肠黏膜组织内神经递质和基质细胞参与炎症性肠病发生——溃疡性结肠炎相关结直肠癌变机制研究进展

Mechanisms underlying development of ulcerative colitis-associated colorectal carcinoma

炎症性肠病(inflammatory bowel disease,IBD)肠黏膜组织内各种免疫细胞通过固有和获得性免疫应答效应,引起激活,释放促炎症细胞因子,导致局部炎症反应.在炎症肠黏膜组织出现肌间神经丛炎,肠黏膜组织内神经纤维细胞通过释放神经递质,调节黏膜组织内淋巴细胞的激活.肠黏膜组织内非免疫细胞如上皮细胞、肥大细胞、血管内皮细胞和基质细胞参与了黏膜免疫病理损伤过程,而成纤维细胞和肌成纤维细胞分泌大量细胞外基质,沉积在组织内,引发肠道纤维化.长期慢性炎症刺激,诱导肠上皮细胞基因突变导致结直肠癌变发生.本焦点论坛通过阐述肠黏膜组织内神经-内分泌-免疫调节,以及非免疫细胞的效应应答,深入探讨炎症性肠病的发生机制,并为临床治疗提供了新的理论基础.

Ulcerative colitis （UC） is a chronic inflammatory disease of the gastrointestinal tract arising from the genetic predisposing factor and the abnormality of the immune system. Long-term course of UC may cause the development of several complications, such as colorectal carcinoma. The mechanisms underlying the development of UC- associated colorectal carcinoma, involving a series of changes from genetic materials to signal transduction, are extremely complicated and differ from those behind the development of sporadic colorectal carcinoma. This article discusses the mechanisms underlying the development of UC- associated colorectal carcinoma.