via metagenomic sequencing. Alpha diversity (Observe, ACE, Shannon-Weaver, Gini-Simpson indices) and beta diversity (PCoA, NMDS) were assessed. Taxonomic profiling, LEfSe analysis, and co-occurrence network construction were performed to identify differential species and microbial interactions. Neutral community modeling evaluated stochastic vs. deterministic assembly processes.
RESULTS: No significant differences were observed in age (62.22 ± 5.74 vs. 58.23 ± 7.55, p = 0.052) or perimenopausal/ postmenopausal status (3/19 vs. 5/18, p = 0.748) between the DM and CT groups. The DM group exhibited significantly higher alpha diversity (p < 0.05) and distinct beta diversity clustering (p < 0.05), marked by reduced Lactobacillus relative abundance (28.7% in CT vs. 6.3% in DM) and increased abundance of opportunistic pathogenic genera (Klebsiella, Gardnerella, Staphylococcus). LEfSe identified Firmicutes as CT biomarkers, while the relative abundance of Bacteroidetes and Prevotella increased in DM group. Both fasting blood glucose and HbA1c levels significantly influenced the relative abundance of vaginal Lactobacillus crispatus, Lactobacillus gasseri, and Lactobacillus iners, showing a significant negative correlation. Co-occurrence networks revealed greater complexity and more integrated in the DM group (more triangles, lower modularity, higher node degrees, higher clustering coefficients, p < 0.0001). Neutral modeling indicated stochastic assembly (R² >0.5), with Lactobacillus species and opportunistic pathogens deviating from neutral predictions in DM.
CONCLUSION: Under perimenopausal and postmenopausal conditions, T2DM disrupts vaginal microbiota homeostasis by diminishing protective Lactobacillus populations and promoting pathogen proliferation.
Additional Links: PMID-41163171
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Citation:
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@article {pmid41163171,
year = {2025},
author = {Qiu, X and Zhang, M and Zhang, L and Chen, H and Gao, M and Li, W and Yu, Z and Hou, Z},
title = {Peculiarities of vaginal microbiota in perimenopausal and postmenopausal women with type 2 diabetes mellitus.},
journal = {Annals of clinical microbiology and antimicrobials},
volume = {24},
number = {1},
pages = {59},
pmid = {41163171},
issn = {1476-0711},
support = {H2020206490//Natural Science Foundation of Hebei Province,China/ ; 20230095//Medical Science Research Subject Plan of Hebei/ ; PD2023002//Clinical Medicine Postdoctoral Research Support Program of Hebei Medical University/ ; B2024003014//Hebei Province Yanzhao Golden Talent Program/ ; 2024YFC2510600//Key R&D Program of the China Ministry of Science and Technology/ ; },
mesh = {Humans ; Female ; *Vagina/microbiology ; *Diabetes Mellitus, Type 2/microbiology ; Middle Aged ; *Postmenopause ; *Microbiota ; *Perimenopause ; Aged ; *Bacteria/classification/genetics/isolation & purification ; Metagenomics ; Dysbiosis/microbiology ; },
abstract = {BACKGROUND: The changes in the vaginal microbiota and potential dysbiosis adjustment strategies in diabetic patients remain inconclusive. This study was designed to investigate the impact of Type 2 diabetes mellitus (T2DM) on the ecological dynamics of the vaginal microbiota in perimenopausal and postmenopausal women, with a focus on microbial community structure and functional homeostasis.
METHODS: Vaginal secretion samples from 22 T2DM patients (DM group) and 23 healthy controls (CT group) under perimenopausal and postmenopausal conditions were analyzed via metagenomic sequencing. Alpha diversity (Observe, ACE, Shannon-Weaver, Gini-Simpson indices) and beta diversity (PCoA, NMDS) were assessed. Taxonomic profiling, LEfSe analysis, and co-occurrence network construction were performed to identify differential species and microbial interactions. Neutral community modeling evaluated stochastic vs. deterministic assembly processes.
RESULTS: No significant differences were observed in age (62.22 ± 5.74 vs. 58.23 ± 7.55, p = 0.052) or perimenopausal/ postmenopausal status (3/19 vs. 5/18, p = 0.748) between the DM and CT groups. The DM group exhibited significantly higher alpha diversity (p < 0.05) and distinct beta diversity clustering (p < 0.05), marked by reduced Lactobacillus relative abundance (28.7% in CT vs. 6.3% in DM) and increased abundance of opportunistic pathogenic genera (Klebsiella, Gardnerella, Staphylococcus). LEfSe identified Firmicutes as CT biomarkers, while the relative abundance of Bacteroidetes and Prevotella increased in DM group. Both fasting blood glucose and HbA1c levels significantly influenced the relative abundance of vaginal Lactobacillus crispatus, Lactobacillus gasseri, and Lactobacillus iners, showing a significant negative correlation. Co-occurrence networks revealed greater complexity and more integrated in the DM group (more triangles, lower modularity, higher node degrees, higher clustering coefficients, p < 0.0001). Neutral modeling indicated stochastic assembly (R² >0.5), with Lactobacillus species and opportunistic pathogens deviating from neutral predictions in DM.
CONCLUSION: Under perimenopausal and postmenopausal conditions, T2DM disrupts vaginal microbiota homeostasis by diminishing protective Lactobacillus populations and promoting pathogen proliferation.},
}
MeSH Terms:
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Humans
Female
*Vagina/microbiology
*Diabetes Mellitus, Type 2/microbiology
Middle Aged
*Postmenopause
*Microbiota
*Perimenopause
Aged
*Bacteria/classification/genetics/isolation & purification
Metagenomics
Dysbiosis/microbiology
RevDate: 2025-10-30
CmpDate: 2025-10-30
Comprehensive multi omics explore the microbial function in metabolic pathway flow during altered diet.
NPJ science of food, 9(1):212.
High-protein diet (HPD) and high-fiber diet (HFiD) are two common types of diet, and the transition from HPD to HFiD frequently happens in people who perform diet control. Gut microbiota provide a bridge between diet and health. However, most of the research left out the metabolic landscape change and gut microbial influence under this kind of altered diet. Here, we examined gut microbiome and metabolites change using multi-omics (16S rRNA gene sequencing, shotgun metagenomics, LC-MS/MS metabolomics), and machine-learning methods were introduced to capture the response of gut microbiota to altered diet and associate the variable metabolites and microbial factors. The results suggest that the conversion from HPD to HFiD improves the gut microbial diversity and promotes the pathways of tryptophan, galactose, fructose, and mannose metabolism, which are associated with different gut microbiota and special metabolites. Among them, Faecalibacterium rodentium and Akkermansia muciniphila indicate potential roles in the multi-metabolism. Although these findings are exploratory and hypothesis-generating, they provide a foundation for future mechanistic investigations and emphasize the importance of diverse diets.
Additional Links: PMID-41162426
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Citation:
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@article {pmid41162426,
year = {2025},
author = {Zhao, Y and Yao, S and Umar, A and Huang, J and Chen, S and Yu, Z},
title = {Comprehensive multi omics explore the microbial function in metabolic pathway flow during altered diet.},
journal = {NPJ science of food},
volume = {9},
number = {1},
pages = {212},
pmid = {41162426},
issn = {2396-8370},
support = {82270564//National Natural Science Foundation of China/ ; 32170071//National Natural Science Foundation of China/ ; 2022JJ30916//Natural Science Foundation of Hunan Province/ ; 2022M713521//China Postdoctoral Science Foundation/ ; 2023CXQD059//Central South University Innovation-Driven Research Programme/ ; },
abstract = {High-protein diet (HPD) and high-fiber diet (HFiD) are two common types of diet, and the transition from HPD to HFiD frequently happens in people who perform diet control. Gut microbiota provide a bridge between diet and health. However, most of the research left out the metabolic landscape change and gut microbial influence under this kind of altered diet. Here, we examined gut microbiome and metabolites change using multi-omics (16S rRNA gene sequencing, shotgun metagenomics, LC-MS/MS metabolomics), and machine-learning methods were introduced to capture the response of gut microbiota to altered diet and associate the variable metabolites and microbial factors. The results suggest that the conversion from HPD to HFiD improves the gut microbial diversity and promotes the pathways of tryptophan, galactose, fructose, and mannose metabolism, which are associated with different gut microbiota and special metabolites. Among them, Faecalibacterium rodentium and Akkermansia muciniphila indicate potential roles in the multi-metabolism. Although these findings are exploratory and hypothesis-generating, they provide a foundation for future mechanistic investigations and emphasize the importance of diverse diets.},
}
RevDate: 2025-10-30
CmpDate: 2025-10-30
Microbiome and well-being: a meta-analysis.
NPJ biofilms and microbiomes, 11(1):201.
The human microbiome may play a significant role in both health and disease. However, most studies to date have focused on the microbiome's role in pathogenesis, while its potential role in promoting well-being remains underexplored. We conducted the first meta-analysis synthesizing empirical evidence on associations between the human microbiome and psychological well-being. Based on eight analyzed studies (N = 2526 participants), we found that both microbial diversity and taxonomic abundance were positively associated with psychological well-being, with diversity emerging as the stronger predictor. Notably, these associations appeared consistent across sex and age. This study provides preliminary evidence that microbiome composition may support salutogenic processes and offers a foundation for future integration of microbiome science into psychological and clinical interventions. However, given the small number of empirical studies included in the meta-analysis, the generalizability of these findings remains limited. Further research is required to strengthen and refine our understanding of the microbiome-well-being relationship.
Additional Links: PMID-41162403
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Citation:
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@article {pmid41162403,
year = {2025},
author = {Kowal, M and Sorokowski, P and David, O and Iuga, IA and Renwick, S and Sorokowska, A},
title = {Microbiome and well-being: a meta-analysis.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {201},
pmid = {41162403},
issn = {2055-5008},
support = {PNRR-III-C9-2023-I8-CF 32/28.07.2023//European Union/ ; PNRR-III-C9-2023-I8-CF 32/28.07.2023//European Union/ ; PNRR-III-C9-2023-I8-CF 32/28.07.2023//European Union/ ; PNRR-III-C9-2023-I8-CF 32/28.07.2023//European Union/ ; PNRR-III-C9-2023-I8-CF 32/28.07.2023//European Union/ ; },
mesh = {Humans ; *Microbiota ; Male ; Female ; *Bacteria/classification/genetics/isolation & purification ; *Mental Health ; },
abstract = {The human microbiome may play a significant role in both health and disease. However, most studies to date have focused on the microbiome's role in pathogenesis, while its potential role in promoting well-being remains underexplored. We conducted the first meta-analysis synthesizing empirical evidence on associations between the human microbiome and psychological well-being. Based on eight analyzed studies (N = 2526 participants), we found that both microbial diversity and taxonomic abundance were positively associated with psychological well-being, with diversity emerging as the stronger predictor. Notably, these associations appeared consistent across sex and age. This study provides preliminary evidence that microbiome composition may support salutogenic processes and offers a foundation for future integration of microbiome science into psychological and clinical interventions. However, given the small number of empirical studies included in the meta-analysis, the generalizability of these findings remains limited. Further research is required to strengthen and refine our understanding of the microbiome-well-being relationship.},
}
MeSH Terms:
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Humans
*Microbiota
Male
Female
*Bacteria/classification/genetics/isolation & purification
*Mental Health
RevDate: 2025-10-29
CmpDate: 2025-10-29
In Vivo Therapeutic Potential of Next-Generation Probiotic Akkermansia muciniphila and Butyrate Combination Therapy in Diabetes.
Journal of microbiology and biotechnology, 35:e2506025 pii:jmb.2506.06025.
Recent studies have found that gut microbiota is closely related to the initiation and progression of T1DM. This study aimed to examine the effects of sodium butyrate and Akkermansia muciniphila (AKK), both individually and combined, on T1DM models. To optimize a T1DM model, a single high dose of streptozotocin (STZ) was administered to C57BL/6J mice to determine the appropriate dose (150 mg/kg). Mice were divided into four groups: a control group, a diabetic group, a diabetic group treated with butyrate, and a diabetic group treated with AKK. The groups treated with butyrate and AKK reduced blood glucose levels, prevented body weight loss, and normalized food and water intake. To explore the synergistic effects of AKK and butyric acid, Sprague-Dawley (SD) rats were assigned to control, diabetic, and treatment groups including butyrate, AKK, and combination therapy. Two weeks of oral treatment showed improved metabolic parameters in the treatment groups. The combination therapy exhibited the most improvements. In the in vitro experiment, the cytotoxic effects of STZ on 3T3-L1 cells treated with both AKK and butyric acid were measured, indicating their protective effects on cell viability. GC-MS/MS analysis was also performed to assess changes and correlations in systemic short-chain fatty acids (SCFAs). SCFAs were significantly increased in the liver after probiotic treatment, especially in the combination therapy group. These findings demonstrate the microbiota-regulating and therapeutic effects of AKK and butyrate, particularly highlighting the potential of combination therapy as an alternative to standard diabetic treatments.
Additional Links: PMID-41162165
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PubMed:
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@article {pmid41162165,
year = {2025},
author = {Ghorbanian, F and Seo, H and Sarafraz, F and Atashi, A and Shuvo, MSH and Chae-Eun, P and Hossain, MS and Tajdozian, H and Kim, S and Song, HY and Yang, H},
title = {In Vivo Therapeutic Potential of Next-Generation Probiotic Akkermansia muciniphila and Butyrate Combination Therapy in Diabetes.},
journal = {Journal of microbiology and biotechnology},
volume = {35},
number = {},
pages = {e2506025},
doi = {10.4014/jmb.2506.06025},
pmid = {41162165},
issn = {1738-8872},
mesh = {Animals ; *Probiotics/administration & dosage/therapeutic use ; *Diabetes Mellitus, Experimental/therapy/drug therapy ; Mice ; Rats, Sprague-Dawley ; Mice, Inbred C57BL ; Rats ; Male ; Blood Glucose/drug effects ; Gastrointestinal Microbiome/drug effects ; *Butyrates/therapeutic use/administration & dosage ; *Butyric Acid/therapeutic use/administration & dosage ; Akkermansia ; Streptozocin ; },
abstract = {Recent studies have found that gut microbiota is closely related to the initiation and progression of T1DM. This study aimed to examine the effects of sodium butyrate and Akkermansia muciniphila (AKK), both individually and combined, on T1DM models. To optimize a T1DM model, a single high dose of streptozotocin (STZ) was administered to C57BL/6J mice to determine the appropriate dose (150 mg/kg). Mice were divided into four groups: a control group, a diabetic group, a diabetic group treated with butyrate, and a diabetic group treated with AKK. The groups treated with butyrate and AKK reduced blood glucose levels, prevented body weight loss, and normalized food and water intake. To explore the synergistic effects of AKK and butyric acid, Sprague-Dawley (SD) rats were assigned to control, diabetic, and treatment groups including butyrate, AKK, and combination therapy. Two weeks of oral treatment showed improved metabolic parameters in the treatment groups. The combination therapy exhibited the most improvements. In the in vitro experiment, the cytotoxic effects of STZ on 3T3-L1 cells treated with both AKK and butyric acid were measured, indicating their protective effects on cell viability. GC-MS/MS analysis was also performed to assess changes and correlations in systemic short-chain fatty acids (SCFAs). SCFAs were significantly increased in the liver after probiotic treatment, especially in the combination therapy group. These findings demonstrate the microbiota-regulating and therapeutic effects of AKK and butyrate, particularly highlighting the potential of combination therapy as an alternative to standard diabetic treatments.},
}
MeSH Terms:
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Animals
*Probiotics/administration & dosage/therapeutic use
*Diabetes Mellitus, Experimental/therapy/drug therapy
Mice
Rats, Sprague-Dawley
Mice, Inbred C57BL
Rats
Male
Blood Glucose/drug effects
Gastrointestinal Microbiome/drug effects
*Butyrates/therapeutic use/administration & dosage
*Butyric Acid/therapeutic use/administration & dosage
Akkermansia
Streptozocin
RevDate: 2025-10-29
Long-term neutralization capacity of vaccine and breakthrough infection induced SARS-CoV-2 specific antibodies against omicron subvariants BA.2, XBB.1.5, and JN.1.
Vaccine, 68:127894 pii:S0264-410X(25)01191-0 [Epub ahead of print].
The long-term effectiveness of COVID-19 vaccines remains a critical area of study, especially with the emergence of new SARS-CoV-2 subvariants. In this study, we investigated the long-term neutralization capacity of SARS-CoV-2 -specific antibodies induced by the third, fourth and fifth vaccine doses, and by SARS-CoV-2 breakthrough infections. Spike (S)-specific antibodies decline relatively rapidly after each vaccine dose, with an estimated half-life of 3-4 months. However, after the third vaccine dose, S-specific serum antibody levels remained comparable at 12 and 24 months post-vaccination. Antibody levels induced by the fourth and fifth vaccine doses were higher, and the decay was slower than after the third vaccine dose. Additionally, nucleocapsid (N)-specific antibody levels increased significantly following multiple breakthrough infections. The neutralization capacity of the antibodies against Omicron XBB.1.5 and JN.1 subvariants were significantly increased by the fifth, XBB.1.5 subvariant specific, mRNA vaccine dose. Our findings strongly indicate that updated booster vaccines based on the latest s of concern are necessary to sustain high neutralizing antibody levels against emerging variants. No exhaustion of vaccine-induced antibody response was observed after repeated COVID-19 vaccinations.
