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Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats
The intestinal microbiota is a complex microbial community, with diverse and stable populations hosted by the gastrointestinal tract since birth. This ecosystem holds multiple anti-infectious, anti-inflammatory, and immune modulating roles decisive for intestinal homeostasis. Among these, colonizati...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362409/ https://www.ncbi.nlm.nih.gov/pubmed/30761120 http://dx.doi.org/10.3389/fmicb.2018.03328 |
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author | Iacob, Simona Iacob, Diana Gabriela Luminos, Luminita Monica |
author_facet | Iacob, Simona Iacob, Diana Gabriela Luminos, Luminita Monica |
author_sort | Iacob, Simona |
collection | PubMed |
description | The intestinal microbiota is a complex microbial community, with diverse and stable populations hosted by the gastrointestinal tract since birth. This ecosystem holds multiple anti-infectious, anti-inflammatory, and immune modulating roles decisive for intestinal homeostasis. Among these, colonization resistance refers to the dynamic antagonistic interactions between commensals and pathogenic flora. Hence, gut bacteria compete for the same intestinal niches and substrates, while also releasing antimicrobial substances such as bacteriocines and changing the environmental conditions. Short chain fatty acids (SCFAs) generated in anaerobic conditions prompt epigenetic regulatory mechanisms that favor a tolerogenic immune response. In addition, the commensal flora is involved in the synthesis of bactericidal products, namely secondary biliary acids or antimicrobial peptides (AMPs) such as cathellicidin-LL37, an immunomodulatory, antimicrobial, and wound healing peptide. Gut microbiota is protected through symbiotic relations with the hosting organism and by quorum sensing, a specific cell-to-cell communication system. Any alterations of these relationships favor the uncontrollable multiplication of the resident pathobionts or external entero-pathogens, prompting systemic translocations, inflammatory reactions, or exacerbations of bacterial virulence mechanisms (T6SS, T3SS) and ultimately lead to gastrointestinal or systemic infections. The article describes the metabolic and immunological mechanisms through which the intestinal microbiota is both an ally of the organism against enteric pathogens and an enemy that favors the development of infections. |
format | Online Article Text |
id | pubmed-6362409 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63624092019-02-13 Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats Iacob, Simona Iacob, Diana Gabriela Luminos, Luminita Monica Front Microbiol Microbiology The intestinal microbiota is a complex microbial community, with diverse and stable populations hosted by the gastrointestinal tract since birth. This ecosystem holds multiple anti-infectious, anti-inflammatory, and immune modulating roles decisive for intestinal homeostasis. Among these, colonization resistance refers to the dynamic antagonistic interactions between commensals and pathogenic flora. Hence, gut bacteria compete for the same intestinal niches and substrates, while also releasing antimicrobial substances such as bacteriocines and changing the environmental conditions. Short chain fatty acids (SCFAs) generated in anaerobic conditions prompt epigenetic regulatory mechanisms that favor a tolerogenic immune response. In addition, the commensal flora is involved in the synthesis of bactericidal products, namely secondary biliary acids or antimicrobial peptides (AMPs) such as cathellicidin-LL37, an immunomodulatory, antimicrobial, and wound healing peptide. Gut microbiota is protected through symbiotic relations with the hosting organism and by quorum sensing, a specific cell-to-cell communication system. Any alterations of these relationships favor the uncontrollable multiplication of the resident pathobionts or external entero-pathogens, prompting systemic translocations, inflammatory reactions, or exacerbations of bacterial virulence mechanisms (T6SS, T3SS) and ultimately lead to gastrointestinal or systemic infections. The article describes the metabolic and immunological mechanisms through which the intestinal microbiota is both an ally of the organism against enteric pathogens and an enemy that favors the development of infections. Frontiers Media S.A. 2019-01-23 /pmc/articles/PMC6362409/ /pubmed/30761120 http://dx.doi.org/10.3389/fmicb.2018.03328 Text en Copyright © 2019 Iacob, Iacob and Luminos. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Microbiology Iacob, Simona Iacob, Diana Gabriela Luminos, Luminita Monica Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title | Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title_full | Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title_fullStr | Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title_full_unstemmed | Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title_short | Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title_sort | intestinal microbiota as a host defense mechanism to infectious threats |
topic | Microbiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362409/ https://www.ncbi.nlm.nih.gov/pubmed/30761120 http://dx.doi.org/10.3389/fmicb.2018.03328 |
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