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 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.

Medienart:

E-Artikel

Erscheinungsjahr:

2020

Erschienen:

2020

Enthalten in:

Zur Gesamtaufnahme - volume:11

Enthalten in:

Gut microbes - 11(2020), 3 vom: 03. Mai, Seite 421-432

Sprache:

Englisch

Beteiligte Personen:

Stephens, Matthew [VerfasserIn]
von der Weid, Pierre-Yves [VerfasserIn]

Links:

Volltext

Themen:

CXCL8 protein, human
Cytokines
Endotoxin
Epithelium
Inflammation
Interleukin-8
Journal Article
Lipopolysaccharides
NF-kappa B
Research Support, Non-U.S. Gov't
TLR4 protein, human
Toll- like receptor 4
Toll-Like Receptor 4

Anmerkungen:

Date Completed 08.04.2021

Date Revised 28.04.2021

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1080/19490976.2019.1629235

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM298202859