Additional Links: PMID-41161045
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PubMed:
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@article {pmid41161045,
year = {2025},
author = {Reinholm, A and Khan, H and Laakso, T and Maljanen, S and Jalkanen, P and Gunell, M and Kallonen, T and Österlund, P and Ritvos, O and Nousiainen, A and Häkkinen, HK and Pakkanen, SH and Välimaa, H and Kantele, A and Lempainen, J and Julkunen, I and Kolehmainen, P and Kakkola, L},
title = {Long-term neutralization capacity of vaccine and breakthrough infection induced SARS-CoV-2 specific antibodies against omicron subvariants BA.2, XBB.1.5, and JN.1.},
journal = {Vaccine},
volume = {68},
number = {},
pages = {127894},
doi = {10.1016/j.vaccine.2025.127894},
pmid = {41161045},
issn = {1873-2518},
abstract = {The long-term effectiveness of COVID-19 vaccines remains a critical area of study, especially with the emergence of new SARS-CoV-2 subvariants. In this study, we investigated the long-term neutralization capacity of SARS-CoV-2 -specific antibodies induced by the third, fourth and fifth vaccine doses, and by SARS-CoV-2 breakthrough infections. Spike (S)-specific antibodies decline relatively rapidly after each vaccine dose, with an estimated half-life of 3-4 months. However, after the third vaccine dose, S-specific serum antibody levels remained comparable at 12 and 24 months post-vaccination. Antibody levels induced by the fourth and fifth vaccine doses were higher, and the decay was slower than after the third vaccine dose. Additionally, nucleocapsid (N)-specific antibody levels increased significantly following multiple breakthrough infections. The neutralization capacity of the antibodies against Omicron XBB.1.5 and JN.1 subvariants were significantly increased by the fifth, XBB.1.5 subvariant specific, mRNA vaccine dose. Our findings strongly indicate that updated booster vaccines based on the latest s of concern are necessary to sustain high neutralizing antibody levels against emerging variants. No exhaustion of vaccine-induced antibody response was observed after repeated COVID-19 vaccinations.},
}
RevDate: 2025-10-29
CmpDate: 2025-10-29
Legends, dogmas, presumptions, and demystifications in antibiotic therapy.
Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia, 38 Suppl 1:70-79.
Suboptimal antimicrobial use is a global challenge driven by entrenched misconceptions and dogmas. This article aims to critically evaluate and debunk several widespread myths in infectious disease management that lead to overdiagnosis and overtreatment. Through a nonsystematic literature review, this manuscript examines key misconceptions across various aspects of antimicrobial therapy, including administration routes, drug mechanisms, treatment duration, and the interplay with infection source control. It also explores the influence of evolving concepts like long-acting antimicrobials and the human microbiome. We challenge the dogmas that intravenous antibiotics are superior to oral agents, that longer courses are always better, and that bactericidal drugs are more effective than bacteriostatic ones. The review highlights the paramount importance of source control and surgical intervention in treating severe infections and cautions against misinformation surrounding the human microbiome. The medical community must critically re-evaluate long-standing clinical practices to improve antibiotic stewardship. By debunking these myths, we can promote a more precise, safe, and effective approach to antimicrobial use, ultimately reducing unnecessary prescribing and combating antimicrobial resistance.
Additional Links: PMID-41159234
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PubMed:
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@article {pmid41159234,
year = {2025},
author = {Blanes Hernández, R and de Cossio Tejido, S and Puchades Gimeno, F and García-Bustos, V and Salavert Lletí, M},
title = {Legends, dogmas, presumptions, and demystifications in antibiotic therapy.},
journal = {Revista espanola de quimioterapia : publicacion oficial de la Sociedad Espanola de Quimioterapia},
volume = {38 Suppl 1},
number = {},
pages = {70-79},
doi = {10.37201/req/s01.11.2025},
pmid = {41159234},
issn = {1988-9518},
mesh = {Humans ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; Antimicrobial Stewardship ; Inappropriate Prescribing ; },
abstract = {Suboptimal antimicrobial use is a global challenge driven by entrenched misconceptions and dogmas. This article aims to critically evaluate and debunk several widespread myths in infectious disease management that lead to overdiagnosis and overtreatment. Through a nonsystematic literature review, this manuscript examines key misconceptions across various aspects of antimicrobial therapy, including administration routes, drug mechanisms, treatment duration, and the interplay with infection source control. It also explores the influence of evolving concepts like long-acting antimicrobials and the human microbiome. We challenge the dogmas that intravenous antibiotics are superior to oral agents, that longer courses are always better, and that bactericidal drugs are more effective than bacteriostatic ones. The review highlights the paramount importance of source control and surgical intervention in treating severe infections and cautions against misinformation surrounding the human microbiome. The medical community must critically re-evaluate long-standing clinical practices to improve antibiotic stewardship. By debunking these myths, we can promote a more precise, safe, and effective approach to antimicrobial use, ultimately reducing unnecessary prescribing and combating antimicrobial resistance.},
}
MeSH Terms:
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Humans
*Anti-Bacterial Agents/therapeutic use/administration & dosage
Antimicrobial Stewardship
Inappropriate Prescribing
RevDate: 2025-10-29
CmpDate: 2025-10-29
Mammary Gland Microbiota in Benign Breast Diseases.
International journal of molecular sciences, 26(20): pii:ijms26209951.
The human microbiome is a critical factor in health and disease. While its association with breast cancer (BC) has been increasingly studied, this review provides a dedicated synthesis of the microbiota's role in benign breast diseases (BBDs)-a common yet microbiologically overlooked spectrum of conditions. The primary aim of this work is to consolidate the current understanding of the composition, origins, and functional mechanisms of the mammary gland (MG) microbiota specifically in the context of BBD and to evaluate its potential for novel diagnostic and therapeutic targets. We detail the distinct MG microbiota, formed via exogenous (e.g., cutaneous, translocation) and endogenous (e.g., enteromammary, lymphohematogenous) pathways, and its interaction with the host through estrogen metabolism, immunomodulation, and epigenetic modifications. This narrative review reveals unique dysbiotic patterns in BBD, characterized by distinct microbial signatures, such as the enrichment of Corynebacterium kroppenstedtii in granulomatous mastitis and the presence of Staphylococcus aureus in fibroadenomas and lactational mastitis. Furthermore, specific gut microbial profiles are identified in BBD patients, including an increased abundance of genera such as Clostridium and Faecalibacterium, alongside a decrease in Collinsella and Alistipes compared to healthy controls. These specific taxa represent compelling candidates for diagnostic biomarkers. We conclude that microbial dysbiosis is a significant component of BBD pathogenesis. A paradigm shift toward multi-omics approaches and mechanistic studies is now essential to translate these associations into clinical applications. Understanding the BBD-specific microbiome holds the promise of revolutionizing patient care through microbiota-based diagnostics for differentiating benign subtypes and novel, personalized therapeutic strategies aimed at restoring microbial homeostasis.
Additional Links: PMID-41155245
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@article {pmid41155245,
year = {2025},
author = {Ukraincev, NI and Kashutina, MI and Kasatkina, LI and Abduraimov, AB and Zhernov, YV},
title = {Mammary Gland Microbiota in Benign Breast Diseases.},
journal = {International journal of molecular sciences},
volume = {26},
number = {20},
pages = {},
doi = {10.3390/ijms26209951},
pmid = {41155245},
issn = {1422-0067},
support = {25-18-00901//Russian Science Foundation/ ; },
mesh = {Humans ; Female ; *Microbiota ; *Mammary Glands, Human/microbiology ; *Breast Diseases/microbiology ; Dysbiosis/microbiology ; Mastitis/microbiology ; Breast Neoplasms/microbiology ; },
abstract = {The human microbiome is a critical factor in health and disease. While its association with breast cancer (BC) has been increasingly studied, this review provides a dedicated synthesis of the microbiota's role in benign breast diseases (BBDs)-a common yet microbiologically overlooked spectrum of conditions. The primary aim of this work is to consolidate the current understanding of the composition, origins, and functional mechanisms of the mammary gland (MG) microbiota specifically in the context of BBD and to evaluate its potential for novel diagnostic and therapeutic targets. We detail the distinct MG microbiota, formed via exogenous (e.g., cutaneous, translocation) and endogenous (e.g., enteromammary, lymphohematogenous) pathways, and its interaction with the host through estrogen metabolism, immunomodulation, and epigenetic modifications. This narrative review reveals unique dysbiotic patterns in BBD, characterized by distinct microbial signatures, such as the enrichment of Corynebacterium kroppenstedtii in granulomatous mastitis and the presence of Staphylococcus aureus in fibroadenomas and lactational mastitis. Furthermore, specific gut microbial profiles are identified in BBD patients, including an increased abundance of genera such as Clostridium and Faecalibacterium, alongside a decrease in Collinsella and Alistipes compared to healthy controls. These specific taxa represent compelling candidates for diagnostic biomarkers. We conclude that microbial dysbiosis is a significant component of BBD pathogenesis. A paradigm shift toward multi-omics approaches and mechanistic studies is now essential to translate these associations into clinical applications. Understanding the BBD-specific microbiome holds the promise of revolutionizing patient care through microbiota-based diagnostics for differentiating benign subtypes and novel, personalized therapeutic strategies aimed at restoring microbial homeostasis.},
}
MeSH Terms:
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Humans
Female
*Microbiota
*Mammary Glands, Human/microbiology
*Breast Diseases/microbiology
Dysbiosis/microbiology
Mastitis/microbiology
Breast Neoplasms/microbiology
RevDate: 2025-10-29
CmpDate: 2025-10-29
Integrative Bioinformatics-Guided Analysis of Glomerular Transcriptome Implicates Potential Therapeutic Targets and Pathogenesis Mechanisms in IgA Nephropathy.
Bioengineering (Basel, Switzerland), 12(10): pii:bioengineering12101040.
(1) Background: IgA nephropathy (IgAN) is a leading cause of chronic kidney disease worldwide. Despite its prevalence, the molecular mechanisms of IgAN remain poorly understood, partly due to limited research scale. Identifying key genes involved in IgAN's pathogenesis is critical for novel diagnostic and therapeutic strategies. (2) Methods: We identified differentially expressed genes (DEGs) by analyzing public datasets from the Gene Expression Omnibus. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed to elucidate the biological roles of DEGs. Hub genes were screened using weighted gene co-expression network analysis combined with machine learning algorithms. Immune infiltration analysis was conducted to explore associations between hub genes and immune cell profiles. The hub genes were validated using receiver operating characteristic curves and area under the curve. (3) Results: We identified 165 DEGs associated with IgAN and revealed pathways such as IL-17 signaling and complement and coagulation cascades, and biological processes including response to xenobiotic stimuli. Four hub genes were screened: three downregulated (FOSB, SLC19A2, PER1) and one upregulated (SOX17). The AUC values for identifying IgAN in the training and testing set ranged from 0.956 to 0.995. Immune infiltration analysis indicated that hub gene expression correlated with immune cell abundance, suggesting their involvement in IgAN's immune pathogenesis. (4) Conclusion: This study identifies FOSB, SLC19A2, PER1, and SOX17 as novel hub genes with high diagnostic accuracy for IgAN. These genes, linked to immune-related pathways such as IL-17 signaling and complement activation, offer promising targets for diagnostic development and therapeutic intervention, enhancing our understanding of IgAN's molecular and immune mechanisms.
Additional Links: PMID-41155038
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@article {pmid41155038,
year = {2025},
author = {Yang, T and Dai, M and Zhang, F and Wen, W},
title = {Integrative Bioinformatics-Guided Analysis of Glomerular Transcriptome Implicates Potential Therapeutic Targets and Pathogenesis Mechanisms in IgA Nephropathy.},
journal = {Bioengineering (Basel, Switzerland)},
volume = {12},
number = {10},
pages = {},
doi = {10.3390/bioengineering12101040},
pmid = {41155038},
issn = {2306-5354},
support = {82304144//National Natural Science Foundation of China/ ; 32372334//National Natural Science Foundation of China/ ; },
abstract = {(1) Background: IgA nephropathy (IgAN) is a leading cause of chronic kidney disease worldwide. Despite its prevalence, the molecular mechanisms of IgAN remain poorly understood, partly due to limited research scale. Identifying key genes involved in IgAN's pathogenesis is critical for novel diagnostic and therapeutic strategies. (2) Methods: We identified differentially expressed genes (DEGs) by analyzing public datasets from the Gene Expression Omnibus. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were performed to elucidate the biological roles of DEGs. Hub genes were screened using weighted gene co-expression network analysis combined with machine learning algorithms. Immune infiltration analysis was conducted to explore associations between hub genes and immune cell profiles. The hub genes were validated using receiver operating characteristic curves and area under the curve. (3) Results: We identified 165 DEGs associated with IgAN and revealed pathways such as IL-17 signaling and complement and coagulation cascades, and biological processes including response to xenobiotic stimuli. Four hub genes were screened: three downregulated (FOSB, SLC19A2, PER1) and one upregulated (SOX17). The AUC values for identifying IgAN in the training and testing set ranged from 0.956 to 0.995. Immune infiltration analysis indicated that hub gene expression correlated with immune cell abundance, suggesting their involvement in IgAN's immune pathogenesis. (4) Conclusion: This study identifies FOSB, SLC19A2, PER1, and SOX17 as novel hub genes with high diagnostic accuracy for IgAN. These genes, linked to immune-related pathways such as IL-17 signaling and complement activation, offer promising targets for diagnostic development and therapeutic intervention, enhancing our understanding of IgAN's molecular and immune mechanisms.},
}
RevDate: 2025-10-29
CmpDate: 2025-10-29
Exploring the Impact of Skin Care Routines on the Skin Microbiome and Possible Skin Disease Risk-A Pilot Study.
Biomedicines, 13(10): pii:biomedicines13102371.
Background/Objectives: Unceasing exposure of skin and its microbiome to various external and internal factors influences its health. Any imbalance ensuing may result in dysbiosis and consequently skin diseases. Thus, it becomes critical to identify and recognize the influence of several factors on the skin microbiome and various disorders associated with it. Methods: In the current investigation, we studied the skin microbiomes of 37 subjects using the next-generation shotgun sequencing method and compared them with 48 healthy subjects from the Human Microbiome Project (HMP). This work focused on the analysis of the impact of different skin care routines-use of sunscreen and moisturizers-on the skin microbiome and related skin diseases. Results: Differences were observed between the microbiomes of subjects who were using only moisturizer (p = 3.1 × 10[-5]) or moisturizer with sunscreen (p = 3.2 × 10[-13]) and those who did not use these products at all. We also observed differences in the skin microbiomes of males vs. females with respect to the use of moisturizer. The composition of the skin microbiomes of female participants showed a higher difference in diversity in comparison to males. The current investigation also found that usage of sunscreen might help in retaining skin-protecting species in the skin microbiome. Conclusions: This work allowed us to understand the impact of moisturizer and sunscreen on skin health. The present evaluation shall pave the way for personalized skin care product development.
Additional Links: PMID-41153658
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PubMed:
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@article {pmid41153658,
year = {2025},
author = {Dubli, K and Balasundaram, P and Chaudhari, R and Vettrivelan, S and Borawake, A and Kapoor, R and Kovalchuk, I and Kapoor, A and Singh, R and Tripathi, MB},
title = {Exploring the Impact of Skin Care Routines on the Skin Microbiome and Possible Skin Disease Risk-A Pilot Study.},
journal = {Biomedicines},
volume = {13},
number = {10},
pages = {},
doi = {10.3390/biomedicines13102371},
pmid = {41153658},
issn = {2227-9059},
support = {IT33301//Mitacs/ ; },
abstract = {Background/Objectives: Unceasing exposure of skin and its microbiome to various external and internal factors influences its health. Any imbalance ensuing may result in dysbiosis and consequently skin diseases. Thus, it becomes critical to identify and recognize the influence of several factors on the skin microbiome and various disorders associated with it. Methods: In the current investigation, we studied the skin microbiomes of 37 subjects using the next-generation shotgun sequencing method and compared them with 48 healthy subjects from the Human Microbiome Project (HMP). This work focused on the analysis of the impact of different skin care routines-use of sunscreen and moisturizers-on the skin microbiome and related skin diseases. Results: Differences were observed between the microbiomes of subjects who were using only moisturizer (p = 3.1 × 10[-5]) or moisturizer with sunscreen (p = 3.2 × 10[-13]) and those who did not use these products at all. We also observed differences in the skin microbiomes of males vs. females with respect to the use of moisturizer. The composition of the skin microbiomes of female participants showed a higher difference in diversity in comparison to males. The current investigation also found that usage of sunscreen might help in retaining skin-protecting species in the skin microbiome. Conclusions: This work allowed us to understand the impact of moisturizer and sunscreen on skin health. The present evaluation shall pave the way for personalized skin care product development.},
}
RevDate: 2025-10-28
Mediated electron transfer in five prevalent human oral microbial species.
Bioelectrochemistry (Amsterdam, Netherlands), 168:109149 pii:S1567-5394(25)00252-X [Epub ahead of print].
An increasing number of microbial species within the human body, many of which are pathogenic, are being reported as "electroactive". However, the mechanisms and kinetics of extracellular electron transfer (EET) and its putative ecological relevance remain understudied. We utilized rotating disk electrodes (RDEs) to assess mediated electron transfer (MET) in five oral species via their ability to reduce riboflavin and ferricyanide. The use of both mediators was confirmed in Streptococcus mutans, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, while A. viscosus only reduced riboflavin. Kinetics of EET (turnover rate per cell) were slow with riboflavin (kcat, RF< 10[4] s[-1]) in all species but F. nucleatum, whereas ferricyanide resulted in fast kinetics (kcat, Ferri(app)> 10[4] s[-1]) in all but S. mutans. Due to its central role in oral biofilms and association to systemic diseases, MET was further characterized in F. nucleatum. Apparent Michaelis-Menten kinetics showed Km values of (0.57 ± 0.16 and 10.43 ± 0.91) μM for ferricyanide and riboflavin. The presence of mediators enhanced acetate production compared to mediator-free controls; when ferricyanide was used, butyrate and formate production was triggered only after its depletion. Finally, the putative molecular mechanisms enabling MET in F. nucleatum are discussed.
