This article describes the importance of TJP on tissue to prevent invasion of pathogenic organisms.
5. Conclusions
In conclusion, some enteric pathogens can target the junctional complex to weaken the intestinal epithelial barrier and promote their invasion. This microbial modulation of the IECs’ permeability involves numerous mechanisms ranging from direct molecular interactions of microorganism with host components to the modulation of various signaling cellular pathways. Whereas many studies highlight the fate of the major TJ proteins (i.e., occludin, claudins and ZO-1) during bacterial, viral, fungal, or parasitic IEC infections, the cellular and molecular mechanisms remain to be specified, including the nature of the microbial effector, its host cellular receptor, the nature of the signaling pathways involved, as well as the direct or indirect impact of their modulation on the TJ complex organization. Finally, most of the observations reported here are based on simplified models of infection (one pathogen interacting with one type of intestinal cell) that do not consider (i) the complexity of the intestinal ecosystem and environmental conditions including the communications between pathogenic and commensal microorganisms, or (ii) the influence of the intestinal microbiota upon pathogens/epithelial cells interactions regarding the gut TJ integrity [163,164,165]. Pathogenic effectors and/or their cellular receptors constitute therapeutic candidates by preventing the weakening of the digestive barrier induced by pathogens.
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