{"title":"应激下肠壁通透性增加的机制研究","authors":"A. O. Vorvul, I. Bobyntsev, O. Medvedeva","doi":"10.21626/vestnik/2022-2/05","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":24060,"journal":{"name":"Курский научно-практический вестник «Человек и его здоровье»","volume":"25 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"On mechanisms of increased intestinal wall permeability under stress\",\"authors\":\"A. O. Vorvul, I. Bobyntsev, O. 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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. 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引用次数: 0
摘要
结肠应激反应的表现之一是在神经内分泌调节和微生物群状态改变的背景下,炎症反应的发生导致结肠壁通透性增加。这些过程伴随着体液稳态和细胞活性的显著变化,这些变化涉及结肠壁炎症反应的发展。我们通过文献综述,分析和总结了有关应激诱导肠道变化的分子、细胞和组织水平机制的现有研究数据,这些机制涉及机体的调节系统。在Web Of Science、Scopus、ScienceDirect、Medline、俄罗斯科学引文索引(RSCI)以及搜索引擎Google Scholar、PubMed、Semantic Scholar、Taylor & Francis、Wiley Online Library和Bielefeld Academic search Engine (BASE)中搜索科学信息。壁透性具有相当复杂的调控机制,涉及促肾上腺皮质激素释放因子、肥大细胞、树突状细胞、嗜酸性粒细胞、巨噬细胞、P物质、神经生长因子、神经紧张素、微生物群代谢因子(血清素、短链脂肪酸、吲哚衍生物和共轭脂肪酸)、表观遗传机制、HES1 (Hairy/Enhancer of Split-1) - GR(糖皮质激素受体)以及应激相关的极性信号通路。在压力下,这些机制的功能发生变化,导致肠壁通透性增加。它导致细菌从管腔转移到下层,引起免疫反应的激活,随后发展为炎症反应。所提出的数据证明了通过影响实现应激反应的中央和局部机制以及微生物群状态来纠正结肠中应激引起的转移的方法的前景和有效性。
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.