Additional Links: PMID-41151427
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PubMed:
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@article {pmid41151427,
year = {2025},
author = {Hernández-Villamor, D and Jeaidi, A and Boydens, R and Rabaey, K and Van de Wiele, T and Prévoteau, A},
title = {Mediated electron transfer in five prevalent human oral microbial species.},
journal = {Bioelectrochemistry (Amsterdam, Netherlands)},
volume = {168},
number = {},
pages = {109149},
doi = {10.1016/j.bioelechem.2025.109149},
pmid = {41151427},
issn = {1878-562X},
abstract = {An increasing number of microbial species within the human body, many of which are pathogenic, are being reported as "electroactive". However, the mechanisms and kinetics of extracellular electron transfer (EET) and its putative ecological relevance remain understudied. We utilized rotating disk electrodes (RDEs) to assess mediated electron transfer (MET) in five oral species via their ability to reduce riboflavin and ferricyanide. The use of both mediators was confirmed in Streptococcus mutans, Fusobacterium nucleatum, Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis, while A. viscosus only reduced riboflavin. Kinetics of EET (turnover rate per cell) were slow with riboflavin (kcat, RF< 10[4] s[-1]) in all species but F. nucleatum, whereas ferricyanide resulted in fast kinetics (kcat, Ferri(app)> 10[4] s[-1]) in all but S. mutans. Due to its central role in oral biofilms and association to systemic diseases, MET was further characterized in F. nucleatum. Apparent Michaelis-Menten kinetics showed Km values of (0.57 ± 0.16 and 10.43 ± 0.91) μM for ferricyanide and riboflavin. The presence of mediators enhanced acetate production compared to mediator-free controls; when ferricyanide was used, butyrate and formate production was triggered only after its depletion. Finally, the putative molecular mechanisms enabling MET in F. nucleatum are discussed.},
}
RevDate: 2025-10-28
CmpDate: 2025-10-28
In Silico Identification and Molecular Characterization of Lentilactobacillus hilgardii Antimicrobial Peptides with Activity Against Carbapenem-Resistant Acinetobacter baumannii.
Antibiotics (Basel, Switzerland), 14(10): pii:antibiotics14101004.
BACKGROUND/OBJECTIVES: Biofilm formation by Acinetobacter baumannii contributes to its persistence in clinical settings and resistance to antibiotic treatment. This study aims to identify and characterize antimicrobials from lactic acid bacteria (LAB) using molecular and in silico approaches that can prevent and disrupt A. baumannii biofilms, assess their antimicrobial host range, and define their synergy with current antibiotics.
METHODS: Thirteen LAB isolates from the Human Microbiome Project were screened for anti-biofilm activity against A. baumannii. Conditioned media was further tested against six ESKAPE pathogens and three skin commensals. Lentilactobacillus hilgardii was selected for detailed study and antimicrobial peptide (AMP) prediction analysis due to limited toxicity toward commensals. In silico identified peptides were synthesized and tested individually and in combination with sub-MIC doses of an antibiotic.
RESULTS: Conditioned media from five LAB species (Lentilactobacillus hilgardii, Lentilactobacillus buchneri, Ligilactobacillus ruminis, Limosilactobacillus fermentum, and Limosilactobacillus antri) significantly inhibited A. baumannii biofilm formation and reduced biomass of mature biofilms. LAB-conditioned media also exhibited broad-spectrum activity against ESKAPE pathogens, though effects on commensals varied. Bioinformatically predicted AMPs from L. hilgardii inhibited planktonic A. baumannii growth but showed no direct biofilm activity even at high doses. However, AMPs were found to synergize with sub-MIC doses of meropenem against mature biofilms leading to decolonization.
CONCLUSIONS: Our study provides a comprehensive platform for the discovery and characterization of AMPs and supports using commensal bacteria to reduce, prevent, and decolonize biofilms from pathogenic bacteria in community and nosocomial settings.
Additional Links: PMID-41148698
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@article {pmid41148698,
year = {2025},
author = {Appel, A and Velazco, L and Alreja, AB and LeClair, K and Duggal, AP and Vashee, I and Taal, AM and Gonzalez-Juarbe, N and Fouts, DE},
title = {In Silico Identification and Molecular Characterization of Lentilactobacillus hilgardii Antimicrobial Peptides with Activity Against Carbapenem-Resistant Acinetobacter baumannii.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {10},
pages = {},
doi = {10.3390/antibiotics14101004},
pmid = {41148698},
issn = {2079-6382},
support = {U54CK000603/CC/CDC HHS/United States ; },
abstract = {BACKGROUND/OBJECTIVES: Biofilm formation by Acinetobacter baumannii contributes to its persistence in clinical settings and resistance to antibiotic treatment. This study aims to identify and characterize antimicrobials from lactic acid bacteria (LAB) using molecular and in silico approaches that can prevent and disrupt A. baumannii biofilms, assess their antimicrobial host range, and define their synergy with current antibiotics.
METHODS: Thirteen LAB isolates from the Human Microbiome Project were screened for anti-biofilm activity against A. baumannii. Conditioned media was further tested against six ESKAPE pathogens and three skin commensals. Lentilactobacillus hilgardii was selected for detailed study and antimicrobial peptide (AMP) prediction analysis due to limited toxicity toward commensals. In silico identified peptides were synthesized and tested individually and in combination with sub-MIC doses of an antibiotic.
RESULTS: Conditioned media from five LAB species (Lentilactobacillus hilgardii, Lentilactobacillus buchneri, Ligilactobacillus ruminis, Limosilactobacillus fermentum, and Limosilactobacillus antri) significantly inhibited A. baumannii biofilm formation and reduced biomass of mature biofilms. LAB-conditioned media also exhibited broad-spectrum activity against ESKAPE pathogens, though effects on commensals varied. Bioinformatically predicted AMPs from L. hilgardii inhibited planktonic A. baumannii growth but showed no direct biofilm activity even at high doses. However, AMPs were found to synergize with sub-MIC doses of meropenem against mature biofilms leading to decolonization.
CONCLUSIONS: Our study provides a comprehensive platform for the discovery and characterization of AMPs and supports using commensal bacteria to reduce, prevent, and decolonize biofilms from pathogenic bacteria in community and nosocomial settings.},
}
RevDate: 2025-10-28
Negotiated Categories: The Co-Construction of the Tunisian Population in Human Microbiome Science and Its Historical Entanglements.
Medical anthropology [Epub ahead of print].
The analysis of the intersection between race and microbiome science is a growing area in the social sciences, but little scholarly attention has been given to how population categories, that often have a racial subtext when applied to the Global South, are constructed, or how they intersect with or diverge from local conceptions of race. Drawing on research on an EU-funded human microbiome project involving Italian and Tunisian researchers, I argue that population categories in microbiome research are not merely imposed, but are continuously negotiated and co-constructed with local, homegrown racial categories.
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@article {pmid41147308,
year = {2025},
author = {Scaglioni, M},
title = {Negotiated Categories: The Co-Construction of the Tunisian Population in Human Microbiome Science and Its Historical Entanglements.},
journal = {Medical anthropology},
volume = {},
number = {},
pages = {1-16},
doi = {10.1080/01459740.2025.2581072},
pmid = {41147308},
issn = {1545-5882},
abstract = {The analysis of the intersection between race and microbiome science is a growing area in the social sciences, but little scholarly attention has been given to how population categories, that often have a racial subtext when applied to the Global South, are constructed, or how they intersect with or diverge from local conceptions of race. Drawing on research on an EU-funded human microbiome project involving Italian and Tunisian researchers, I argue that population categories in microbiome research are not merely imposed, but are continuously negotiated and co-constructed with local, homegrown racial categories.},
}
RevDate: 2025-10-28
Heavy metal detoxification of gut environment: potential application of probiotic supplementation and challenges.
Journal of the science of food and agriculture [Epub ahead of print].
The human microbiome is a diverse group of microbes that regulates the host's environment and health. Probiotic microorganisms improve gastrointestinal microbial balance. However, frequent exposure to heavy metals (HMs) such as arsenic, lead, cadmium, chromium and mercury can disrupt the delicate balance gut microbiota, altering its composition. Exopolysaccharide (EPS) from probiotics can effectively reduce HM toxicity and mobility in the environment, potentially enhancing the gut microbiota's ability to regulate the host's environment. The current paper discusses the role of probiotic supplementation on HM biosorption to build awareness about the health effects of HMs on human metabolism and raises concerns about their sources, distribution and the potential effects on human gut health. HM toxicity occurs through reactive oxygen species which can cause damage to cellular components such as DNA, proteins and lipids. This oxidative damage can lead to various health issues, including neurodegenerative diseases, cardiovascular problems and impaired immune function. EPS biopolymers have shown promising results in the removal of HMs from contaminated environments through binding with metal ions, preventing their harmful effects on living organisms. Thus, EPS biopolymers have been found to enhance the growth and activity of probiotic microorganisms, further aiding in the bioremediation process. Vigorous research is needed to understand the underlying mechanism and cell surface morphology of bacteria for better sorption and removal of HMs. © 2025 Society of Chemical Industry.
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@article {pmid41146567,
year = {2025},
author = {Bhowmik, B and Hossain, MN and Afrin, S and Jui, AH and Naumovski, N},
title = {Heavy metal detoxification of gut environment: potential application of probiotic supplementation and challenges.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.70280},
pmid = {41146567},
issn = {1097-0010},
abstract = {The human microbiome is a diverse group of microbes that regulates the host's environment and health. Probiotic microorganisms improve gastrointestinal microbial balance. However, frequent exposure to heavy metals (HMs) such as arsenic, lead, cadmium, chromium and mercury can disrupt the delicate balance gut microbiota, altering its composition. Exopolysaccharide (EPS) from probiotics can effectively reduce HM toxicity and mobility in the environment, potentially enhancing the gut microbiota's ability to regulate the host's environment. The current paper discusses the role of probiotic supplementation on HM biosorption to build awareness about the health effects of HMs on human metabolism and raises concerns about their sources, distribution and the potential effects on human gut health. HM toxicity occurs through reactive oxygen species which can cause damage to cellular components such as DNA, proteins and lipids. This oxidative damage can lead to various health issues, including neurodegenerative diseases, cardiovascular problems and impaired immune function. EPS biopolymers have shown promising results in the removal of HMs from contaminated environments through binding with metal ions, preventing their harmful effects on living organisms. Thus, EPS biopolymers have been found to enhance the growth and activity of probiotic microorganisms, further aiding in the bioremediation process. Vigorous research is needed to understand the underlying mechanism and cell surface morphology of bacteria for better sorption and removal of HMs. © 2025 Society of Chemical Industry.},
}
RevDate: 2025-10-27
EasyAmplicon 2: Expanding PacBio and Nanopore Long Amplicon Sequencing Analysis Pipeline for Microbiome.
Advanced science (Weinheim, Baden-Wurttemberg, Germany) [Epub ahead of print].
In the past decade, third-generation sequencing technologies (such as PacBio (Pacific Biosciences) and Nanopore) have become gradually matured and are widely used for microbial taxonomy and quantification. Compared with Illumina sequencing, PacBio or Nanopore has advantages with long reads and high resolution in taxonomic classification. However, there is currently a lack of an easy-to-use, reproducible, and community-supported pipeline for PacBio or Nanopore amplicon sequencing data analysis. To address this shortcoming, the highly cited EasyAmplicon is updated to version 2, a pipeline fully supporting third-generation full-length amplicon data. EasyAmplicon 2 is a user-friendly pipeline that embraces data analysis and visualization options for data obtained from various sequencing technologies (Illumina, BGI (Beijing Genomics Institution), PacBio, Nanopore or Qitan). It integrates popular tools such as DADA2 and Emu, and provides a workflow from raw data to publication-ready visualizations. EasyAmplicon 2 inherits the advantages of the previous version and further optimizes the visualization part. The updated version of the pipeline includes data preprocessing, annotation, and quantification of amplicon sequence variants, intergroup comparison, and visualization for third-generation sequencing. EasyAmplicon 2 provides a simple and easy-to-use analysis environment for long-read amplicon sequencing data analysis. It is available for free on GitHub (https://github.com/YongxinLiu/EasyAmplicon).
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@article {pmid41144790,
year = {2025},
author = {Luo, H and Bai, D and Zhu, Z and Yousuf, S and Yang, H and Xun, J and Zeng, M and Wang, Y and Gao, Y and Peng, K and Xu, S and Zhou, Y and Zhang, T and Ma, C and Hou, H and Wan, X and Zhou, Y and Jia, B and Huang, S and Gan, R and Wen, T and Chen, T and Chen, X and Li, X and Liu, YX},
title = {EasyAmplicon 2: Expanding PacBio and Nanopore Long Amplicon Sequencing Analysis Pipeline for Microbiome.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e12447},
doi = {10.1002/advs.202512447},
pmid = {41144790},
issn = {2198-3844},
support = {32522001//Natural Science Foundation of China/ ; 32470055//Natural Science Foundation of China/ ; CAAS-BRC-CB-2025-01//Agricultural Science and Technology Innovation Program/ ; },
abstract = {In the past decade, third-generation sequencing technologies (such as PacBio (Pacific Biosciences) and Nanopore) have become gradually matured and are widely used for microbial taxonomy and quantification. Compared with Illumina sequencing, PacBio or Nanopore has advantages with long reads and high resolution in taxonomic classification. However, there is currently a lack of an easy-to-use, reproducible, and community-supported pipeline for PacBio or Nanopore amplicon sequencing data analysis. To address this shortcoming, the highly cited EasyAmplicon is updated to version 2, a pipeline fully supporting third-generation full-length amplicon data. EasyAmplicon 2 is a user-friendly pipeline that embraces data analysis and visualization options for data obtained from various sequencing technologies (Illumina, BGI (Beijing Genomics Institution), PacBio, Nanopore or Qitan). It integrates popular tools such as DADA2 and Emu, and provides a workflow from raw data to publication-ready visualizations. EasyAmplicon 2 inherits the advantages of the previous version and further optimizes the visualization part. The updated version of the pipeline includes data preprocessing, annotation, and quantification of amplicon sequence variants, intergroup comparison, and visualization for third-generation sequencing. EasyAmplicon 2 provides a simple and easy-to-use analysis environment for long-read amplicon sequencing data analysis. It is available for free on GitHub (https://github.com/YongxinLiu/EasyAmplicon).},
}
RevDate: 2025-10-24
Prevalence of oxalotrophy in the human microbiome.
BMC genomics, 26(1):954.
BACKGROUND: Incomplete degradation of oxalate, a compound commonly found in the diet, can lead to disease in humans, particularly affecting the kidneys. The concentration of oxalate in the body depends on several factors, one of which is intestinal absorption-an aspect influenced by oxalotrophy among enteric bacteria. Despite its potential significance, oxalotrophy in the human microbiome remains poorly understood.
RESULTS: In this study, we conducted a systematic search for the co-occurrence of three key oxalotrophy genes-frc, oxc, and oxlT. We developed and validated specific conservation models for each gene and applied them to genomes and metagenomes associated with the human digestive tract, oral cavity, and lungs. Our analysis revealed that oxalotrophy, defined as the capacity to use oxalate as an energy source, is a rare metabolic trait predominantly confined to the gut. We also found evidence that this capacity can be acquired via horizontal gene transfer.
CONCLUSIONS: While oxalotrophy is relatively uncommon, the broader capacity for oxalate degradation is more widespread. Notably, the genes frc and oxc are frequently found in close proximity within genomes, suggesting a selective advantage for organisms possessing this capability. Incomplete degradation of oxalate, a compound commonly found in the diet, can cause disease in humans, particularly affecting the kidney. Its concentration in the body depends on several factors, one of which is intestinal absorption, which is itself affected by oxalotrophy among enteric bacteria. Oxalotrophy in the human microbiome is poorly known. In this study, we perform a systematic search for the simultaneous presence of the three oxalotrophy genes, namely frc, oxc and oxlT. Thanks to the construction and validation of specific conservation models for all three genes, we were able to search for oxalotrophy in genomes and metagenomes associated with the human digestive tract, oral cavity, and lungs. We report that oxalotrophy-the capacity to use oxalate as an energy source-is a rare metabolic trait, mostly confined to the gut, and also find evidence that it can be acquired by horizontal gene transfer. By contrast, the capacity for oxalate degradation is more widespread, and two genes responsible for it (frc and oxc) are almost always close together in the genome, suggesting selection pressure.
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@article {pmid41136898,
year = {2025},
author = {Junier, T and Palmieri, F and Ubags, ND and Trompette, A and Koutsokera, A and Junier, P and Pagni, M and Neuenschwander, S},
title = {Prevalence of oxalotrophy in the human microbiome.},
journal = {BMC genomics},
volume = {26},
number = {1},
pages = {954},
pmid = {41136898},
issn = {1471-2164},
support = {40B2-0_194701//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung/ ; GRS-064/18//Gebert Rüf Stiftung/ ; },
abstract = {BACKGROUND: Incomplete degradation of oxalate, a compound commonly found in the diet, can lead to disease in humans, particularly affecting the kidneys. The concentration of oxalate in the body depends on several factors, one of which is intestinal absorption-an aspect influenced by oxalotrophy among enteric bacteria. Despite its potential significance, oxalotrophy in the human microbiome remains poorly understood.
RESULTS: In this study, we conducted a systematic search for the co-occurrence of three key oxalotrophy genes-frc, oxc, and oxlT. We developed and validated specific conservation models for each gene and applied them to genomes and metagenomes associated with the human digestive tract, oral cavity, and lungs. Our analysis revealed that oxalotrophy, defined as the capacity to use oxalate as an energy source, is a rare metabolic trait predominantly confined to the gut. We also found evidence that this capacity can be acquired via horizontal gene transfer.
CONCLUSIONS: While oxalotrophy is relatively uncommon, the broader capacity for oxalate degradation is more widespread. Notably, the genes frc and oxc are frequently found in close proximity within genomes, suggesting a selective advantage for organisms possessing this capability. Incomplete degradation of oxalate, a compound commonly found in the diet, can cause disease in humans, particularly affecting the kidney. Its concentration in the body depends on several factors, one of which is intestinal absorption, which is itself affected by oxalotrophy among enteric bacteria. Oxalotrophy in the human microbiome is poorly known. In this study, we perform a systematic search for the simultaneous presence of the three oxalotrophy genes, namely frc, oxc and oxlT. Thanks to the construction and validation of specific conservation models for all three genes, we were able to search for oxalotrophy in genomes and metagenomes associated with the human digestive tract, oral cavity, and lungs. We report that oxalotrophy-the capacity to use oxalate as an energy source-is a rare metabolic trait, mostly confined to the gut, and also find evidence that it can be acquired by horizontal gene transfer. By contrast, the capacity for oxalate degradation is more widespread, and two genes responsible for it (frc and oxc) are almost always close together in the genome, suggesting selection pressure.},
}
RevDate: 2025-10-24
CmpDate: 2025-10-24
Akkermansia muciniphila Muc[T] harnesses dietary polyphenols as xenosiderophores for enhanced iron uptake.
Nature communications, 16(1):9428.
