Dignass A U
Department of Medicine, Charité-Campus Virchow Clinic, Berlin, Germany.
Inflamm Bowel Dis. 2001 Feb;7(1):68-77. doi: 10.1097/00054725-200102000-00014.
The mucosal epithelium of the alimentary tract represents a crucial barrier to a broad spectrum of noxious and immunogenic substances within the intestinal lumen. An impairment of the integrity of the mucosal epithelial barrier is observed in the course of various intestinal disorders including inflammatory bowel diseases (IBD), celiac disease, intestinal infections, and various other diseases. Furthermore, even under physiologic conditions temporary damage of the epithelial surface mucosa may be caused by proteases, residential flora, dietary compounds, or other factors. Generally, the integrity of the intestinal mucosal surface barrier is rapidly reestablished even after extensive destruction because of an enormous regenerative capability of the mucosal surface epithelium. Rapid resealing of the surface epithelium is accomplished by epithelial cell migration, also termed epithelial restitution, epithelial cell proliferation, and differentiation. Healing of the intestinal surface epithelium is regulated by a complex network of highly divergent factors, among them a broad spectrum of structurally distinct regulatory peptides that have been identified within the mucosa of the intestinal tract. These regulatory peptides, conventionally designated as growth factors and cytokines, play an essential role in regulating differential epithelial cell functions to preserve normal homeostasis and integrity of the intestinal mucosa. In addition, a number of other peptide molecules such as extracellular matrix factors and blood clotting factors, and also nonpeptide molecules including phospholipids, shortchain fatty acids, adenine nucleotides, trace elements, and pharmacological agents, have been demonstrated to modulate intestinal epithelial repair mechanisms. Some of these molecules may be released by platelets, adjacent stromal cells, inflammatory cells, or injured epithelial and nonepithelial cells and may play an important role in the modulation of intestinal injury. Repeated damage and injury of the intestinal surface are key features of various intestinal disorders including IBD and require constant repair of the epithelium. Enhancement of intestinal repair mechanisms by regulatory peptides or other modulatory factors may provide future approaches for the treatment of diseases that are characterized by injuries of the epithelial surface.
消化道的黏膜上皮是肠道腔内多种有害物质和免疫原性物质的关键屏障。在包括炎症性肠病（IBD）、乳糜泻、肠道感染及其他各种疾病在内的多种肠道疾病过程中，均可观察到黏膜上皮屏障完整性受损。此外，即使在生理条件下，上皮表面黏膜的暂时损伤也可能由蛋白酶、常驻菌群、膳食化合物或其他因素引起。一般来说，由于黏膜表面上皮具有巨大的再生能力，即使在广泛破坏后，肠道黏膜表面屏障的完整性也能迅速重建。表面上皮的快速重新封闭是通过上皮细胞迁移（也称为上皮修复）、上皮细胞增殖和分化来实现的。肠道表面上皮的愈合受一系列高度不同的因素组成的复杂网络调控，其中包括在肠道黏膜内已鉴定出的多种结构不同的调节肽。这些调节肽通常被称为生长因子和细胞因子，在调节上皮细胞不同功能以维持肠道黏膜正常稳态和完整性方面发挥着重要作用。此外，许多其他肽分子，如细胞外基质因子和凝血因子，以及包括磷脂、短链脂肪酸、腺嘌呤核苷酸、微量元素和药物制剂在内的非肽分子，已被证明可调节肠道上皮修复机制。其中一些分子可能由血小板、相邻基质细胞、炎症细胞或受损的上皮和非上皮细胞释放，并可能在调节肠道损伤中发挥重要作用。肠道表面的反复损伤是包括IBD在内的各种肠道疾病的关键特征，需要上皮的持续修复。通过调节肽或其他调节因子增强肠道修复机制可能为治疗以上皮表面损伤为特征的疾病提供未来的方法。
