Theories explaining the etiopathogenesis of inflammatory bowel disease (IBD) have been proposed ever since Crohn's disease (CD) and ulcerative colitis (UC) were recognized as the two major forms of the disease. Although the exact cause(s) and mechanisms of tissue damage in CD and UC have yet to be completely understood, enough progress has occurred to accept the following hypothesis as valid: IBD is an inappropriate immune response that occurs in genetically susceptible individuals as the result of a complex interaction among environmental factors, microbial factors, and the intestinal immune system. Among an almost endless list of environmental factors, smoking has been identified as a risk factor for CD and a protective factor for UC. Among microbial factors, no convincing evidence indicates that classical infectious agents cause IBD, while mounting evidence points to an abnormal immune response against the normal enteric flora as being of central importance. Gut inflammation is mediated by cells of the innate as well as adaptive immune systems, with the additional contribution of non-immune cells, such as epithelial, mesenchymal and endothelial cells, and platelets.

译文

自从克罗恩病 (CD) 和溃疡性结肠炎 (UC) 被认为是炎症性肠病 (IBD) 的两种主要形式以来,就提出了解释炎症性肠病 (IBD) 病因的理论。尽管CD和UC组织损伤的确切原因和机制尚未完全了解,但已经取得了足够的进展,接受以下假设是有效的: IBD是一种不适当的免疫反应,由于遗传易感个体的结果环境因素之间的复杂相互作用,微生物因素和肠道免疫系统。在几乎无穷无尽的环境因素列表中,吸烟已被确定为CD的危险因素和UC的保护因素。在微生物因素中,没有令人信服的证据表明经典的感染因子引起IBD,而越来越多的证据表明针对正常肠道菌群的异常免疫反应至关重要。肠道炎症是由先天免疫系统和适应性免疫系统的细胞介导的,非免疫细胞 (例如上皮,间充质和内皮细胞以及血小板) 的额外贡献。

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