Dietary proanthocyanidins (PACs) are polyphenols that promote a healthy gut microbiome. PACs are notable for their rich catechol moieties with high affinity for iron, enabling them to interfere with pathogens' iron uptake. PACs selectively increase the abundance of Akkermansia muciniphila, a symbiont known for supporting metabolic and immune health. We discovered that A. muciniphila Muc[T] utilizes distinct iron-acquisition systems to take up iron sequestered by PACs, supporting its metabolic activity. Integrative proteomics and transcriptomics revealed that A. muciniphila has an active catechol-type siderophore-mediated iron uptake (Fe[3+]) system, involving membrane ATP-binding cassette transporters and lipocalins. Simultaneously, the expression of ferrous iron (Fe[2+]) transporters, zinc uptake, and iron storage proteins was upregulated. Administering iron-laden PACs in an iron-depleted medium restored the A. muciniphila growth to levels comparable to those in iron-amended conditions. This was associated with an increased expression of the A. muciniphila siderophore operon and lipocalin genes, indicating that iron-laden PACs are recognized as xenosiderophores to cope with iron depletion. Hence, we identified novel signaling mechanisms for iron acquisition and siderophore uptake regulation in A. muciniphila Muc[T] upon exposure to PACs, enhancing our understanding of the role of dietary PACs in selectively promoting this gut symbiont and potentially outcompeting pathogenic bacteria.
Additional Links: PMID-41136386
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@article {pmid41136386,
year = {2025},
author = {Rodríguez-Daza, MC and Boeren, S and Tytgat, HLP and Desjardins, Y and de Vos, WM},
title = {Akkermansia muciniphila Muc[T] harnesses dietary polyphenols as xenosiderophores for enhanced iron uptake.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {9428},
pmid = {41136386},
issn = {2041-1723},
support = {Grant 024.002.002//Stiftelsen Siamon/ ; },
mesh = {*Iron/metabolism ; *Polyphenols/metabolism/pharmacology ; *Siderophores/metabolism ; *Akkermansia/metabolism/genetics ; Gastrointestinal Microbiome/drug effects ; *Verrucomicrobia/metabolism/genetics ; Proteomics ; Zinc/metabolism ; ATP-Binding Cassette Transporters/metabolism ; },
abstract = {Dietary proanthocyanidins (PACs) are polyphenols that promote a healthy gut microbiome. PACs are notable for their rich catechol moieties with high affinity for iron, enabling them to interfere with pathogens' iron uptake. PACs selectively increase the abundance of Akkermansia muciniphila, a symbiont known for supporting metabolic and immune health. We discovered that A. muciniphila Muc[T] utilizes distinct iron-acquisition systems to take up iron sequestered by PACs, supporting its metabolic activity. Integrative proteomics and transcriptomics revealed that A. muciniphila has an active catechol-type siderophore-mediated iron uptake (Fe[3+]) system, involving membrane ATP-binding cassette transporters and lipocalins. Simultaneously, the expression of ferrous iron (Fe[2+]) transporters, zinc uptake, and iron storage proteins was upregulated. Administering iron-laden PACs in an iron-depleted medium restored the A. muciniphila growth to levels comparable to those in iron-amended conditions. This was associated with an increased expression of the A. muciniphila siderophore operon and lipocalin genes, indicating that iron-laden PACs are recognized as xenosiderophores to cope with iron depletion. Hence, we identified novel signaling mechanisms for iron acquisition and siderophore uptake regulation in A. muciniphila Muc[T] upon exposure to PACs, enhancing our understanding of the role of dietary PACs in selectively promoting this gut symbiont and potentially outcompeting pathogenic bacteria.},
}
MeSH Terms:
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*Iron/metabolism
*Polyphenols/metabolism/pharmacology
*Siderophores/metabolism
*Akkermansia/metabolism/genetics
Gastrointestinal Microbiome/drug effects
*Verrucomicrobia/metabolism/genetics
Proteomics
Zinc/metabolism
ATP-Binding Cassette Transporters/metabolism
RevDate: 2025-10-24
Dietary urbanization destabilizes host-gut microbiome homeostasis and informs precision nutrition for human health.
Cell metabolism pii:S1550-4131(25)00398-5 [Epub ahead of print].
Since the industrial revolution, human dietary habits have invariably trended toward dietary urbanization, during which the human gut microbiota has rapidly changed. However, the human genome cannot change substantially over one generation, leaving it potentially ill-equipped to adapt to evolving microbial functions associated with rising non-communicable diseases (NCDs). In this review, we map the chronological alterations in dietary patterns and incidences of NCDs during global urbanization while emphasizing the gut microbiome as the centerpiece. We then illustrate losses and acquisitions of gut microbes during worldwide urbanization and delineate the mechanisms by which urbanized diets may disrupt host-microbiome interactions, linking to the onset of NCDs. Building on this, we further propose a microbiome-directed precision-nutrition framework that integrates both inter-population and intra-population variations to promote diet-fueled host-microbiome synergism and hence to counteract urbanization-associated diseases. These insights will instruct future microbiome-targeted diets to thwart NCDs.
Additional Links: PMID-41135513
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@article {pmid41135513,
year = {2025},
author = {Zhang, F and Zhou, G and Schewe, M and Kulling, SE and Ding, Y and Mozaffarian, D and Zuo, T},
title = {Dietary urbanization destabilizes host-gut microbiome homeostasis and informs precision nutrition for human health.},
journal = {Cell metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmet.2025.09.013},
pmid = {41135513},
issn = {1932-7420},
abstract = {Since the industrial revolution, human dietary habits have invariably trended toward dietary urbanization, during which the human gut microbiota has rapidly changed. However, the human genome cannot change substantially over one generation, leaving it potentially ill-equipped to adapt to evolving microbial functions associated with rising non-communicable diseases (NCDs). In this review, we map the chronological alterations in dietary patterns and incidences of NCDs during global urbanization while emphasizing the gut microbiome as the centerpiece. We then illustrate losses and acquisitions of gut microbes during worldwide urbanization and delineate the mechanisms by which urbanized diets may disrupt host-microbiome interactions, linking to the onset of NCDs. Building on this, we further propose a microbiome-directed precision-nutrition framework that integrates both inter-population and intra-population variations to promote diet-fueled host-microbiome synergism and hence to counteract urbanization-associated diseases. These insights will instruct future microbiome-targeted diets to thwart NCDs.},
}
RevDate: 2025-10-22
CmpDate: 2025-10-22
Gut microbiota alterations and their association with tumorigenic pathways in colorectal cancer: insights from a pooled analysis of 109 microbiome datasets.
Gut pathogens, 17(1):82.
BACKGROUND: Colorectal cancer (CRC) is a significant global health burden, ranking amongst the top causes of cancer-associated mortality. Emerging evidences implicate gut microbiota as a prominent mediator of cell signalling, immune, and metabolic pathways in the pathophysiology of CRC.
METHODS: We analysed 16S rRNA amplicon sequencing data (PRJEB7774) from faecal samples of 46 CRC patients and 63 healthy controls to assess shifts in microbial composition, diversity, and biomarker taxa. Differential abundances of microbiota were determined using Linear Discriminant Analysis Effect Size (LEfSe) and Random Forest (RF) models. Host-microbiota interactions were explored using the Human Microbiome Affect the Host Epigenome (MIAOME) and Host Genetic and Immune Factors Shaping Human Microbiota (GIMICA) databases, with key host genes validated using Gene Expression Profiling Interactive Analysis (GEPIA) and The Cancer Genome Atlas (TCGA) datasets. Functional enrichment analyses were performed to uncover associated biological processes and pathways.
RESULTS: CRC samples exhibited significantly reduced alpha diversity and distinct beta diversity profiles, compared to controls. Taxonomic profiling revealed an enrichment of potentially pathogenic bacteria, including Prevotella copri, Methanobrevibacter smithii, Bacteroides eggerthii, and Dialister invisus, and depletion of beneficial microbes such as Bifidobacterium animalis and Ruminococcus sp. Predicted host-microbe interactions highlighted associations between key microbial biomarkers and inflammation-related genes (CD44, CXCL8, DUSP16, FOXP3, IFNGR2, IL18), all significantly overexpressed in CRC samples. Enrichment analyses linked these genes to immune pathways, including NF-κB, TLR and cytokine signalling.
CONCLUSIONS: Our study reveals a distinct gut microbiota signature in CRC and suggests functional interactions between microbial dysbiosis and host inflammatory responses. These findings emphasize the potential of microbiota-based interventions and microbial metabolites as adjunctive strategies for the management of CRC.
Additional Links: PMID-41121269
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Citation:
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@article {pmid41121269,
year = {2025},
author = {Haque, S and Bantun, F and Jalal, NA and Faidah, H and Babalghith, AO and Alobaidy, MA and Aldairi, AF and Ahmad, F},
title = {Gut microbiota alterations and their association with tumorigenic pathways in colorectal cancer: insights from a pooled analysis of 109 microbiome datasets.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {82},
pmid = {41121269},
issn = {1757-4749},
abstract = {BACKGROUND: Colorectal cancer (CRC) is a significant global health burden, ranking amongst the top causes of cancer-associated mortality. Emerging evidences implicate gut microbiota as a prominent mediator of cell signalling, immune, and metabolic pathways in the pathophysiology of CRC.
METHODS: We analysed 16S rRNA amplicon sequencing data (PRJEB7774) from faecal samples of 46 CRC patients and 63 healthy controls to assess shifts in microbial composition, diversity, and biomarker taxa. Differential abundances of microbiota were determined using Linear Discriminant Analysis Effect Size (LEfSe) and Random Forest (RF) models. Host-microbiota interactions were explored using the Human Microbiome Affect the Host Epigenome (MIAOME) and Host Genetic and Immune Factors Shaping Human Microbiota (GIMICA) databases, with key host genes validated using Gene Expression Profiling Interactive Analysis (GEPIA) and The Cancer Genome Atlas (TCGA) datasets. Functional enrichment analyses were performed to uncover associated biological processes and pathways.
RESULTS: CRC samples exhibited significantly reduced alpha diversity and distinct beta diversity profiles, compared to controls. Taxonomic profiling revealed an enrichment of potentially pathogenic bacteria, including Prevotella copri, Methanobrevibacter smithii, Bacteroides eggerthii, and Dialister invisus, and depletion of beneficial microbes such as Bifidobacterium animalis and Ruminococcus sp. Predicted host-microbe interactions highlighted associations between key microbial biomarkers and inflammation-related genes (CD44, CXCL8, DUSP16, FOXP3, IFNGR2, IL18), all significantly overexpressed in CRC samples. Enrichment analyses linked these genes to immune pathways, including NF-κB, TLR and cytokine signalling.
CONCLUSIONS: Our study reveals a distinct gut microbiota signature in CRC and suggests functional interactions between microbial dysbiosis and host inflammatory responses. These findings emphasize the potential of microbiota-based interventions and microbial metabolites as adjunctive strategies for the management of CRC.},
}
RevDate: 2025-10-21
Travel-Associated Carbapenemase-Producing Enterobacterales: Epidemiology and Risk Factors in a Finnish Cohort.
Travel medicine and infectious disease pii:S1477-8939(25)00132-2 [Epub ahead of print].
BACKGROUND: Carbapenemase-producing Enterobacterales (CPE) are increasing worldwide and are associated with difficult-to-treat infections. We previously reported that international travel is a major source of CPE acquisition in the Helsinki region, Finland. To clarify the extent of importation, we investigated the epidemiology and associated risk factors of foreign-acquired CPEs.
METHODS: We revisited two earlier cohorts. Cohort A (n=187 after a one-year extension) comprised patients from 2010 through 2024 presumed to have acquired CPE abroad; CPE types were categorized by travel region. Cohort B included 3,029 patients screened for CPE from 2010 through 2019 within 12 months after hospitalization abroad. Multivariable analysis identified factors that predispose to colonization.
RESULTS: Among patients hospitalized abroad (Cohort B), CPE rates were particularly high for South Asia (14.6%) and North Africa (13.7%). Across the 24 individual countries with data, the highest CPE colonization risks were observed for Egypt (20.8%) and India (16.4%). In addition to destination, independent risk factors included antibiotic use, travel type, short interval between discharge from a foreign hospital and screening (within one week or one month) and male sex. For South/Southeast Asia and sub-Saharan Africa, over 70% of CPE carriers (Cohort A) had metallo-β-lactamase-producing Enterobacterales, predominantly NDM, whereas OXA-48-like enzymes predominated in North Africa and the Middle East.
CONCLUSIONS: Hospitalization in high-prevalence countries and antibiotic use emerged as key risk factors for CPE acquisition. Regional variation was evident: OXA-48-like enzymes dominated among CPEs linked to the Middle East and North Africa, whereas NDM was prevalent elsewhere in Eurasia and Africa.
Additional Links: PMID-41120038
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@article {pmid41120038,
year = {2025},
author = {Kajova, M and Khawaja, T and Kainulainen, K and Kantele, A},
title = {Travel-Associated Carbapenemase-Producing Enterobacterales: Epidemiology and Risk Factors in a Finnish Cohort.},
journal = {Travel medicine and infectious disease},
volume = {},
number = {},
pages = {102926},
doi = {10.1016/j.tmaid.2025.102926},
pmid = {41120038},
issn = {1873-0442},
abstract = {BACKGROUND: Carbapenemase-producing Enterobacterales (CPE) are increasing worldwide and are associated with difficult-to-treat infections. We previously reported that international travel is a major source of CPE acquisition in the Helsinki region, Finland. To clarify the extent of importation, we investigated the epidemiology and associated risk factors of foreign-acquired CPEs.
METHODS: We revisited two earlier cohorts. Cohort A (n=187 after a one-year extension) comprised patients from 2010 through 2024 presumed to have acquired CPE abroad; CPE types were categorized by travel region. Cohort B included 3,029 patients screened for CPE from 2010 through 2019 within 12 months after hospitalization abroad. Multivariable analysis identified factors that predispose to colonization.
RESULTS: Among patients hospitalized abroad (Cohort B), CPE rates were particularly high for South Asia (14.6%) and North Africa (13.7%). Across the 24 individual countries with data, the highest CPE colonization risks were observed for Egypt (20.8%) and India (16.4%). In addition to destination, independent risk factors included antibiotic use, travel type, short interval between discharge from a foreign hospital and screening (within one week or one month) and male sex. For South/Southeast Asia and sub-Saharan Africa, over 70% of CPE carriers (Cohort A) had metallo-β-lactamase-producing Enterobacterales, predominantly NDM, whereas OXA-48-like enzymes predominated in North Africa and the Middle East.
CONCLUSIONS: Hospitalization in high-prevalence countries and antibiotic use emerged as key risk factors for CPE acquisition. Regional variation was evident: OXA-48-like enzymes dominated among CPEs linked to the Middle East and North Africa, whereas NDM was prevalent elsewhere in Eurasia and Africa.},
}
RevDate: 2025-10-21
CmpDate: 2025-10-21
Microbiome network: a robust biomarker of skin health.
The British journal of dermatology, 193(Supplement_2):ii1-ii5.
The skin microbiome is an integral part of the skin barrier. Its activity is shaped by microbe-microbe and microbe-host interactions. Understanding such interactions is an evolving field essential for uncovering the ecology and functions of a human microbiome community. Various studies have adapted network theory to explore the relationships of the microbiome community and its functional importance in health and diseases. The microbiome network is described as a biomarker depicting the interaction or correlation between two species, rather than their concentrations or abundances as in traditional molecular biomarkers. In skin diseases, the collapse of microbial community network structure has been reported in patients with atopic dermatitis, vitiligo and seborrhoeic dermatitis. More recently, we have reported that a fragile skin microbiome network is becoming a marker consistently observed across skin conditions, such as acne, in preclinical concerns like dry skin and premature ageing, as well as in pollution-compromised skin. In this review, we describe how advanced microbiome networks are constructed to reveal hidden microbiome features based on the nature of polymicrobial interaction from a systems perspective. We discuss the skin microbiome network as a robust network biomarker by capturing skin-microbiome interactions, specifically in conditions where a differential abundance of microbial species is absent, and further as a dynamic network biomarker by capturing skin microbiome dynamics.
Additional Links: PMID-41118314
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PubMed:
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@article {pmid41118314,
year = {2025},
author = {Yue, X and Wang, H and Xu, YN and Chu, CC and Chen, L},
title = {Microbiome network: a robust biomarker of skin health.},
journal = {The British journal of dermatology},
volume = {193},
number = {Supplement_2},
pages = {ii1-ii5},
doi = {10.1093/bjd/ljaf230},
pmid = {41118314},
issn = {1365-2133},
support = {T2341007//Natural Science Foundation of China/ ; T2350003//Natural Science Foundation of China/ ; 12131020//Natural Science Foundation of China/ ; 42450084//Natural Science Foundation of China/ ; 42450135//Natural Science Foundation of China/ ; 12326614//Natural Science Foundation of China/ ; 12426310//Natural Science Foundation of China/ ; 23JS1401300//Science and Technology Commission of Shanghai Municipality/ ; 2025C01114//Science and Technology Commission of Shanghai Municipality/ ; //Institute for advanced study/ ; 2024HIAS-P004//UCAS/ ; //Unilever/ ; },
mesh = {Humans ; *Microbiota/physiology ; *Skin/microbiology ; Biomarkers/metabolism ; *Skin Diseases/microbiology ; Host Microbial Interactions/physiology ; },
abstract = {The skin microbiome is an integral part of the skin barrier. Its activity is shaped by microbe-microbe and microbe-host interactions. Understanding such interactions is an evolving field essential for uncovering the ecology and functions of a human microbiome community. Various studies have adapted network theory to explore the relationships of the microbiome community and its functional importance in health and diseases. The microbiome network is described as a biomarker depicting the interaction or correlation between two species, rather than their concentrations or abundances as in traditional molecular biomarkers. In skin diseases, the collapse of microbial community network structure has been reported in patients with atopic dermatitis, vitiligo and seborrhoeic dermatitis. More recently, we have reported that a fragile skin microbiome network is becoming a marker consistently observed across skin conditions, such as acne, in preclinical concerns like dry skin and premature ageing, as well as in pollution-compromised skin. In this review, we describe how advanced microbiome networks are constructed to reveal hidden microbiome features based on the nature of polymicrobial interaction from a systems perspective. We discuss the skin microbiome network as a robust network biomarker by capturing skin-microbiome interactions, specifically in conditions where a differential abundance of microbial species is absent, and further as a dynamic network biomarker by capturing skin microbiome dynamics.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Microbiota/physiology
*Skin/microbiology
Biomarkers/metabolism
*Skin Diseases/microbiology
Host Microbial Interactions/physiology
RevDate: 2025-10-20
CmpDate: 2025-10-20
Enrichment of prevotella melaninogenica in the lower respiratory tract links to checkpoint inhibitor pneumonitis and radiation pneumonitis.
