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Mechanisms of tissue damage in inflammatory bowel disease

机译:炎症性肠病中组织损伤的机制

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摘要

Crohn disease and ulcerative colitis are caused by an excessive immune-inflammatory reaction in the intestinal wall. Analysis of the types of immune response ongoing in the inflamed intestine has revealed that in Crohn disease there is predominantly a T helper cell type 1 response, with exaggerated production of interleukin (IL)-12 and interferon-gamma, whereas in ulcerative colitis the lesion seems to be more of an antibody-mediated hypersensitivity reaction. Despite these differences, downstream inflammatory events are probably similar in both conditions, in both Crohn disease and ulcerative colitis there is an increased synthesis of proinflammatory cytokines, including IL-1beta, IL-6, IL-8, IL-16, and tumor necrosis factor-alpha accompanying the influx of nonspecific inflammatory cells into the mucosa. These cytokines contribute to the tissue damage either directly or indirectly by enhancing the production of matrix metalloproteinases and growth factors, which produce ulceration as well as mucosal repair.
机译:克罗恩病和溃疡性结肠炎是由肠壁过度的免疫炎症反应引起的。对发炎的肠道中正在进行的免疫反应类型的分析表明,在克罗恩病中主要存在1型T辅助细胞反应,白细胞介素(IL)-12和干扰素-γ的产生过大,而溃疡性结肠炎则病变似乎更多是抗体介导的超敏反应。尽管存在这些差异,但在两种情况下下游炎症事件可能都相似,在克罗恩病和溃疡性结肠炎中,促炎细胞因子(包括IL-1beta,IL-6,IL-8,IL-16和肿瘤坏死)的合成增加伴随非特异性炎性细胞流入粘膜的α-因子。这些细胞因子通过增强基质金属蛋白酶和生长因子的产生而直接或间接地导致组织损伤,所述基质金属蛋白酶和生长因子产生溃疡以及粘膜修复。

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