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Intestinal fibrosis in human and experimental inflammatory bowel disease

机译:人和实验性炎症性肠病中的肠纤维化

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Fibrosis is a serious complication of Crohn disease for which there is no effective therapy. It is unclear why fibrosis, particularly fibrosis of the mucosal layer, develops in Crohn disease and not in ulcerative colitis. Smooth muscle cells, subepithelial myofibroblasts, and fibroblasts have traditionally been considered mediators of fibrosis, but new information points to a role of interstitial cells of Cajal and mast cells. Recent evidence about the role of each of these cell types in fibrosis in Crohn disease or other inflammatory bowel diseases is described. Hypothetical models to describe how altered function of these cells could underlie fibrosis of the mucosa or submucosal layers are presented. Fibrosis is not well characterized in any animal model of inflammatory bowel disease. The merits of several animal models for defining the mechanisms of inflammation-induced intestinal fibrosis are reviewed.
机译:纤维化是克罗恩病的一种严重并发症,目前尚无有效的治疗方法。目前尚不清楚为什么在克罗恩病而不是溃疡性结肠炎中发生纤维化,特别是粘膜层纤维化。传统上,平滑肌细胞,上皮下肌成纤维细胞和成纤维细胞被认为是纤维化的介质,但是新的信息指出了间质细胞在Cajal和肥大细胞中的作用。描述了关于这些细胞类型中的每一种在克罗恩病或其他炎性肠病中的纤维化中作用的最新证据。提出了描述这些细胞功能改变如何可能成为粘膜或粘膜下层纤维化基础的假想模型。在任何炎症性肠病动物模型中,纤维化的特征均不充分。审查了几种动物模型的优点,用于定义炎症诱导的肠道纤维化的机制。

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