Frontiers in cellular and infection microbiology, 15:1594460.
BACKGROUND: Checkpoint inhibitor pneumonitis (CIP) and radiation pneumonitis (RP) lead to anti-cancer therapy discontinuation and poor diagnosis. The human microbiome is related to various respiratory diseases. However, the role of the lung microbiome in CIP and RP remains unknown. Our study aimed to explore the lower respiratory tract (LRT) microbiome in CIP/RP patients.
METHODS: The study enrolled 61 patients with pneumonitis or pneumonia, including 23 with CIP/RP, and 38 with lung cancer with pneumonia (LC-P). Metagenomic next-generation sequencing (mNGS) was performed to identify the microbiota in bronchoalveolar lavage fluid (BALF), and bioinformatics methods were used to compare the microbial differences between CIP/RP and LC-P groups. Correlation analysis was conducted to explore the relationship between LRT microbiota and clinical features.
RESULTS: The Prevotella was the dominant genus in both groups. The Prevotella melaninogenica, which belongs to the Prevotella genus, was the dominant species in the CIP/RP group and the second most abundant species in the LC-P group. Compared to the LC-P group, the CIP/RP group had significantly high levels of Prevotella melaninogenica species and lymphocyte percentage in BALF but significantly low levels of lymphocytes, eosinophils and albumin in peripheral blood. In addition, the Prevotella melaninogenica species had a negative correlation with peripheral blood lymphocytes.
CONCLUSION: The enrichment of Prevotella melaninogenica species in LRT and a decreased level of peripheral blood lymphocytes are associated with CIP/RP.
Additional Links: PMID-41112578
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Citation:
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@article {pmid41112578,
year = {2025},
author = {Chen, J and Xu, Q and Zhang, L and Zhang, D and Wu, X},
title = {Enrichment of prevotella melaninogenica in the lower respiratory tract links to checkpoint inhibitor pneumonitis and radiation pneumonitis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1594460},
pmid = {41112578},
issn = {2235-2988},
mesh = {Humans ; Male ; Female ; Middle Aged ; Aged ; Bronchoalveolar Lavage Fluid/microbiology ; *Radiation Pneumonitis/microbiology ; *Prevotella/isolation & purification/genetics/classification ; Microbiota ; Lung Neoplasms/drug therapy ; *Immune Checkpoint Inhibitors/adverse effects ; High-Throughput Nucleotide Sequencing ; Metagenomics ; *Pneumonia/microbiology ; Lung/microbiology ; },
abstract = {BACKGROUND: Checkpoint inhibitor pneumonitis (CIP) and radiation pneumonitis (RP) lead to anti-cancer therapy discontinuation and poor diagnosis. The human microbiome is related to various respiratory diseases. However, the role of the lung microbiome in CIP and RP remains unknown. Our study aimed to explore the lower respiratory tract (LRT) microbiome in CIP/RP patients.
METHODS: The study enrolled 61 patients with pneumonitis or pneumonia, including 23 with CIP/RP, and 38 with lung cancer with pneumonia (LC-P). Metagenomic next-generation sequencing (mNGS) was performed to identify the microbiota in bronchoalveolar lavage fluid (BALF), and bioinformatics methods were used to compare the microbial differences between CIP/RP and LC-P groups. Correlation analysis was conducted to explore the relationship between LRT microbiota and clinical features.
RESULTS: The Prevotella was the dominant genus in both groups. The Prevotella melaninogenica, which belongs to the Prevotella genus, was the dominant species in the CIP/RP group and the second most abundant species in the LC-P group. Compared to the LC-P group, the CIP/RP group had significantly high levels of Prevotella melaninogenica species and lymphocyte percentage in BALF but significantly low levels of lymphocytes, eosinophils and albumin in peripheral blood. In addition, the Prevotella melaninogenica species had a negative correlation with peripheral blood lymphocytes.
CONCLUSION: The enrichment of Prevotella melaninogenica species in LRT and a decreased level of peripheral blood lymphocytes are associated with CIP/RP.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Male
Female
Middle Aged
Aged
Bronchoalveolar Lavage Fluid/microbiology
*Radiation Pneumonitis/microbiology
*Prevotella/isolation & purification/genetics/classification
Microbiota
Lung Neoplasms/drug therapy
*Immune Checkpoint Inhibitors/adverse effects
High-Throughput Nucleotide Sequencing
Metagenomics
*Pneumonia/microbiology
Lung/microbiology
RevDate: 2025-10-20
CmpDate: 2025-10-20
What is the relationship between microorganisms in the human body and upper tract urothelial carcinoma?.
Frontiers in immunology, 16:1636782.
Upper Tract Urothelial Carcinoma (UTUC) is a highly malignant tumor originating from the epithelium of the upper urinary tract with diverse pathogenesis, but currently available diagnostic and therapeutic strategies have some limitations. In recent years, human microbiome-related studies have provided new ideas for the exploration of the pathogenesis and treatment of UTUC. In this paper, we review the research progress of human microbiome related to UTUC. Focusing on the urinary microbiome, the role of the microbiome in the pathogenesis of UTUC is investigated through the mechanisms of chronic inflammation, genotoxic damage, immune microenvironmental imbalance and metabolic reprogramming. The pyelo-ureteric microbiome of healthy populations is dominated by commensal bacteria such as Lactobacillus and Streptococcus, whereas pathogenic bacteria such as Escherichia coli (E. coli) and Enterococcus faecalis are significantly enriched in patients with UTUC, which results in the development of DNA damage, inflammatory response and immunosuppression. In addition, microbiome metabolites (e.g., short-chain fatty acids, tryptophan derivatives) can influence tumor progression by modulating immune checkpoints (e.g., PD-1/PD-L1, B7-H4) and metabolic pathways (e.g., Warburg effect). In diagnostic and therapeutic applications, urinary microbial markers (e.g., E. coli-specific gene clusters) can be combined with circulating tumor DNA (ctDNA) assays to improve diagnostic sensitivity and specificity, and indices of intestinal flora diversity (e.g., Simpson's index) are significantly correlated with the response rate to chemotherapy and prognostic course. In the future, we need to overcome the challenges of difficult sample acquisition, unknown causal mechanisms, and etiologic heterogeneity interference, and promote multi-omics joint modeling as well as cross-ethnicity and geographic research, and bidirectional regulation mechanisms of the gut-kidney axis in order to develop more accurate UTUC diagnosis and treatment strategies.
Additional Links: PMID-41112283
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Citation:
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@article {pmid41112283,
year = {2025},
author = {Pei, X and Yu, M and Wang, Y and Zong, S and Qi, F and Wang, K},
title = {What is the relationship between microorganisms in the human body and upper tract urothelial carcinoma?.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1636782},
pmid = {41112283},
issn = {1664-3224},
mesh = {Humans ; *Microbiota/immunology ; *Urologic Neoplasms/microbiology ; Tumor Microenvironment/immunology ; *Carcinoma, Transitional Cell/microbiology ; },
abstract = {Upper Tract Urothelial Carcinoma (UTUC) is a highly malignant tumor originating from the epithelium of the upper urinary tract with diverse pathogenesis, but currently available diagnostic and therapeutic strategies have some limitations. In recent years, human microbiome-related studies have provided new ideas for the exploration of the pathogenesis and treatment of UTUC. In this paper, we review the research progress of human microbiome related to UTUC. Focusing on the urinary microbiome, the role of the microbiome in the pathogenesis of UTUC is investigated through the mechanisms of chronic inflammation, genotoxic damage, immune microenvironmental imbalance and metabolic reprogramming. The pyelo-ureteric microbiome of healthy populations is dominated by commensal bacteria such as Lactobacillus and Streptococcus, whereas pathogenic bacteria such as Escherichia coli (E. coli) and Enterococcus faecalis are significantly enriched in patients with UTUC, which results in the development of DNA damage, inflammatory response and immunosuppression. In addition, microbiome metabolites (e.g., short-chain fatty acids, tryptophan derivatives) can influence tumor progression by modulating immune checkpoints (e.g., PD-1/PD-L1, B7-H4) and metabolic pathways (e.g., Warburg effect). In diagnostic and therapeutic applications, urinary microbial markers (e.g., E. coli-specific gene clusters) can be combined with circulating tumor DNA (ctDNA) assays to improve diagnostic sensitivity and specificity, and indices of intestinal flora diversity (e.g., Simpson's index) are significantly correlated with the response rate to chemotherapy and prognostic course. In the future, we need to overcome the challenges of difficult sample acquisition, unknown causal mechanisms, and etiologic heterogeneity interference, and promote multi-omics joint modeling as well as cross-ethnicity and geographic research, and bidirectional regulation mechanisms of the gut-kidney axis in order to develop more accurate UTUC diagnosis and treatment strategies.},
}
MeSH Terms:
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Humans
*Microbiota/immunology
*Urologic Neoplasms/microbiology
Tumor Microenvironment/immunology
*Carcinoma, Transitional Cell/microbiology
RevDate: 2025-10-20
CmpDate: 2025-10-20
Gut microbial-derived 3,4-dihydroxyphenylacetic acid ameliorates reproductive phenotype of polycystic ovary syndrome.
iMeta, 4(5):e70065.
Polycystic ovary syndrome (PCOS) is a prevalent endocrine and reproductive disorder affecting women of reproductive age. While the gut microbiota has been implicated in PCOS pathophysiology, the role of microbial-derived metabolites as mediators of host-microbe interactions remains poorly defined. Here, we integrated untargeted gut metabolomics with metagenomic profiling in patients with PCOS and identified a marked depletion of 3,4-dihydroxyphenylacetic acid (DHPAA), a flavonoid-derived microbial catabolite. Oral administration of DHPAA ameliorated PCOS-like phenotypes in two mouse models by suppressing bone morphogenetic protein signaling and reducing anti-Müllerian hormone (AMH) levels. We found that DHPAA production depends on gut microbial degradation of dietary flavonoids. We further identified a bacterial species, Streptococcus thermophilus, consistently depleted in PCOS across two human cohorts and a mouse model, restored DHPAA levels and improved reproductive outcomes in mice. Conversely, a β-galactosidase-deficient mutant of S. thermophilus failed to confer these benefits, highlighting β-galactosidase as a critical enzyme in DHPAA biosynthesis. Our findings establish DHPAA as a key microbial metabolite linking diet, microbiota, and reproductive health, and propose its potential as a novel therapeutic candidate for PCOS.
Additional Links: PMID-41112053
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@article {pmid41112053,
year = {2025},
author = {Li, P and Xie, L and Zheng, H and Feng, Y and Mai, F and Tang, W and Wang, J and Lan, Z and Lv, S and Jayawardana, T and Koentgen, S and Xu, S and Wan, Z and Chen, Y and Xu, H and Shen, S and Zhang, F and Yang, Y and Hold, G and He, F and El-Omar, EM and Yu, G and Chen, X},
title = {Gut microbial-derived 3,4-dihydroxyphenylacetic acid ameliorates reproductive phenotype of polycystic ovary syndrome.},
journal = {iMeta},
volume = {4},
number = {5},
pages = {e70065},
pmid = {41112053},
issn = {2770-596X},
abstract = {Polycystic ovary syndrome (PCOS) is a prevalent endocrine and reproductive disorder affecting women of reproductive age. While the gut microbiota has been implicated in PCOS pathophysiology, the role of microbial-derived metabolites as mediators of host-microbe interactions remains poorly defined. Here, we integrated untargeted gut metabolomics with metagenomic profiling in patients with PCOS and identified a marked depletion of 3,4-dihydroxyphenylacetic acid (DHPAA), a flavonoid-derived microbial catabolite. Oral administration of DHPAA ameliorated PCOS-like phenotypes in two mouse models by suppressing bone morphogenetic protein signaling and reducing anti-Müllerian hormone (AMH) levels. We found that DHPAA production depends on gut microbial degradation of dietary flavonoids. We further identified a bacterial species, Streptococcus thermophilus, consistently depleted in PCOS across two human cohorts and a mouse model, restored DHPAA levels and improved reproductive outcomes in mice. Conversely, a β-galactosidase-deficient mutant of S. thermophilus failed to confer these benefits, highlighting β-galactosidase as a critical enzyme in DHPAA biosynthesis. Our findings establish DHPAA as a key microbial metabolite linking diet, microbiota, and reproductive health, and propose its potential as a novel therapeutic candidate for PCOS.},
}
RevDate: 2025-10-20
CmpDate: 2025-10-20
The microbiome in cancer.
iMeta, 4(5):e70070.
The human microbiome is now recognized as a central regulator of cancer biology, intricately shaping tumor development, immune dynamics, and therapeutic response. This comprehensive review delineates the multifaceted roles of bacteria, viruses, and fungi in modulating the tumor microenvironment and systemic immunity across diverse cancer types. We synthesize current evidence on how microbial dysbiosis promotes carcinogenesis via chronic inflammation, metabolic reprogramming, genotoxic stress, immune evasion, and epigenetic remodeling. This review emphasizes organ-specific microbiome signatures and highlights their potential as non-invasive biomarkers for early detection, treatment stratification, and prognosis. Furthermore, we explore the impact of intratumoral microbiota on cancer therapies, uncovering how microbial metabolites and host-microbe interactions shape therapeutic efficacy and resistance. Finally, advances in microbiome-targeted strategies, such as probiotics, fecal microbiota transplantation, and engineered microbes offer new avenues for adjunctive cancer therapy. This review provides a roadmap for future investigation and underscores the transformative promise of microbiome modulation in cancer prevention and treatment.
Additional Links: PMID-41112042
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@article {pmid41112042,
year = {2025},
author = {Lin, A and Xiong, M and Jiang, A and Huang, L and Wong, HZH and Feng, S and Zhang, C and Li, Y and Chen, L and Chi, H and Zhang, P and Ye, B and Zhang, H and Zhang, N and Zhu, L and Mou, W and Shen, J and Li, K and Xu, W and Ying, H and Zhang, C and Zeng, D and Xie, J and Deng, X and Wang, Q and Xu, J and Shi, W and Qi, C and Qu, C and Huang, X and Hajdu, A and Li, C and Peng, C and Cao, X and Pei, G and Zhang, L and Huo, Y and Xu, J and Glaviano, A and Szöllősi, AG and Bian, S and Li, Z and Tang, H and Tang, B and Liu, Z and Zhang, J and Miao, K and Cheng, Q and Wei, T and Yuan, S and Luo, P},
title = {The microbiome in cancer.},
journal = {iMeta},
volume = {4},
number = {5},
pages = {e70070},
pmid = {41112042},
issn = {2770-596X},
abstract = {The human microbiome is now recognized as a central regulator of cancer biology, intricately shaping tumor development, immune dynamics, and therapeutic response. This comprehensive review delineates the multifaceted roles of bacteria, viruses, and fungi in modulating the tumor microenvironment and systemic immunity across diverse cancer types. We synthesize current evidence on how microbial dysbiosis promotes carcinogenesis via chronic inflammation, metabolic reprogramming, genotoxic stress, immune evasion, and epigenetic remodeling. This review emphasizes organ-specific microbiome signatures and highlights their potential as non-invasive biomarkers for early detection, treatment stratification, and prognosis. Furthermore, we explore the impact of intratumoral microbiota on cancer therapies, uncovering how microbial metabolites and host-microbe interactions shape therapeutic efficacy and resistance. Finally, advances in microbiome-targeted strategies, such as probiotics, fecal microbiota transplantation, and engineered microbes offer new avenues for adjunctive cancer therapy. This review provides a roadmap for future investigation and underscores the transformative promise of microbiome modulation in cancer prevention and treatment.},
}
RevDate: 2025-10-19
Forensic application of metagenomics: Methods and future directions.
Journal of microbiological methods pii:S0167-7012(25)00216-7 [Epub ahead of print].
The microbial communities are found commonly in our environment, making it impossible to touch any surface without interfering with them. The human microbiome, primarily bacteria in the saliva, skin, and gut, can be used for forensic purposes. Human-associated and environmental samples, such as soil, water, etc., carry the microbiome, which can be used for geolocation inference. These microbiomes have considerable potential for use in forensic investigations, including many instances of sexual violence, post-mortem examinations, individual identification, and location identification. Recent developments in metagenomic sequencing have greatly contributed to microbial analysis. Yet, because of certain issues and challenges, the forensic application of microbiomes is still in its infancy. This article reviewed the use of metagenomics in forensic science and some of the main obstacles that are faced by experts in this area. The first and foremost issues noted were the lack of standardization protocols and a poor reference database for research studies. Some limitations, such as storage sensitivity and limited samples, are also indicated. Future research studies should concentrate on more standardized investigations to overcome these difficulties and explore the enormous potential of microbiomes for beneficial applications in forensic contexts.
Additional Links: PMID-41110780
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@article {pmid41110780,
year = {2025},
author = {Sreekutti, S and Ndomondo, S and Sharma, P and Patel, R and Mevada, V},
title = {Forensic application of metagenomics: Methods and future directions.},
journal = {Journal of microbiological methods},
volume = {},
number = {},
pages = {107300},
doi = {10.1016/j.mimet.2025.107300},
pmid = {41110780},
issn = {1872-8359},
abstract = {The microbial communities are found commonly in our environment, making it impossible to touch any surface without interfering with them. The human microbiome, primarily bacteria in the saliva, skin, and gut, can be used for forensic purposes. Human-associated and environmental samples, such as soil, water, etc., carry the microbiome, which can be used for geolocation inference. These microbiomes have considerable potential for use in forensic investigations, including many instances of sexual violence, post-mortem examinations, individual identification, and location identification. Recent developments in metagenomic sequencing have greatly contributed to microbial analysis. Yet, because of certain issues and challenges, the forensic application of microbiomes is still in its infancy. This article reviewed the use of metagenomics in forensic science and some of the main obstacles that are faced by experts in this area. The first and foremost issues noted were the lack of standardization protocols and a poor reference database for research studies. Some limitations, such as storage sensitivity and limited samples, are also indicated. Future research studies should concentrate on more standardized investigations to overcome these difficulties and explore the enormous potential of microbiomes for beneficial applications in forensic contexts.},
}
RevDate: 2025-10-17
Microbiome-active drug delivery systems (MADDS): Leveraging microbial stimuli for controlled drug release.
