Department of Pathology, University of Michigan, Ann Arbor, Michigan 48109, USA; email:
Annu Rev Physiol. 2019 Feb 10;81:189-209. doi: 10.1146/annurev-physiol-020518-114504. Epub 2018 Oct 24.
The gastrointestinal mucosa, structurally formed by the epithelium and lamina propria, serves as a selective barrier that separates luminal contents from the underlying tissues. Gastrointestinal mucosal wound repair is orchestrated by a series of spatial and temporal events that involve the epithelium, recruited immune cells, resident stromal cells, and the microbiota present in the wound bed. Upon injury, repair of the gastrointestinal barrier is mediated by collective migration, proliferation, and subsequent differentiation of epithelial cells. Epithelial repair is intimately regulated by a number of wound-associated cells that include immune cells and stromal cells in addition to mediators released by luminal microbiota. The highly regulated interaction of these cell types is perturbed in chronic inflammatory diseases that are associated with impaired wound healing. An improved understanding of prorepair mechanisms in the gastrointestinal mucosa will aid in the development of novel therapeutics that promote mucosal healing and reestablish the critical epithelial barrier function.
胃肠道黏膜由上皮和固有层构成,形成选择性屏障,将腔内容物与下面的组织分隔开。胃肠道黏膜创面修复由一系列时空事件协调,涉及上皮、募集的免疫细胞、固有基质细胞以及创面床中的微生物群。损伤后,胃肠道屏障的修复由上皮细胞的集体迁移、增殖和随后的分化介导。上皮修复受到多种与创面相关的细胞的密切调控,包括免疫细胞和基质细胞,以及腔内分泌物释放的介质。这些细胞类型的高度调控相互作用在与创面愈合受损相关的慢性炎症性疾病中受到干扰。对胃肠道黏膜中促修复机制的更好理解将有助于开发促进黏膜愈合和重建关键上皮屏障功能的新型治疗方法。