Damage-associated molecular patterns in inflammatory bowel disease:From biomarkers to therapeutic targets
作者机构：Servico de Gastroenterologia e Laboratorio Multidisciplinar de PesquisaDepartamento de Clinica MedicaHospital Universitario Clementino Fraga FilhoUniversidade Federal do Rio de JaneiroRio de JaneiroRJ 21941-913Brazil D’Or Institute for Research and Education(IDOR)Rua Diniz Cordeiro 30BotafogoRio de JaneiroRJ 22281-100Brazil
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2018年第24卷第41期
页 面：4622-4634页
核心收录：
基 金：Supported by the Brazilian research foundations Fundacao de Amparo à Pesquisa do Estado do Rio de Janeiro--FAPERJ,No.E26/202.781/2017 Conselho Nacional de Desenvolvimento Científico e Tecnológico-CNPq,No.302401/2016-4
主 题：Damage-associated molecular patterns Environmental factors Epigenetics Inflammatory bowel disease Therapeutic targets
摘 要：The chronic inflammatory process underlying inflammatory bowel disease (IBD), comprising Crohn s disease and ulcerative colitis, derives from the interplay of several components in a genetically susceptible host. These components include environmental elements and gut microbiota a dysbiosis. For decades, immune abnormalities have been investigated as critically important in IBD pathogenesis, and attempts to develop effective therapies have predominantly targeted the immune system. Nevertheless, immune events represent only one of the constituents contributing to IBD pathogenesis within the context of the complex cellular and molecular network underlying chronic intestinal inflammation. These factors need to be appreciated within the milieu of nonimmune components. Damage-associated molecular patterns (DAMPs), which are essentially endogenous stress proteins expressed or released as a result of cell or tissue damage, have been shown to act as direct proinflammatory mediators. Excessive or persistent signalling mediated by such molecules can underlie several chronic inflammatory disorders, including IBD. The release of endogenous DAMPs amplifies the inflammatory response driven by immune and non-immune cells and promotes epigenetic reprogramming in IBD.The effects determine pathologic changes,which may sustain chronic intestinal inflammation and also underlie specific disease phenotypes.In addition to highlighting the potential use of DAMPs such as calprotectin as biomarkers,research on DAMPs may reveal novel mechanistic associations in IBD pathogenesis and is expected to uncover putative therapeutic targets.
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