Advanced drug delivery reviews pii:S0169-409X(25)00205-4 [Epub ahead of print].
The human microbiome comprises diverse microbial communities that inhabit tissues and biofluids throughout the body, including the gastrointestinal tract, lungs, vagina, and skin. These sites create dynamic microenvironments rich in enzymes, metabolites, and chemical gradients that act both as biological barriers and as localised targets for drug delivery. This review provides an overview of Microbiome-Active Drug Delivery Systems (MADDS), an emerging class of platforms that exploit microbial stimuli for site-specific therapeutic release. Unlike conventional systems that simply coexist with the microbiome, MADDS harness resident microbes and their metabolites to trigger drug activation, retention, or release. This enables spatially precise delivery of small molecules, biologics, and live biotherapeutic products (LBPs). Key strategies include enzyme-, environment-, metabolite-, biofilm-, and receptor-responsive designs, each tailored to microbial niches and applied across infectious, inflammatory, and metabolic disorders. However, challenges remain, including microbiome variability between individuals, regulatory uncertainty around hybrid biologic-material systems, and the need for scalable GMP-compliant manufacturing. This review therefore outlines the current approaches for engineering MADDS and the future steps required for clinical translation. By exploiting microbial cues for controlled drug release, MADDS offer a practical route to more targeted and patient-specific therapies.
Additional Links: PMID-41106731
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@article {pmid41106731,
year = {2025},
author = {Kamath, S and Ariaee, A and Abdelhafez, A and Asif, Z and Chan, NSL and Collins, K and Hunter, A and Joyce, P},
title = {Microbiome-active drug delivery systems (MADDS): Leveraging microbial stimuli for controlled drug release.},
journal = {Advanced drug delivery reviews},
volume = {},
number = {},
pages = {115720},
doi = {10.1016/j.addr.2025.115720},
pmid = {41106731},
issn = {1872-8294},
abstract = {The human microbiome comprises diverse microbial communities that inhabit tissues and biofluids throughout the body, including the gastrointestinal tract, lungs, vagina, and skin. These sites create dynamic microenvironments rich in enzymes, metabolites, and chemical gradients that act both as biological barriers and as localised targets for drug delivery. This review provides an overview of Microbiome-Active Drug Delivery Systems (MADDS), an emerging class of platforms that exploit microbial stimuli for site-specific therapeutic release. Unlike conventional systems that simply coexist with the microbiome, MADDS harness resident microbes and their metabolites to trigger drug activation, retention, or release. This enables spatially precise delivery of small molecules, biologics, and live biotherapeutic products (LBPs). Key strategies include enzyme-, environment-, metabolite-, biofilm-, and receptor-responsive designs, each tailored to microbial niches and applied across infectious, inflammatory, and metabolic disorders. However, challenges remain, including microbiome variability between individuals, regulatory uncertainty around hybrid biologic-material systems, and the need for scalable GMP-compliant manufacturing. This review therefore outlines the current approaches for engineering MADDS and the future steps required for clinical translation. By exploiting microbial cues for controlled drug release, MADDS offer a practical route to more targeted and patient-specific therapies.},
}
RevDate: 2025-10-17
Emerging Concepts in Periprosthetic Joint Infection Research: Infection Recurrence and Microbe Persistence.
The Journal of arthroplasty pii:S0883-5403(25)01310-5 [Epub ahead of print].
Recurrent periprosthetic joint infection (PJI) is a highly morbid complication following total joint arthroplasty (TJA). Despite appropriate medical and surgical management with targeted antimicrobial therapies, many patients who suffer from a PJI experience clinically relevant episodes of recurrence. Though the majority of these recurrent infections are due to microbes that are different from the species initially isolated at the index infection, approximately 15 to 50% of subsequent PJIs are attributed to recurrence with the same causative organism. Treatment resistance, contamination during revision surgery, hematogenous spread of bacteria from a distant source, and the presence of resilient biofilms have long been implicated in these recurrent infections. However, recent preclinical and clinical evidence has demonstrated that certain organisms that commonly cause PJI, namely staphylococcal species, can undergo phenotypic transformation into viable, but non-culturable (VBNC) and quasi-dormant small colony variant (SCV) forms that may persist intracellularly and lead to recurrent infection. Moreover, some organisms are known to infiltrate the osteocyte lacuno-canalicular network (OLCN) and invade eukaryotic cells to avoid targeting by the host immune system and antimicrobial agents. In doing so, they create microbial reservoirs that may be capable of reactivating to cause symptomatic infection locally or after being transported to the joint by circulating phagocytic cells. Commensal species present in the human microbiome may also become pathogenic and lead to recurrent PJI. Evidence suggests dysbiosis, a pathological imbalance in the composition and function of the microbiome, may induce the translocation of resident organisms from the gut into the bloodstream. Recent studies have also identified joint microbiota signatures that vary in accordance with the presence or absence of certain pathologies, including PJI.
Additional Links: PMID-41106704
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Citation:
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@article {pmid41106704,
year = {2025},
author = {Heckmann, ND and Culler, M and Atallah, LM and Mont, MA and Lieberman, JR and Parvizi, J},
title = {Emerging Concepts in Periprosthetic Joint Infection Research: Infection Recurrence and Microbe Persistence.},
journal = {The Journal of arthroplasty},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.arth.2025.10.033},
pmid = {41106704},
issn = {1532-8406},
abstract = {Recurrent periprosthetic joint infection (PJI) is a highly morbid complication following total joint arthroplasty (TJA). Despite appropriate medical and surgical management with targeted antimicrobial therapies, many patients who suffer from a PJI experience clinically relevant episodes of recurrence. Though the majority of these recurrent infections are due to microbes that are different from the species initially isolated at the index infection, approximately 15 to 50% of subsequent PJIs are attributed to recurrence with the same causative organism. Treatment resistance, contamination during revision surgery, hematogenous spread of bacteria from a distant source, and the presence of resilient biofilms have long been implicated in these recurrent infections. However, recent preclinical and clinical evidence has demonstrated that certain organisms that commonly cause PJI, namely staphylococcal species, can undergo phenotypic transformation into viable, but non-culturable (VBNC) and quasi-dormant small colony variant (SCV) forms that may persist intracellularly and lead to recurrent infection. Moreover, some organisms are known to infiltrate the osteocyte lacuno-canalicular network (OLCN) and invade eukaryotic cells to avoid targeting by the host immune system and antimicrobial agents. In doing so, they create microbial reservoirs that may be capable of reactivating to cause symptomatic infection locally or after being transported to the joint by circulating phagocytic cells. Commensal species present in the human microbiome may also become pathogenic and lead to recurrent PJI. Evidence suggests dysbiosis, a pathological imbalance in the composition and function of the microbiome, may induce the translocation of resident organisms from the gut into the bloodstream. Recent studies have also identified joint microbiota signatures that vary in accordance with the presence or absence of certain pathologies, including PJI.},
}
RevDate: 2025-10-17
CmpDate: 2025-10-17
Beyond just correlation: causal machine learning for the microbiome, from prediction to health policy with econometric tools.
Frontiers in microbiology, 16:1691503.
The human microbiome is increasingly recognized as a key mediator of health and disease, yet translating microbial associations into actionable interventions remains challenging. This review synthesizes advances in machine learning (ML) and causal inference applied to human microbiome research, emphasizing policy-relevant applications. Explainable ML approaches, have identified microbial drivers, guiding targeted strategies. Econometric tools, including instrumental variables, difference-in-differences, and panel data models, provide robust frameworks for validating causal relationships, while hybrid methods like Double Machine Learning (Double ML) and Deep Instrumental Variables (Deep IV) address high-dimensional and non-linear effects, enabling precise evaluation of microbiome-mediated interventions. Policy translation is further enhanced by federated learning, standardized analytical pipelines, and model visualization frameworks, which collectively improve reproducibility, scalability, and data privacy compliance. By integrating predictive power with causal rigor, microbiome research can move beyond observational associations to generate interventions that are biologically grounded, clinically actionable, and policy-ready. This roadmap provides a blueprint for translating mechanistic microbial insights into real-world health solutions, emphasizing interdisciplinary collaboration, standardized reporting, and evidence-based policymaking.
Additional Links: PMID-41103759
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@article {pmid41103759,
year = {2025},
author = {Khelfaoui, I and Wang, W and Meskher, H and Shehata, AI and El Basuini, MF and Abouelenein, MF and Degha, HE and Alhoshy, M and Teiba, II and Mahmoud, SS},
title = {Beyond just correlation: causal machine learning for the microbiome, from prediction to health policy with econometric tools.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1691503},
pmid = {41103759},
issn = {1664-302X},
abstract = {The human microbiome is increasingly recognized as a key mediator of health and disease, yet translating microbial associations into actionable interventions remains challenging. This review synthesizes advances in machine learning (ML) and causal inference applied to human microbiome research, emphasizing policy-relevant applications. Explainable ML approaches, have identified microbial drivers, guiding targeted strategies. Econometric tools, including instrumental variables, difference-in-differences, and panel data models, provide robust frameworks for validating causal relationships, while hybrid methods like Double Machine Learning (Double ML) and Deep Instrumental Variables (Deep IV) address high-dimensional and non-linear effects, enabling precise evaluation of microbiome-mediated interventions. Policy translation is further enhanced by federated learning, standardized analytical pipelines, and model visualization frameworks, which collectively improve reproducibility, scalability, and data privacy compliance. By integrating predictive power with causal rigor, microbiome research can move beyond observational associations to generate interventions that are biologically grounded, clinically actionable, and policy-ready. This roadmap provides a blueprint for translating mechanistic microbial insights into real-world health solutions, emphasizing interdisciplinary collaboration, standardized reporting, and evidence-based policymaking.},
}
RevDate: 2025-10-16
CmpDate: 2025-10-16
EPheClass: ensemble-based phenotype classifier from 16S rRNA gene sequences.
Frontiers in bioinformatics, 5:1514880.
One area of bioinformatics that is currently attracting particular interest is the classification of polymicrobial diseases using machine learning (ML), with data obtained from high-throughput amplicon sequencing of the 16S rRNA gene in human microbiome samples. The microbial dysbiosis underlying these types of diseases is particularly challenging to classify, as the data is highly dimensional, with potentially hundreds or even thousands of predictive features. In addition, the imbalance in the composition of the microbial community is highly heterogeneous across samples. In this paper, we propose a curated pipeline for binary phenotype classification based on a count table of 16S rRNA gene amplicons, which can be applied to any microbiome. To evaluate our proposal, raw 16S rRNA gene sequences from samples of healthy and periodontally affected oral microbiomes that met certain quality criteria were downloaded from public repositories. In the end, a total of 2,581 samples were analysed. In our approach, we first reduced the dimensionality of the data using feature selection methods. After tuning and evaluating different machine learning (ML) models and ensembles created using Dynamic Ensemble Selection (DES) techniques, we found that all DES models performed similarly and were more robust than individual models. Although the margin over other methods was minimal, DES-P achieved the highest AUC and was therefore selected as the representative technique in our analysis. When diagnosing periodontal disease with saliva samples, it achieved with only 13 features an F1 score of 0.913, a precision of 0.881, a recall (sensitivity) of 0.947, an accuracy of 0.929, and an AUC of 0.973. In addition, we used EPheClass to diagnose inflammatory bowel disease (IBD) and obtained better results than other works in the literature using the same dataset. We also evaluated its effectiveness in detecting antibiotic exposure, where it again demonstrated competitive results. This highlights the importance and generalisation aspect of our classification approach, which is applicable to different phenotypes, study niches, and sample types. The code is available at https://gitlab.citius.usc.es/lara.vazquez/epheclass.
Additional Links: PMID-41099014
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@article {pmid41099014,
year = {2025},
author = {Vázquez-González, L and Peña-Reyes, C and Regueira-Iglesias, A and Balsa-Castro, C and Tomás, I and Carreira, MJ},
title = {EPheClass: ensemble-based phenotype classifier from 16S rRNA gene sequences.},
journal = {Frontiers in bioinformatics},
volume = {5},
number = {},
pages = {1514880},
pmid = {41099014},
issn = {2673-7647},
abstract = {One area of bioinformatics that is currently attracting particular interest is the classification of polymicrobial diseases using machine learning (ML), with data obtained from high-throughput amplicon sequencing of the 16S rRNA gene in human microbiome samples. The microbial dysbiosis underlying these types of diseases is particularly challenging to classify, as the data is highly dimensional, with potentially hundreds or even thousands of predictive features. In addition, the imbalance in the composition of the microbial community is highly heterogeneous across samples. In this paper, we propose a curated pipeline for binary phenotype classification based on a count table of 16S rRNA gene amplicons, which can be applied to any microbiome. To evaluate our proposal, raw 16S rRNA gene sequences from samples of healthy and periodontally affected oral microbiomes that met certain quality criteria were downloaded from public repositories. In the end, a total of 2,581 samples were analysed. In our approach, we first reduced the dimensionality of the data using feature selection methods. After tuning and evaluating different machine learning (ML) models and ensembles created using Dynamic Ensemble Selection (DES) techniques, we found that all DES models performed similarly and were more robust than individual models. Although the margin over other methods was minimal, DES-P achieved the highest AUC and was therefore selected as the representative technique in our analysis. When diagnosing periodontal disease with saliva samples, it achieved with only 13 features an F1 score of 0.913, a precision of 0.881, a recall (sensitivity) of 0.947, an accuracy of 0.929, and an AUC of 0.973. In addition, we used EPheClass to diagnose inflammatory bowel disease (IBD) and obtained better results than other works in the literature using the same dataset. We also evaluated its effectiveness in detecting antibiotic exposure, where it again demonstrated competitive results. This highlights the importance and generalisation aspect of our classification approach, which is applicable to different phenotypes, study niches, and sample types. The code is available at https://gitlab.citius.usc.es/lara.vazquez/epheclass.},
}
RevDate: 2025-10-16
CmpDate: 2025-10-16
The role of oral microbiota in digestive system diseases: current advances and perspectives.
Journal of oral microbiology, 17(1):2566403.
The oral microbiota is intimately linked to human health and various disease states. With the advent of the Human Microbiome Project, our comprehension of the oral microbiota has substantially improved. This microbial community is not only associated with a range of oral diseases, such as dental caries and periodontal diseases, but also with numerous digestive disorders, as demonstrated by recent clinical studies. Specific bacteria residing in the oral cavity, such as Porphyromonas gingivalis, Fusobacterium species and Streptococcus species, have been shown to translocate to the gastrointestinal tract, thereby establishing a potential connection between the oral and gut microbiota. The transfer and ectopic colonization of oral microbiota within the gastrointestinal tract may contribute to both the onset and exacerbation of gastrointestinal diseases. Following the principles of dysregulation characteristics, mechanism research and innovative treatment, this paper systematically reviews the association between the oral microbiota and various digestive system diseases. This paper explores how specific oral microbiota drive digestive system diseases mechanisms and evaluates treatments including probiotics, prebiotics, fecal microbiota transplantation, and targeted antimicrobial therapies. By clarifying the oral-gut microbiota-disease link, it highlights oral microbiota monitoring as a promising tool for early detection, diagnosis, and therapy.
Additional Links: PMID-41098769
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@article {pmid41098769,
year = {2025},
author = {Li, Y and Xin, Y and Zong, W and Li, X},
title = {The role of oral microbiota in digestive system diseases: current advances and perspectives.},
journal = {Journal of oral microbiology},
volume = {17},
number = {1},
pages = {2566403},
pmid = {41098769},
issn = {2000-2297},
abstract = {The oral microbiota is intimately linked to human health and various disease states. With the advent of the Human Microbiome Project, our comprehension of the oral microbiota has substantially improved. This microbial community is not only associated with a range of oral diseases, such as dental caries and periodontal diseases, but also with numerous digestive disorders, as demonstrated by recent clinical studies. Specific bacteria residing in the oral cavity, such as Porphyromonas gingivalis, Fusobacterium species and Streptococcus species, have been shown to translocate to the gastrointestinal tract, thereby establishing a potential connection between the oral and gut microbiota. The transfer and ectopic colonization of oral microbiota within the gastrointestinal tract may contribute to both the onset and exacerbation of gastrointestinal diseases. Following the principles of dysregulation characteristics, mechanism research and innovative treatment, this paper systematically reviews the association between the oral microbiota and various digestive system diseases. This paper explores how specific oral microbiota drive digestive system diseases mechanisms and evaluates treatments including probiotics, prebiotics, fecal microbiota transplantation, and targeted antimicrobial therapies. By clarifying the oral-gut microbiota-disease link, it highlights oral microbiota monitoring as a promising tool for early detection, diagnosis, and therapy.},
}
RevDate: 2025-10-15
Predicting functions of uncharacterized gene products from microbial communities.
Nature biotechnology [Epub ahead of print].
The majority of genes in microbial communities remain uncharacterized. Here we develop a method to infer putative function for microbial proteins at scale by assessing community-wide multiomics data. We predict high-confidence functions for >443,000 protein families (~82.3% previously uncharacterized), including >27,000 protein families with weak homology to known proteins and >6,000 protein families without homology. These were drawn from 1,595 gut metagenomes and 800 metatranscriptomes from the Integrative Human Microbiome Project (HMP2/iHMP). Integrating additional information such as sequence similarity, genomic proximity and domain-domain interactions improves performance of the method. Our method's implementation, FUGAsseM, is generalizable and predicts protein function in both well-studied and undercharacterized communities. FUGAsseM achieves similar levels of accuracy in the context of microbial communities when compared to state-of-the-art approaches designed for application to single organisms while simultaneously providing much greater breadth of coverage. This initial study expands the functional landscape of the human gut microbiome and allows for exploration of microbial proteins in undercharacterized communities.
