Division of Pediatric Gastroenterology and Nutrition, Children's Medical Center, Medical College of Virginia/Virginia Commonwealth University, Richmond, Virginia, U.S.A.
Inflamm Bowel Dis. 1995 Fall;1(3):220-7.
: Stricture formation in Crohn's disease is a complication of an important wound healing process in the intestine. The smooth muscle cells of the intestinal musculares bear a responsibility for the repair of injured intestine, and effect this wound healing process by proliferating and laying down collagen at the site of injury. Injury in the submucosa, and chronicity of injury, are important factors in the development of stricture. The resultant accumulation of collagenous scar, thickening of the muscle layers, and contracture, all play a role in producing the critical architectural changes in the intestinal wall that impede the aboral movement of chyme. Important putative facets of intestinal smooth muscle cell biology that are involved in stricture formation include: the synthesis and secretion of procollagen; the peculiar response of these cells to cytokines, ascorbate, and corticosteroids; and changes in cell phenotype that result from chronic inflammation. Therapeutic modalities designed to ameliorate the stricturing process will need to modulate these biological activities in resident intestinal smooth muscle cells.
克罗恩病的狭窄形成是肠道重要愈合过程的并发症。肠平滑肌细胞负责修复受损的肠道,并通过在损伤部位增殖和沉积胶原蛋白来实现这一愈合过程。黏膜下层的损伤和损伤的慢性化是狭窄形成的重要因素。胶原瘢痕的积累、肌肉层的增厚和挛缩,都在产生阻碍食糜逆行运动的肠壁关键结构变化中发挥作用。涉及狭窄形成的肠道平滑肌细胞生物学的重要假定方面包括:原胶原蛋白的合成和分泌;这些细胞对细胞因子、抗坏血酸和皮质类固醇的特殊反应;以及慢性炎症导致的细胞表型变化。旨在改善狭窄过程的治疗方式将需要调节驻留的肠道平滑肌细胞中的这些生物学活性。