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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Published in:	Gut microbes Vol. 11; no. 3; pp. 421 - 432
Main Authors:	Stephens, Matthew, von der Weid, Pierre-Yves
Format:	Journal Article
Language:	English
Published:	United States Taylor & Francis 03.05.2020 Taylor & Francis Group
Subjects:	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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Abstract	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.
AbstractList	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. 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.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.
Author	von der Weid, Pierre-Yves Stephens, Matthew
Author_xml	– sequence: 1 givenname: Matthew surname: Stephens fullname: Stephens, Matthew organization: University of Calgary – sequence: 2 givenname: Pierre-Yves surname: von der Weid fullname: von der Weid, Pierre-Yves email: vonderwe@ucalgary.ca organization: University of Calgary
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SubjectTerms	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
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Title	Lipopolysaccharides modulate intestinal epithelial permeability and inflammation in a species-specific manner
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