Additional Links: PMID-41094150
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@article {pmid41094150,
year = {2025},
author = {Zhang, Y and Bhosle, A and Bae, S and Eckenrode, K and Huang, X and Tang, J and Lavrentovich, D and Awad, L and Hua, J and Wang, Y and Morgan, XC and Li, B and Krueger, A and Garrett, WS and Franzosa, EA and Huttenhower, C},
title = {Predicting functions of uncharacterized gene products from microbial communities.},
journal = {Nature biotechnology},
volume = {},
number = {},
pages = {},
pmid = {41094150},
issn = {1546-1696},
support = {R24DK110499//U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases)/ ; U19AI110820//Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID)/ ; },
abstract = {The majority of genes in microbial communities remain uncharacterized. Here we develop a method to infer putative function for microbial proteins at scale by assessing community-wide multiomics data. We predict high-confidence functions for >443,000 protein families (~82.3% previously uncharacterized), including >27,000 protein families with weak homology to known proteins and >6,000 protein families without homology. These were drawn from 1,595 gut metagenomes and 800 metatranscriptomes from the Integrative Human Microbiome Project (HMP2/iHMP). Integrating additional information such as sequence similarity, genomic proximity and domain-domain interactions improves performance of the method. Our method's implementation, FUGAsseM, is generalizable and predicts protein function in both well-studied and undercharacterized communities. FUGAsseM achieves similar levels of accuracy in the context of microbial communities when compared to state-of-the-art approaches designed for application to single organisms while simultaneously providing much greater breadth of coverage. This initial study expands the functional landscape of the human gut microbiome and allows for exploration of microbial proteins in undercharacterized communities.},
}
RevDate: 2025-10-15
CmpDate: 2025-10-15
Microbiome therapeutic PMC101 inhibits the translocation of carbapenem-resistant Klebsiella while enhancing eubiosis in antibiotic-induced dysbiosis mice.
Medical microbiology and immunology, 214(1):49.
Carbapenem-resistant Enterobacteriaceae (CRE), known for their extensive antibiotic resistance, pose a severe global medical threat. Therefore, developing novel therapeutics beyond conventional antibiotics is urgently needed, and the importance of microbiome therapeutics is increasingly being recognized. This study explores the expanded systemic efficacy of PMC101, a microbiome therapeutic, beyond intestinal CRE infections and investigates its mechanism of action from a microbiome perspective. First, the genetic characteristics of the novel strain were identified through whole-genome analysis, and a scalable cultivation process was established as part of the overall development of this microbiome therapeutic. PMC101 increased the survival rate to 100%, significantly reduced disease severity scores, and prevented weight loss in CRE-infected mice treated with antibiotics. These effects are attributed to the inhibition of CRE growth in stool and the reduced detection of CRE in the lungs and kidneys, indicating suppression of systemic translocation. Metagenomic analysis revealed that PMC101 prevented the reduction in microbial population caused by antibiotics and CRE infection, restored species diversity indices, and mitigated dysbiosis while promoting eubiosis. This CRE translocation suppression was closely associated with increased CRE translocation-microbiome index, defined as the ratio of Bacteroidetes to Proteobacteria. This relationship was further confirmed through simulations using a human intestinal microbial ecosystem model. Additionally, increases in short-chain fatty acids, reductions in excessive inflammatory responses, and decreases in tissue damage were observed, all of which contribute to preventing CRE translocation. Finally, pathogen inhibition effects and safety tests were conducted, confirming the prophylactic potential of PMC101 as a microbiome therapeutic. These findings strongly support PMC101 as a promising candidate for future microbiome-based therapies against CRE infections.
Additional Links: PMID-41091222
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@article {pmid41091222,
year = {2025},
author = {Tajdozian, H and Seo, H and Kim, S and Rahim, MA and Park, HA and Sarafraz, F and Yoon, Y and Kim, H and Barman, I and Park, CE and Ghorbanian, F and Lee, S and Jeong, HR and Song, HY},
title = {Microbiome therapeutic PMC101 inhibits the translocation of carbapenem-resistant Klebsiella while enhancing eubiosis in antibiotic-induced dysbiosis mice.},
journal = {Medical microbiology and immunology},
volume = {214},
number = {1},
pages = {49},
pmid = {41091222},
issn = {1432-1831},
support = {No. RS-2023-00219563//Ministry of Science and ICT, South Korea/ ; P248400003//Korea Institute for Advancement of Technology/ ; },
mesh = {Animals ; *Dysbiosis/chemically induced/microbiology/therapy ; *Carbapenem-Resistant Enterobacteriaceae/drug effects/physiology ; *Anti-Bacterial Agents/adverse effects/pharmacology ; Mice ; *Gastrointestinal Microbiome/drug effects ; Disease Models, Animal ; *Klebsiella Infections/microbiology/therapy ; *Bacterial Translocation/drug effects ; Carbapenems/pharmacology ; Humans ; Mice, Inbred C57BL ; Feces/microbiology ; },
abstract = {Carbapenem-resistant Enterobacteriaceae (CRE), known for their extensive antibiotic resistance, pose a severe global medical threat. Therefore, developing novel therapeutics beyond conventional antibiotics is urgently needed, and the importance of microbiome therapeutics is increasingly being recognized. This study explores the expanded systemic efficacy of PMC101, a microbiome therapeutic, beyond intestinal CRE infections and investigates its mechanism of action from a microbiome perspective. First, the genetic characteristics of the novel strain were identified through whole-genome analysis, and a scalable cultivation process was established as part of the overall development of this microbiome therapeutic. PMC101 increased the survival rate to 100%, significantly reduced disease severity scores, and prevented weight loss in CRE-infected mice treated with antibiotics. These effects are attributed to the inhibition of CRE growth in stool and the reduced detection of CRE in the lungs and kidneys, indicating suppression of systemic translocation. Metagenomic analysis revealed that PMC101 prevented the reduction in microbial population caused by antibiotics and CRE infection, restored species diversity indices, and mitigated dysbiosis while promoting eubiosis. This CRE translocation suppression was closely associated with increased CRE translocation-microbiome index, defined as the ratio of Bacteroidetes to Proteobacteria. This relationship was further confirmed through simulations using a human intestinal microbial ecosystem model. Additionally, increases in short-chain fatty acids, reductions in excessive inflammatory responses, and decreases in tissue damage were observed, all of which contribute to preventing CRE translocation. Finally, pathogen inhibition effects and safety tests were conducted, confirming the prophylactic potential of PMC101 as a microbiome therapeutic. These findings strongly support PMC101 as a promising candidate for future microbiome-based therapies against CRE infections.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Animals
*Dysbiosis/chemically induced/microbiology/therapy
*Carbapenem-Resistant Enterobacteriaceae/drug effects/physiology
*Anti-Bacterial Agents/adverse effects/pharmacology
Mice
*Gastrointestinal Microbiome/drug effects
Disease Models, Animal
*Klebsiella Infections/microbiology/therapy
*Bacterial Translocation/drug effects
Carbapenems/pharmacology
Humans
Mice, Inbred C57BL
Feces/microbiology
RevDate: 2025-10-11
Environmental determinants of immune tolerance in asthma and allergy.
Immunology letters pii:S0165-2478(25)00135-X [Epub ahead of print].
Prevalence of allergic diseases has increased globally, reflecting environmental and behavioral changes. The exposome concept encompasses cumulative chemical, microbial, nutritional, psychosocial, and physical exposures across the life course, offering a unifying framework to understand how immune tolerance is shaped or disrupted. Emerging evidence highlights that early-life exposures are particularly critical. Pollutants, endocrine disruptors, microbial deprivation, dietary shifts, and psychosocial stress contribute to barrier dysfunction, dysbiosis, and immune dysregulation, favoring Th2 dominance and allergy development. In contrast, exposures that enhance biodiversity, microbial diversity, pollution-free air, and balanced nutrition support active tolerance development, especially via regulatory T cells. Mechanistic insights point to the barrier-microbiota-immune axis as central pathways linking the environment to allergic outcomes. Translational studies, including biodiversity enrichment interventions, maternal and infant dietary strategies, and microbiome-based therapies, illustrate the potential of exposome-informed approaches to allergy prevention. However, major challenges remain in measuring complex exposure mixtures, identifying causal pathways, and integrating exposome data with systems immunology. This review synthesizes current knowledge on how the exposome modulates immune tolerance and outlines future research directions toward precision prevention. A deeper understanding of these interactions is essential to address the rising global allergy burden.
Additional Links: PMID-41076098
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@article {pmid41076098,
year = {2025},
author = {Karisola, P and Alenius, H},
title = {Environmental determinants of immune tolerance in asthma and allergy.},
journal = {Immunology letters},
volume = {},
number = {},
pages = {107102},
doi = {10.1016/j.imlet.2025.107102},
pmid = {41076098},
issn = {1879-0542},
abstract = {Prevalence of allergic diseases has increased globally, reflecting environmental and behavioral changes. The exposome concept encompasses cumulative chemical, microbial, nutritional, psychosocial, and physical exposures across the life course, offering a unifying framework to understand how immune tolerance is shaped or disrupted. Emerging evidence highlights that early-life exposures are particularly critical. Pollutants, endocrine disruptors, microbial deprivation, dietary shifts, and psychosocial stress contribute to barrier dysfunction, dysbiosis, and immune dysregulation, favoring Th2 dominance and allergy development. In contrast, exposures that enhance biodiversity, microbial diversity, pollution-free air, and balanced nutrition support active tolerance development, especially via regulatory T cells. Mechanistic insights point to the barrier-microbiota-immune axis as central pathways linking the environment to allergic outcomes. Translational studies, including biodiversity enrichment interventions, maternal and infant dietary strategies, and microbiome-based therapies, illustrate the potential of exposome-informed approaches to allergy prevention. However, major challenges remain in measuring complex exposure mixtures, identifying causal pathways, and integrating exposome data with systems immunology. This review synthesizes current knowledge on how the exposome modulates immune tolerance and outlines future research directions toward precision prevention. A deeper understanding of these interactions is essential to address the rising global allergy burden.},
}
RevDate: 2025-10-08
CmpDate: 2025-10-08
Microbiome characterization of a pre-Hispanic man from Zimapán, Mexico: Insights into ancient gut microbial communities.
PloS one, 20(10):e0331137 pii:PONE-D-24-21607.
The research of microbiome derived from mummified human remains, coprolites and paleofeces has gained significant interest over several decades, aiming to elucidate the evolution of microbial interactions and shed light on the lifestyles of past populations. In this study, we analyzed the gut microbiome of a pre-Hispanic male individual referred to as the Zimapán man, dated to 936 BP, discovered on the border between Mesoamerica and Aridoamerica. Employing high-throughput 16S rRNA gene sequencing on both the paleofeces and mummified intestinal tissue, we conducted a comprehensive characterization of the Zimapán man's gut microbiome. The bacterial community was described, and a weighted UniFrac-based principal coordinates analysis (PCoA) was performed. The multivariate analysis incorporated microbiome samples from diverse environments, such as soils, compost, and both contemporary and ancient human gut microbiota. The analysis revealed bacterial groups associated with the human microbiome, including families such as Peptostreptococcaceae, Clostridiaceae, Enterobacteriaceae, and Enterococcaceae. Notably, a high abundance of the Clostridiaceae group was found, similar to those discovered in the intestinal tissue of mummies from other geographic regions. Additionally, unique groups such as Romboutsia hominis, exclusively isolated from human intestines and not previously reported in ancient human microbiomes, were identified. Furthermore, our analysis demonstrated that the bacterial composition did not resemble soil and compost environments. This initial characterization successfully achieved the goal of identifying bacterial groups of the gut microbiome in the Zimapán samples. Consequently, this study contributes to the ongoing expansion of knowledge regarding ancient microbiomes across diverse temporal, historical, geographical, and environmental contexts.
Additional Links: PMID-41060894
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PubMed:
Citation:
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@article {pmid41060894,
year = {2025},
author = {Rosas-Plaza, S and Mainou, L and Delgado, G and Morales, R and Aguilar-Romero, A and Escalante, AE and Cerritos, R},
title = {Microbiome characterization of a pre-Hispanic man from Zimapán, Mexico: Insights into ancient gut microbial communities.},
journal = {PloS one},
volume = {20},
number = {10},
pages = {e0331137},
doi = {10.1371/journal.pone.0331137},
pmid = {41060894},
issn = {1932-6203},
mesh = {Humans ; Male ; *Gastrointestinal Microbiome/genetics ; Mexico ; RNA, Ribosomal, 16S/genetics ; *Bacteria/genetics/classification/isolation & purification ; Phylogeny ; Mummies/microbiology ; },
abstract = {The research of microbiome derived from mummified human remains, coprolites and paleofeces has gained significant interest over several decades, aiming to elucidate the evolution of microbial interactions and shed light on the lifestyles of past populations. In this study, we analyzed the gut microbiome of a pre-Hispanic male individual referred to as the Zimapán man, dated to 936 BP, discovered on the border between Mesoamerica and Aridoamerica. Employing high-throughput 16S rRNA gene sequencing on both the paleofeces and mummified intestinal tissue, we conducted a comprehensive characterization of the Zimapán man's gut microbiome. The bacterial community was described, and a weighted UniFrac-based principal coordinates analysis (PCoA) was performed. The multivariate analysis incorporated microbiome samples from diverse environments, such as soils, compost, and both contemporary and ancient human gut microbiota. The analysis revealed bacterial groups associated with the human microbiome, including families such as Peptostreptococcaceae, Clostridiaceae, Enterobacteriaceae, and Enterococcaceae. Notably, a high abundance of the Clostridiaceae group was found, similar to those discovered in the intestinal tissue of mummies from other geographic regions. Additionally, unique groups such as Romboutsia hominis, exclusively isolated from human intestines and not previously reported in ancient human microbiomes, were identified. Furthermore, our analysis demonstrated that the bacterial composition did not resemble soil and compost environments. This initial characterization successfully achieved the goal of identifying bacterial groups of the gut microbiome in the Zimapán samples. Consequently, this study contributes to the ongoing expansion of knowledge regarding ancient microbiomes across diverse temporal, historical, geographical, and environmental contexts.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
Male
*Gastrointestinal Microbiome/genetics
Mexico
RNA, Ribosomal, 16S/genetics
*Bacteria/genetics/classification/isolation & purification
Phylogeny
Mummies/microbiology
RevDate: 2025-10-07
CmpDate: 2025-10-07
Concentrations of ciprofloxacin in food defined as safe alter the gut microbiome and ciprofloxacin susceptibility in humans: an interventional clinical study.
Scientific reports, 15(1):34908.
It is unknown if the low residual concentrations of ciprofloxacin/enrofloxacin allowed in food could influence the human microbiome. The European Medicines Agency reports that it is safe for an average human to ingest 372 µg of enrofloxacin/ciprofloxacin daily. We randomized 30 individuals to either 372 µg of ciprofloxacin or placebo daily for 27 days in a 2:1 fashion and measured the effect on the gut microbiome and the susceptibility of Escherichia coli to ciprofloxacin. After 27 days the E. coli of the individuals in the ciprofloxacin, but not the placebo arm, had reduced ciprofloxacin susceptibility. The receipt of ciprofloxacin was also associated with a reduction in the number of E. coli colony forming units in the gut. The low concentration of antimicrobials allowed in food may have an impact on the composition of the gut microbiome and antimicrobial susceptibility.
Additional Links: PMID-41057417
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Citation:
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@article {pmid41057417,
year = {2025},
author = {Manoharan-Basil, S and Gestels, Z and Abdellati, S and Vanbaelen, T and Van Den Bossche, D and van Alebeek, L and Van Herrewege, Y and Poppe, L and Vandenhove, L and Bracke, S and Smekens, B and Jacobs, B and Genbrugge, E and Kenyon, C},
title = {Concentrations of ciprofloxacin in food defined as safe alter the gut microbiome and ciprofloxacin susceptibility in humans: an interventional clinical study.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {34908},
pmid = {41057417},
issn = {2045-2322},
mesh = {Humans ; *Ciprofloxacin/pharmacology/administration & dosage ; *Gastrointestinal Microbiome/drug effects ; Escherichia coli/drug effects ; Male ; Female ; *Anti-Bacterial Agents/pharmacology/administration & dosage ; Adult ; Microbial Sensitivity Tests ; Middle Aged ; Young Adult ; Enrofloxacin ; Drug Resistance, Bacterial ; },
abstract = {It is unknown if the low residual concentrations of ciprofloxacin/enrofloxacin allowed in food could influence the human microbiome. The European Medicines Agency reports that it is safe for an average human to ingest 372 µg of enrofloxacin/ciprofloxacin daily. We randomized 30 individuals to either 372 µg of ciprofloxacin or placebo daily for 27 days in a 2:1 fashion and measured the effect on the gut microbiome and the susceptibility of Escherichia coli to ciprofloxacin. After 27 days the E. coli of the individuals in the ciprofloxacin, but not the placebo arm, had reduced ciprofloxacin susceptibility. The receipt of ciprofloxacin was also associated with a reduction in the number of E. coli colony forming units in the gut. The low concentration of antimicrobials allowed in food may have an impact on the composition of the gut microbiome and antimicrobial susceptibility.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Ciprofloxacin/pharmacology/administration & dosage
*Gastrointestinal Microbiome/drug effects
Escherichia coli/drug effects
Male
Female
*Anti-Bacterial Agents/pharmacology/administration & dosage
Adult
Microbial Sensitivity Tests
Middle Aged
Young Adult
Enrofloxacin
Drug Resistance, Bacterial
RevDate: 2025-10-06
CmpDate: 2025-10-06
The role of dysbiosis in shaping host immunity in endometrial cancer development.
Frontiers in immunology, 16:1627285.
