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Contribution of the Gut Barrier to Host-Microbiome Communication

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 4308

Special Issue Editors


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Guest Editor
Greater Los Angeles Helathcare System and David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
Interests: gut barrier function; host–microbiome interactions; intestinal transport, metabolite chemosensing, intestinal ectoenzymes

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Guest Editor
David Geffen School of Medicine at UCLA, Los Angeles, CA, USA
Interests: gastroduodenal mocosal defenses; epithelial ion transporters and secretion; luminal chemosensing; DUOX enzymes

Special Issue Information

There has been considerable interest in the gut microbiome in the past decade, leading to an explosion of publications reporting on how the composition of the microbiome changes with disease states and with attempts to alter the composition of the microbiome in an effort to treat illness. What has not been studied to the same extent is how the microbiome affects host functions. At present, bacterial metabolites and bacterial toxins have been implicated in disease pathogenesis, although the mechanisms by which these substances interact with the host are not well known. Although it is assumed that intact bacteria and their toxins penetrate the gut barrier through tight junctions, few in vivo data support this concept. It appears that intact bacteria, bacterial components, and bacterial metabolites do not simply diffuse between epithelial cells but rather cross the barrier through specialized pathways or interact with specific receptors in order to affect the host.

In this Special Issue, we shall focus on the mechanisms by which the gut microbiome communicates with the host, hoping to provide insight into why so many diseases are associated with alterations of the composition of the gut microbiome.

Prof. Jonathan D. Kaunitz
Dr. Akiba Yasutada
Guest Editors

Manuscript Submission Information

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Keywords

  • Bacterial toxins
  • Gut barrier function
  • Toll-like receptors
  • Endocytosis
  • Bacterial metabolites
  • Gut immune system
  • Gut–liver axis

Published Papers (1 paper)

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Research

18 pages, 2753 KiB  
Article
Bifidobacterium bifidum Enhances the Intestinal Epithelial Tight Junction Barrier and Protects against Intestinal Inflammation by Targeting the Toll-like Receptor-2 Pathway in an NF-κB-Independent Manner
by Rana Al-Sadi, Viszwapriya Dharmaprakash, Prashant Nighot, Shuhong Guo, Meghali Nighot, Toan Do and Thomas Y. Ma
Int. J. Mol. Sci. 2021, 22(15), 8070; https://doi.org/10.3390/ijms22158070 - 28 Jul 2021
Cited by 47 | Viewed by 3851
Abstract
Defective intestinal tight junction (TJ) barrier is a hallmark in the pathogenesis of inflammatory bowel disease (IBD). To date, there are no effective therapies that specifically target the intestinal TJ barrier. Among the various probiotic bacteria, Bifidobacterium, is one of the most [...] Read more.
Defective intestinal tight junction (TJ) barrier is a hallmark in the pathogenesis of inflammatory bowel disease (IBD). To date, there are no effective therapies that specifically target the intestinal TJ barrier. Among the various probiotic bacteria, Bifidobacterium, is one of the most widely studied to have beneficial effects on the intestinal TJ barrier. The main purpose of this study was to identify Bifidobacterium species that cause a sustained enhancement in the intestinal epithelial TJ barrier and can be used therapeutically to target the intestinal TJ barrier and to protect against or treat intestinal inflammation. Our results showed that Bifidobacterium bifidum caused a marked, sustained enhancement in the intestinal TJ barrier in Caco-2 monolayers. The Bifidobacterium bifidum effect on TJ barrier was strain-specific, and only the strain designated as BB1 caused a maximal enhancement in TJ barrier function. The mechanism of BB1 enhancement of intestinal TJ barrier required live bacterial cell/enterocyte interaction and was mediated by the BB1 attachment to Toll-like receptor-2 (TLR-2) at the apical membrane surface. The BB1 enhancement of the intestinal epithelial TJ barrier function was mediated by the activation of the p38 kinase pathway, but not the NF-κB signaling pathway. Moreover, the BB1 caused a marked enhancement in mouse intestinal TJ barrier in a TLR-2-dependent manner and protected against dextran sodium sulfate (DSS)-induced increase in mouse colonic permeability, and treated the DSS-induced colitis in a TJ barrier-dependent manner. These studies show that probiotic bacteria BB1 causes a strain-specific enhancement of the intestinal TJ barrier through a novel mechanism involving BB1 attachment to the enterocyte TLR-2 receptor complex and activation of p38 kinase pathway. Full article
(This article belongs to the Special Issue Contribution of the Gut Barrier to Host-Microbiome Communication)
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