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Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases

Lipopolysaccharides (LPSs) are bacterial surface glycolipids, produced by Gram-negative bacteria. LPS is known to determine acute inflammatory reactions, particularly in the context of sepsis. However, LPS can also trigger chronic inflammation. In this case, the source of LPS is not an external infe...

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Autores principales: Candelli, Marcello, Franza, Laura, Pignataro, Giulia, Ojetti, Veronica, Covino, Marcello, Piccioni, Andrea, Gasbarrini, Antonio, Franceschi, Francesco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8226948/
https://www.ncbi.nlm.nih.gov/pubmed/34200555
http://dx.doi.org/10.3390/ijms22126242
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author Candelli, Marcello
Franza, Laura
Pignataro, Giulia
Ojetti, Veronica
Covino, Marcello
Piccioni, Andrea
Gasbarrini, Antonio
Franceschi, Francesco
author_facet Candelli, Marcello
Franza, Laura
Pignataro, Giulia
Ojetti, Veronica
Covino, Marcello
Piccioni, Andrea
Gasbarrini, Antonio
Franceschi, Francesco
author_sort Candelli, Marcello
collection PubMed
description Lipopolysaccharides (LPSs) are bacterial surface glycolipids, produced by Gram-negative bacteria. LPS is known to determine acute inflammatory reactions, particularly in the context of sepsis. However, LPS can also trigger chronic inflammation. In this case, the source of LPS is not an external infection, but rather an increase in endogenous production, which is usually sustained by gut microbiota (GM), and LPS contained in food. The first site in which LPS can exert its inflammatory action is the gut: both GM and gut-associated lymphoid tissue (GALT) are influenced by LPS and shift towards an inflammatory pattern. The changes in GM and GALT induced by LPS are quite similar to the ones seen in IBD: GM loses diversity, while GALT T regulatory (Tregs) lymphocytes are reduced in number, with an increase in Th17 and Th1 lymphocytes. Additionally, the innate immune system is triggered, through the activation of toll-like receptor (TLR)-4, while the epithelium is directly damaged, further triggering inflammation. In this review, we will discuss the importance of the crosstalk between LPS, GM, and GALT, and discuss the possible implications.
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spelling pubmed-82269482021-06-26 Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases Candelli, Marcello Franza, Laura Pignataro, Giulia Ojetti, Veronica Covino, Marcello Piccioni, Andrea Gasbarrini, Antonio Franceschi, Francesco Int J Mol Sci Review Lipopolysaccharides (LPSs) are bacterial surface glycolipids, produced by Gram-negative bacteria. LPS is known to determine acute inflammatory reactions, particularly in the context of sepsis. However, LPS can also trigger chronic inflammation. In this case, the source of LPS is not an external infection, but rather an increase in endogenous production, which is usually sustained by gut microbiota (GM), and LPS contained in food. The first site in which LPS can exert its inflammatory action is the gut: both GM and gut-associated lymphoid tissue (GALT) are influenced by LPS and shift towards an inflammatory pattern. The changes in GM and GALT induced by LPS are quite similar to the ones seen in IBD: GM loses diversity, while GALT T regulatory (Tregs) lymphocytes are reduced in number, with an increase in Th17 and Th1 lymphocytes. Additionally, the innate immune system is triggered, through the activation of toll-like receptor (TLR)-4, while the epithelium is directly damaged, further triggering inflammation. In this review, we will discuss the importance of the crosstalk between LPS, GM, and GALT, and discuss the possible implications. MDPI 2021-06-10 /pmc/articles/PMC8226948/ /pubmed/34200555 http://dx.doi.org/10.3390/ijms22126242 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Candelli, Marcello
Franza, Laura
Pignataro, Giulia
Ojetti, Veronica
Covino, Marcello
Piccioni, Andrea
Gasbarrini, Antonio
Franceschi, Francesco
Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases
title Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases
title_full Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases
title_fullStr Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases
title_full_unstemmed Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases
title_short Interaction between Lipopolysaccharide and Gut Microbiota in Inflammatory Bowel Diseases
title_sort interaction between lipopolysaccharide and gut microbiota in inflammatory bowel diseases
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8226948/
https://www.ncbi.nlm.nih.gov/pubmed/34200555
http://dx.doi.org/10.3390/ijms22126242
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