On mechanisms of increased intestinal wall permeability under stress

One of the manifestations of the stress reaction in the colon is an increase in the permeability of its wall due to the development of an inflammatory reaction against the background of changes in neuroendocrine regulation and microbiota state. These processes are accompanied by significant changes in humoral homeostasis and cell activity involved in the development of an inflammatory response in the colon wall. We performed a literature review to analyze and summarize the available research data on the mechanisms of stress-induced changes in the intestine at the molecular, cellular and tissue levels involving the regulatory systems of the body. Scientific information was searched in Web Of Science, Scopus, ScienceDirect, Medline, Russian Science Citation Index (RSCI), as well as in the search engines Google Scholar, PubMed, Semantic Scholar, Taylor & Francis, Wiley Online Library and Bielefeld Academic Search Engine (BASE). Wall permeability has been shown to have a rather complex regulation involving corticotropin-releasing factor, mast cells, dendritic cells, eosinophils, macrophages, Substance P, nerve growth factor, neurotensin, microbiota metabolic factors (serotonin, short-chain fatty acids, indole derivatives and conjugated fatty acids), epigenetic mechanisms, the HES1 (Hairy/Enhancer of Split-1) - GR (glucocorticoid receptor), and the stress-associated polarity signaling pathway. Under stress, there is a change in the functioning of these mechanisms, leading to an increase in the permeability of the intestinal wall. It results in translocation of bacteria from the lumen into the underlying layers which causes activation of the immune response with subsequent development of an inflammatory reaction. The presented data testify to the prospects and validity of the development of methods of correction of stress-induced shifts in the colon by influencing the central and local mechanisms of realization of the stress response and the state of the microbiota.