In recent years, research into the background of carcinogenic processes has increasingly focused on the role of the tumor microenvironment (TME) in tumorigenesis. In addition to the presence of tumor cells and non-malignant components, which include immune cells, extracellular matrix elements, stroma, and endothelial cells, the microbiome is now increasingly being classified as an integral part of the TME. The establishment of the Human Microbiome Project (HMP) in 2007 along with the development of next-generation sequencing (NGS) techniques proved to be a breakthrough in terms of human microbiota research, shedding new light on the existing knowledge of microorganisms inhabiting various niches of the human body and their functions. Emerging scientific evidence from preclinical and clinical studies indicates significant differences in the microbiome composition between tumor tissues and benign controls. The presence of specific pathogenic strains within a tissue may play a key role in the initiation and progression of inflammation, which not only may be directly responsible for the stimulation of tumorigenic processes but may also affect the destabilization of the host genome, causing significant disruption of its metabolism. The role of microorganisms in the induction and promotion of pathological processes, including cancer, has been confirmed in many studies to date. Recent years of research on the microbiota of the female reproductive tract (FRT) have not only indicated that the endometrium has its unique microbial composition but have also made it possible to point out differences in composition between the microbiome of healthy and tumor-lesioned tissue, suggesting a potential role for dysbiotic disorders in the pathogenesis of endometrial cancer (EC). In this review, we aim to highlight the complex interplay between bacterial interactions and host immunity, and how this phenomenon contributes to the development and progression of endometrial cancer.
Additional Links: PMID-41050662
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@article {pmid41050662,
year = {2025},
author = {Wierzbińska, W and Kuźmycz, O and Kowalczyk, A and Stączek, P},
title = {The role of dysbiosis in shaping host immunity in endometrial cancer development.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1627285},
pmid = {41050662},
issn = {1664-3224},
mesh = {Humans ; *Dysbiosis/immunology/microbiology ; *Endometrial Neoplasms/immunology/microbiology/pathology/etiology ; Female ; Tumor Microenvironment/immunology ; Animals ; Microbiota/immunology ; Carcinogenesis/immunology ; },
abstract = {In recent years, research into the background of carcinogenic processes has increasingly focused on the role of the tumor microenvironment (TME) in tumorigenesis. In addition to the presence of tumor cells and non-malignant components, which include immune cells, extracellular matrix elements, stroma, and endothelial cells, the microbiome is now increasingly being classified as an integral part of the TME. The establishment of the Human Microbiome Project (HMP) in 2007 along with the development of next-generation sequencing (NGS) techniques proved to be a breakthrough in terms of human microbiota research, shedding new light on the existing knowledge of microorganisms inhabiting various niches of the human body and their functions. Emerging scientific evidence from preclinical and clinical studies indicates significant differences in the microbiome composition between tumor tissues and benign controls. The presence of specific pathogenic strains within a tissue may play a key role in the initiation and progression of inflammation, which not only may be directly responsible for the stimulation of tumorigenic processes but may also affect the destabilization of the host genome, causing significant disruption of its metabolism. The role of microorganisms in the induction and promotion of pathological processes, including cancer, has been confirmed in many studies to date. Recent years of research on the microbiota of the female reproductive tract (FRT) have not only indicated that the endometrium has its unique microbial composition but have also made it possible to point out differences in composition between the microbiome of healthy and tumor-lesioned tissue, suggesting a potential role for dysbiotic disorders in the pathogenesis of endometrial cancer (EC). In this review, we aim to highlight the complex interplay between bacterial interactions and host immunity, and how this phenomenon contributes to the development and progression of endometrial cancer.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Dysbiosis/immunology/microbiology
*Endometrial Neoplasms/immunology/microbiology/pathology/etiology
Female
Tumor Microenvironment/immunology
Animals
Microbiota/immunology
Carcinogenesis/immunology
RevDate: 2025-10-06
Microbiome: Friend or Friendly Foe.
Microbial physiology pii:000548748 [Epub ahead of print].
The human microbiome is a dynamic, polymicrobial ecosystem that plays an essential role in nutrition, immune development, barrier integrity, and host physiology, acting as a mutualistic partner under balanced conditions. However, its ecological complexity, genetic adaptability through horizontal gene transfer, and interactions with other prokaryotes as well as protozoan and metazoan parasites can transform commensals into pathobionts, resulting in weakened host's barriers, immunity declines with the progression of age, and community composition shifts toward dysbiosis. Factors such as diet, genetics, aging, immune-senescence, impaired autophagy, and environmental exposure, all influence this delicate balance, determining whether the microbiome remains protective or becomes an opportunistic source of inflammation and disease. This review focuses on the study of the intestinal microbiome in humans. Maintaining microbiome homeostasis is promoted through (a) dietary diversity, (b) limited antimicrobial use, (c) use of probiotics, (d) support for gut barrier function, and (e) healthy lifestyle improvements. These actions and considerations are critical to prevent the emergence of pathogenic states and preserving the microbiome's vital role in host health throughout life.
Additional Links: PMID-41047836
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@article {pmid41047836,
year = {2025},
author = {Reddy, LB and Saier, MH},
title = {Microbiome: Friend or Friendly Foe.},
journal = {Microbial physiology},
volume = {},
number = {},
pages = {},
doi = {10.1159/000548748},
pmid = {41047836},
issn = {2673-1673},
abstract = {The human microbiome is a dynamic, polymicrobial ecosystem that plays an essential role in nutrition, immune development, barrier integrity, and host physiology, acting as a mutualistic partner under balanced conditions. However, its ecological complexity, genetic adaptability through horizontal gene transfer, and interactions with other prokaryotes as well as protozoan and metazoan parasites can transform commensals into pathobionts, resulting in weakened host's barriers, immunity declines with the progression of age, and community composition shifts toward dysbiosis. Factors such as diet, genetics, aging, immune-senescence, impaired autophagy, and environmental exposure, all influence this delicate balance, determining whether the microbiome remains protective or becomes an opportunistic source of inflammation and disease. This review focuses on the study of the intestinal microbiome in humans. Maintaining microbiome homeostasis is promoted through (a) dietary diversity, (b) limited antimicrobial use, (c) use of probiotics, (d) support for gut barrier function, and (e) healthy lifestyle improvements. These actions and considerations are critical to prevent the emergence of pathogenic states and preserving the microbiome's vital role in host health throughout life.},
}
RevDate: 2025-10-06
CmpDate: 2025-10-06
Autologous fecal microbiota capsules are safe and potentially preserve beta-cell function in individuals with type 1 diabetes.
Gut microbes, 17(1):2563155.
This study investigated the safety and feasibility of daily ingestion of autologous lyophilized fecal microbiota capsules (a-LFMCs) for preserving beta-cell function in individuals with type 1 diabetes (T1D). We evaluated a-LFMC in an open-label, single-arm pilot study (NCT05323162) with 10 individuals with T1D. The study included a 3-month run-in period, 3 months of daily a-LFMC treatment, and a 3-month follow-up. Beta-cell function was assessed using mixed-meal stimulated C-peptide area under the curve (AUC). During the run-in period, beta-cell function significantly declined (mean ΔAUC -12.02 ± 5.09 nmol/L*min, p = 0.025). There was no decrease in beta-cell function during the a-LFMC treatment period (mean ΔAUC 0.76 ± 5.09 nmol/L*min, p = 0.88) and the follow-up period (mean ΔAUC 0.96 ± 5.09 nmol/L*min, p = 0.85). No serious adverse events occurred, though constipation increased during the treatment period (0% vs. 30%, p = 0.021). a-LFMC treatment was found to be safe and potentially contributes to preserving beta-cell function in T1D patients. A larger randomized placebo-controlled trial is needed to confirm these promising findings.
Additional Links: PMID-41047724
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PubMed:
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@article {pmid41047724,
year = {2025},
author = {de Groen, P and Fuhri Snethlage, CM and Wortelboer, K and Tokgöz, S and Davids, M and Verdoes, X and Westerbeke, FHM and Meijer, RI and Gotthardt, M and de Vos, WM and Herrema, H and Nieuwdorp, M and Hanssen, NMJ},
title = {Autologous fecal microbiota capsules are safe and potentially preserve beta-cell function in individuals with type 1 diabetes.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2563155},
doi = {10.1080/19490976.2025.2563155},
pmid = {41047724},
issn = {1949-0984},
mesh = {Humans ; *Diabetes Mellitus, Type 1/therapy ; *Insulin-Secreting Cells/physiology/metabolism ; Male ; Female ; Adult ; *Feces/microbiology ; Pilot Projects ; Capsules/administration & dosage ; *Fecal Microbiota Transplantation/adverse effects/methods ; Young Adult ; Middle Aged ; C-Peptide/blood/metabolism ; Adolescent ; Gastrointestinal Microbiome ; },
abstract = {This study investigated the safety and feasibility of daily ingestion of autologous lyophilized fecal microbiota capsules (a-LFMCs) for preserving beta-cell function in individuals with type 1 diabetes (T1D). We evaluated a-LFMC in an open-label, single-arm pilot study (NCT05323162) with 10 individuals with T1D. The study included a 3-month run-in period, 3 months of daily a-LFMC treatment, and a 3-month follow-up. Beta-cell function was assessed using mixed-meal stimulated C-peptide area under the curve (AUC). During the run-in period, beta-cell function significantly declined (mean ΔAUC -12.02 ± 5.09 nmol/L*min, p = 0.025). There was no decrease in beta-cell function during the a-LFMC treatment period (mean ΔAUC 0.76 ± 5.09 nmol/L*min, p = 0.88) and the follow-up period (mean ΔAUC 0.96 ± 5.09 nmol/L*min, p = 0.85). No serious adverse events occurred, though constipation increased during the treatment period (0% vs. 30%, p = 0.021). a-LFMC treatment was found to be safe and potentially contributes to preserving beta-cell function in T1D patients. A larger randomized placebo-controlled trial is needed to confirm these promising findings.},
}
MeSH Terms:
show MeSH Terms
hide MeSH Terms
Humans
*Diabetes Mellitus, Type 1/therapy
*Insulin-Secreting Cells/physiology/metabolism
Male
Female
Adult
*Feces/microbiology
Pilot Projects
Capsules/administration & dosage
*Fecal Microbiota Transplantation/adverse effects/methods
Young Adult
Middle Aged
C-Peptide/blood/metabolism
Adolescent
Gastrointestinal Microbiome
RevDate: 2025-10-05
Repurposing the bacterial surface display technology for drug delivery.
Advanced drug delivery reviews pii:S0169-409X(25)00186-3 [Epub ahead of print].
Bacteria have emerged as versatile platforms for therapeutic delivery, owing to their inherent adaptability, genetic tractability, and ability to interface with the human microbiome and immune system. This review explores the evolution of bacterial engineering for medical applications, emphasizing drug delivery strategies enabled by bacterial surface display technologies. We outline the advantages of surface display-such as enhanced localization, prolonged therapeutic activity, and reduced systemic toxicity-over conventional bacterial secretion and lysis-based delivery methods. The review details key biological mechanisms of surface display in both Gram-negative and Gram-positive bacteria, including outer membrane proteins, sortase-mediated anchoring, and spore-based systems. We also highlight emerging applications of surface-displayed cytokines, nanobodies, and immunomodulatory proteins in cancer therapy, vaccine development, microbiome engineering, and animal health. Innovative approaches combining bacterial display with conjugation systems and biosensors expand the potential of these living therapeutics for precise, responsive, and programmable interventions. Furthermore, we propose a future roadmap that leverages computational tools such as AlphaFold and in silico screening to rationally identify optimal outer membrane anchors, accelerating the design of next-generation surface display platforms. While challenges remain-including regulatory hurdles and microbial stability-continued interdisciplinary innovation with synthetic biology promises to transform engineered bacteria into clinically viable therapeutic agents. This review positions bacterial surface display as a powerful and underexplored modality for targeted drug delivery, bridging synthetic biology, immune engineering, and translational medicine.
Additional Links: PMID-41046872
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PubMed:
Citation:
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@article {pmid41046872,
year = {2025},
author = {Yang, S and Yang, M and Jennings, M and Timek, H and Haley, AE and Romee, R and Li, J},
title = {Repurposing the bacterial surface display technology for drug delivery.},
journal = {Advanced drug delivery reviews},
volume = {},
number = {},
pages = {115701},
doi = {10.1016/j.addr.2025.115701},
pmid = {41046872},
issn = {1872-8294},
abstract = {Bacteria have emerged as versatile platforms for therapeutic delivery, owing to their inherent adaptability, genetic tractability, and ability to interface with the human microbiome and immune system. This review explores the evolution of bacterial engineering for medical applications, emphasizing drug delivery strategies enabled by bacterial surface display technologies. We outline the advantages of surface display-such as enhanced localization, prolonged therapeutic activity, and reduced systemic toxicity-over conventional bacterial secretion and lysis-based delivery methods. The review details key biological mechanisms of surface display in both Gram-negative and Gram-positive bacteria, including outer membrane proteins, sortase-mediated anchoring, and spore-based systems. We also highlight emerging applications of surface-displayed cytokines, nanobodies, and immunomodulatory proteins in cancer therapy, vaccine development, microbiome engineering, and animal health. Innovative approaches combining bacterial display with conjugation systems and biosensors expand the potential of these living therapeutics for precise, responsive, and programmable interventions. Furthermore, we propose a future roadmap that leverages computational tools such as AlphaFold and in silico screening to rationally identify optimal outer membrane anchors, accelerating the design of next-generation surface display platforms. While challenges remain-including regulatory hurdles and microbial stability-continued interdisciplinary innovation with synthetic biology promises to transform engineered bacteria into clinically viable therapeutic agents. This review positions bacterial surface display as a powerful and underexplored modality for targeted drug delivery, bridging synthetic biology, immune engineering, and translational medicine.},
}
RevDate: 2025-10-02
Oral and fecal microbiome alterations in pancreatic cancer: insights into potential diagnostic biomarkers.
BMC microbiology, 25(1):624.
BACKGROUND: The human microbiome plays a pivotal role in pancreatic cancer (PC). This study investigates the abundance of specific gut and oral microbes in PC patients compared to healthy controls.
METHODS: A cohort of 20 diagnosed PC patients and an equivalent control group were recruited. Comprehensive lifestyle data, such as overall food consumption, were collected. Saliva and stool samples were prepared. Microbial DNA was extracted from stool and saliva samples using specialized kits. Primers were designed targeting the conserved regions of the 16 S rRNA genes from Neisseria elongata, Granulicatella adiacens, Fusobacterium nucleatum, Roseburia intestinalis, and Bifidobacterium bifidum. The quantities of selected bacterial species were evaluated using real-time quantitative PCR.
RESULTS: Granulicatella adiacens and Fusobacterium nucleatum were significantly increased in the PC group (medians: 7.35 and 4.37 log10 CFU/g, respectively) compared to controls (medians: 2.43 and 1.20 log10 CFU/g ; P < 0.001 for both). Conversely, Neisseria elongata, Roseburia intestinalis, and Bifidobacterium bifidum levels were significantly lower in PC patients (medians: 2.37, 2.34, and 3.45 log10 CFU/g, respectively) compared to controls (medians: 5.63, 5.07, and 4.34 log10 CFU/g; P < 0.001). The principal component analysis confirmed distinct clustering of microbiota profiles between the two groups, with key microorganisms associated with PC. The discriminatory performance of clinical and microbiota variables demonstrated notable accuracy in classifying PC, particularly metrics such as hemoglobin and hematocrit, achieving an area under the curve (AUC) of 1.00.
CONCLUSIONS: In summary, these findings highlight the significant association between microbiome composition and PC, underscoring the potential of microbiota profiles as non-invasive diagnostic biomarkers that warrant further investigation for early detection and therapeutic targeting in clinical practice.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-025-04344-2.
Additional Links: PMID-41039266
PubMed:
Citation:
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@article {pmid41039266,
year = {2025},
author = {Tavanaeian, S and Feizabadi, MM and Falsafi, S and Aghdaei, HA and Houri, H},
title = {Oral and fecal microbiome alterations in pancreatic cancer: insights into potential diagnostic biomarkers.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {624},
pmid = {41039266},
issn = {1471-2180},
abstract = {BACKGROUND: The human microbiome plays a pivotal role in pancreatic cancer (PC). This study investigates the abundance of specific gut and oral microbes in PC patients compared to healthy controls.
METHODS: A cohort of 20 diagnosed PC patients and an equivalent control group were recruited. Comprehensive lifestyle data, such as overall food consumption, were collected. Saliva and stool samples were prepared. Microbial DNA was extracted from stool and saliva samples using specialized kits. Primers were designed targeting the conserved regions of the 16 S rRNA genes from Neisseria elongata, Granulicatella adiacens, Fusobacterium nucleatum, Roseburia intestinalis, and Bifidobacterium bifidum. The quantities of selected bacterial species were evaluated using real-time quantitative PCR.
RESULTS: Granulicatella adiacens and Fusobacterium nucleatum were significantly increased in the PC group (medians: 7.35 and 4.37 log10 CFU/g, respectively) compared to controls (medians: 2.43 and 1.20 log10 CFU/g ; P < 0.001 for both). Conversely, Neisseria elongata, Roseburia intestinalis, and Bifidobacterium bifidum levels were significantly lower in PC patients (medians: 2.37, 2.34, and 3.45 log10 CFU/g, respectively) compared to controls (medians: 5.63, 5.07, and 4.34 log10 CFU/g; P < 0.001). The principal component analysis confirmed distinct clustering of microbiota profiles between the two groups, with key microorganisms associated with PC. The discriminatory performance of clinical and microbiota variables demonstrated notable accuracy in classifying PC, particularly metrics such as hemoglobin and hematocrit, achieving an area under the curve (AUC) of 1.00.
CONCLUSIONS: In summary, these findings highlight the significant association between microbiome composition and PC, underscoring the potential of microbiota profiles as non-invasive diagnostic biomarkers that warrant further investigation for early detection and therapeutic targeting in clinical practice.
SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12866-025-04344-2.},
}
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ESP Quick Facts
ESP Origins
In the early 1990's, Robert Robbins was a faculty member at Johns Hopkins, where he directed the informatics core of GDB — the human gene-mapping database of the international human genome project. To share papers with colleagues around the world, he set up a small paper-sharing section on his personal web page. This small project evolved into The Electronic Scholarly Publishing Project.
ESP Support
In 1995, Robbins became the VP/IT of the Fred Hutchinson Cancer Research Center in Seattle, WA. Soon after arriving in Seattle, Robbins secured funding, through the ELSI component of the US Human Genome Project, to create the original ESP.ORG web site, with the formal goal of providing free, world-wide access to the literature of classical genetics.
ESP Rationale
Although the methods of molecular biology can seem almost magical to the uninitiated, the original techniques of classical genetics are readily appreciated by one and all: cross individuals that differ in some inherited trait, collect all of the progeny, score their attributes, and propose mechanisms to explain the patterns of inheritance observed.
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.