Lipopolysaccharides modulate intestinal epithelial permeability and inflammation in a species-specific manner

Patients presenting with Inflammatory bowel disease have been shown to exhibit an altered microbiome in both Crohn's disease and Ulcerative colitis. This shift in the microbial content led us to question whether several of these microbes are important in inflammatory processes present in these...

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Vydáno v:	Gut microbes Ročník 11; číslo 3; s. 421 - 432
Hlavní autoři:	Stephens, Matthew, von der Weid, Pierre-Yves
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Taylor & Francis 03.05.2020 Taylor & Francis Group
Témata:	Caco-2 Cells Cell Line Cell Survival Cytokines - metabolism Endotoxin Epithelial Cells - immunology Epithelial Cells - metabolism Epithelium Gram-Negative Bacteria - immunology Gram-Negative Bacteria - pathogenicity Humans Inflammation Inflammation - immunology Inflammatory Bowel Diseases - immunology Inflammatory Bowel Diseases - microbiology Interleukin-8 - metabolism Intestines - cytology Intestines - immunology Lipopolysaccharides Lipopolysaccharides - immunology Lipopolysaccharides - toxicity NF-kappa B - metabolism Permeability Research Paper/Report Species Specificity Tight Junctions - metabolism Toll- like receptor 4 Toll-Like Receptor 4 - immunology Inflammation Epithelium Endotoxin Toll- like receptor 4 Lipopolysaccharides
ISSN:	1949-0976, 1949-0984, 1949-0984
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Shrnutí:	Patients presenting with Inflammatory bowel disease have been shown to exhibit an altered microbiome in both Crohn's disease and Ulcerative colitis. This shift in the microbial content led us to question whether several of these microbes are important in inflammatory processes present in these diseases and more specifically whether lipopolysaccharides from the gram-negative cell wall differentially stimulates resident cells. We, therefore, investigated the possible contribution of five major species of gram-negative bacteria found to be altered in presence during disease progression and evaluate their pathogenicity through LPS. We demonstrated that LPS from these different species had individual capacities to induce NF-κB and pro-inflammatory IL-8 production from HEK-TLR4 cells in a TLR4 dependent manner. Additional work using human intestinal colonic epithelial cell monolayers (Caco-2) demonstrated that the cells responded to the serotype specific LPS in a distinct manner, inducing many inflammatory mediators such as TNF-α and IL-10 in significantly altered proportions. Furthermore, the permeability of Caco-2 monolayers, as a test for their ability to alter intestinal permeability, was also differentially altered by the serotype specific LPS modulating trans-epithelial electrical resistance, small molecule movement, and tight junction integrity. Our results suggest that specific species of bacteria may be potentiating the pathogenesis of IBD and chronic inflammatory diseases through their serotype specific LPS responses.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1949-0976 1949-0984 1949-0984
DOI:	10.1080/19490976.2019.1629235