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...
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doaj-3f7d62e4898e474b998b8ff123638bec2020-11-25T00:36:09ZengFrontiers Media S.A.Frontiers in Microbiology1664-302X2019-01-01910.3389/fmicb.2018.03328426119Intestinal Microbiota as a Host Defense Mechanism to Infectious ThreatsSimona Iacob0Simona Iacob1Diana Gabriela Iacob2Luminita Monica Luminos3Luminita Monica Luminos4Department of Infectious Diseases, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaNational Institute of Infectious Diseases “Prof. Dr. Matei Bals”, Bucharest, RomaniaNational Institute of Infectious Diseases “Prof. Dr. Matei Bals”, Bucharest, RomaniaDepartment of Infectious Diseases, Carol Davila University of Medicine and Pharmacy, Bucharest, RomaniaNational Institute of Infectious Diseases “Prof. Dr. Matei Bals”, Bucharest, RomaniaThe 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.https://www.frontiersin.org/article/10.3389/fmicb.2018.03328/fullintestinal microbiotainfectioncommensal florabacterial enteropathogenscolonization resistancemucosal immunity |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Simona Iacob Simona Iacob Diana Gabriela Iacob Luminita Monica Luminos Luminita Monica Luminos |
spellingShingle |
Simona Iacob Simona Iacob Diana Gabriela Iacob Luminita Monica Luminos Luminita Monica Luminos Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats Frontiers in Microbiology intestinal microbiota infection commensal flora bacterial enteropathogens colonization resistance mucosal immunity |
author_facet |
Simona Iacob Simona Iacob Diana Gabriela Iacob Luminita Monica Luminos Luminita Monica Luminos |
author_sort |
Simona Iacob |
title |
Intestinal Microbiota as a Host Defense Mechanism to Infectious Threats |
title_short |
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_sort |
intestinal microbiota as a host defense mechanism to infectious threats |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Microbiology |
issn |
1664-302X |
publishDate |
2019-01-01 |
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. |
topic |
intestinal microbiota infection commensal flora bacterial enteropathogens colonization resistance mucosal immunity |
url |
https://www.frontiersin.org/article/10.3389/fmicb.2018.03328/full |
work_keys_str_mv |
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