Microbiological mechanisms of immune response modulation: clinical implications
5 affiliations
- 1Department of Propaedeutics of Medicine and Infection Prevention, Collegium Medicum , ,
- 2Tczew Hospitals S.A. , ,
- 3University Hospital No. 2 Dr Jan Biziel , ,
- 4Student Research Club of Clinical Immunology, Department of Allergology, Clinical Immunology and Internal Diseases, Collegium Medicum Bydgoszcz, Nicolaus Copernicus University , ,
- 5Department of Allergology, Clinical Immunology and Internal Diseases, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University , ,
Abstract
The human microbiota is a major regulator of immune development, mucosal barrier integrity, and systemic immune tone. Its effects are mediated by microbe-associated molecular patterns, pattern-recognition receptors, microbial metabolites such as short-chain fatty acids, tryptophan-derived indoles, secondary bile acids and vitamin-pathway metabolites, and direct interactions with epithelial and immune cells. A balanced microbiota supports regulatory T-cell responses, secretory IgA production, innate-like lymphocyte maturation and epithelial barrier function, whereas dysbiosis may promote barrier dysfunction, inflammatory polarization and abnormal responses to dietary, environmental or self-antigens. This narrative review integrates mechanistic and translational evidence across early-life immune maturation, innate and adaptive immune sensing, microbial metabolites, cross-kingdom interactions, gut-organ axes, immune-mediated diseases and microbiota-targeted interventions. Particular emphasis is placed on distinguishing mechanistic evidence from association. Although microbiome-directed therapies are promising, routine clinical translation requires standardized sampling and multi-omics workflows, controlled interventional studies, mechanistic validation, reproducible biomarkers and indication-specific evidence.
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BibTeX
@article{deptula2026microbiological,
title = {{Microbiological mechanisms of immune response modulation: clinical implications}},
author = {Aleksander Deptuła and Aleksandra Ćwirko-Godycka and Agata Majcherczak and Amanda Zoń and Wiktoria Rosiek and Katarzyna Napiórkowska-Baran},
journal = {Frontiers in immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1927480},
url = {https://europepmc.org/article/PMC/PMC13673331},
note = {CC BY},
}
RIS
TY - JOUR
TI - Microbiological mechanisms of immune response modulation: clinical implications
AU - Aleksander Deptuła
AU - Aleksandra Ćwirko-Godycka
AU - Agata Majcherczak
AU - Amanda Zoń
AU - Wiktoria Rosiek
AU - Katarzyna Napiórkowska-Baran
PY - 2026
DA - 2026/10/02
JO - Frontiers in immunology
DO - 10.3389/fimmu.2026.1927480
UR - https://europepmc.org/article/PMC/PMC13673331
AB - The human microbiota is a major regulator of immune development, mucosal barrier integrity, and systemic immune tone. Its effects are mediated by microbe-associated molecular patterns, pattern-recognition receptors, microbial metabolites such as short-chain fatty acids, tryptophan-derived indoles, secondary bile acids and vitamin-pathway metabolites, and direct interactions with epithelial and immune cells. A balanced microbiota supports regulatory T-cell responses, secretory IgA production, innate-like lymphocyte maturation and epithelial barrier function, whereas dysbiosis may promote barrier dysfunction, inflammatory polarization and abnormal responses to dietary, environmental or self-antigens. This narrative review integrates mechanistic and translational evidence across early-life immune maturation, innate and adaptive immune sensing, microbial metabolites, cross-kingdom interactions, gut-organ axes, immune-mediated diseases and microbiota-targeted interventions. Particular emphasis is placed on distinguishing mechanistic evidence from association. Although microbiome-directed therapies are promising, routine clinical translation requires standardized sampling and multi-omics workflows, controlled interventional studies, mechanistic validation, reproducible biomarkers and indication-specific evidence.
SN - 1664-3224
ER -