Podolsky D K
Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, USA.
Am J Physiol. 1999 Sep;277(3):G495-9. doi: 10.1152/ajpgi.1999.277.3.G495.
Well-coordinated mechanisms have evolved that provide both innate protection against gastrointestinal mucosal injury and facilitation of rapid mucosal repair following mucosal damage. Generic protection from injury is provided by intrinsic structural features of the epithelium that form a highly competent barrier and a complex formed at the apical surface by trefoil peptides that comprise the interface between mucosa and lumen. When the epithelial barrier has been broken, regardless of the nature of the injury, epithelial surface continuity is rapidly reestablished through restitution as cells migrate and elongate. This process is promoted by trefoil peptides at the apical surface and a large array of cytokines and growth factors acting at the basolateral pole. Many of these regulatory peptides are products of the immune and other lamina propria cell populations, which are activated following disruption of the mucosal barrier. Thus efforts to repair the epithelium follow inherently from inflammatory effects after initial damage; the repair process in turn may allow abrogation of further inflammation. Ultimate repair of injury requires both proliferative replacement of damaged epithelial cells and remodeling of extracellular matrix and deeper cell populations to restore normal architecture and a fully functional mucosa.
已经进化出了协调良好的机制，这些机制既能提供针对胃肠道黏膜损伤的固有保护，又能在黏膜损伤后促进快速的黏膜修复。上皮细胞的固有结构特征形成了一个高度有效的屏障，以及由三叶肽在顶端表面形成的复合物，该复合物构成了黏膜与管腔之间的界面，从而提供了对损伤的一般保护。当上皮屏障被破坏时，无论损伤的性质如何，随着细胞迁移和伸长，上皮表面的连续性会通过再生迅速重新建立。这一过程由顶端表面的三叶肽以及大量作用于基底外侧极的细胞因子和生长因子促进。这些调节肽中的许多是免疫细胞和其他固有层细胞群体的产物，它们在黏膜屏障破坏后被激活。因此，上皮修复的努力本质上是在初始损伤后的炎症效应之后进行的；反过来，修复过程可能会消除进一步的炎症。损伤的最终修复既需要受损上皮细胞的增殖替代，也需要细胞外基质和更深层细胞群体的重塑，以恢复正常结构和功能完全正常的黏膜。
