Abstract
Alterations in the gut microbiota composition play a crucial role in the pathogenesis of inflammatory bowel disease (IBD) as specific commensal bacterial species are underrepresented in the microbiota of IBD patients. In this study, we examined the therapeutic potential of three commensal bacterial species, Faecalibacterium prausnitzii (F. prausnitzii), Roseburia intestinalis (R. intestinalis) and Bacteroides faecis (B. faecis) in an in vitro model of intestinal inflammation, by using differentiated Caco-2 and HT29-MTX cells, stimulated with a pro-inflammatory cocktail consisting of interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), interferon-γ (IFNγ), and lipopolysaccharide (LPS). Results obtained in this work demonstrated that all three bacterial species are able to recover the impairment of the epithelial barrier function induced by the inflammatory stimulus, as determined by an amelioration of the transepithelial electrical resistance (TEER) and the paracellular permeability of the cell monolayer. Moreover, inflammatory stimulus increased claudin-2 expression and decreased occludin expression were improved in the cells treated with commensal bacteria. Furthermore, the commensals were able to counteract the increased release of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) induced by the inflammatory stimulus. These findings indicated that F. prausnitzii, R. intestinalis and B. faecis improve the epithelial barrier integrity and limit inflammatory responses.
Highlights
The intestinal mucosa is a critical barrier that separates the inner and outer areas of intestinal lumen and is essential for the maintenance of mucosal homeostasis
In order make our data more relevant for the in vivo situation, the Caco-2 and HT29-MTX cells were stimulated with live F. prausnitzii, B. faecis and R. intestinalis under anaerobic culture conditions
In the set of experiments, we studied the effect of the three bacterial species on inflamed epithelial cell monolayers
Summary
The intestinal mucosa is a critical barrier that separates the inner and outer areas of intestinal lumen and is essential for the maintenance of mucosal homeostasis This barrier consists of a single epithelial cell layer, an intraepithelial tight junction (TJ) complex and is considered to be the first line of defense against the hostile luminal environment [1]. TJ proteins such as claudins, occludin, the zonula occludens, junctional adhesion molecule, and the adherence junction protein E-cadherin, located at the apical-lateral membrane [2,3] These proteins regulate the passage of solute and macromolecules through the paracellular pathway, thereby playing a vital role in regulating intestinal barrier function [1]. The dysregulation of intracellular TJs contributes to the uncontrolled translocation of microorganisms, pathogens and antigens throughout the epithelium, resulting in an Nutrients 2020, 12, 2251; doi:10.3390/nu12082251 www.mdpi.com/journal/nutrients
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