Ernst P B, Jin Y, Reyes V E, Crowe S E
Dept. of Pediatrics, University of Texas Medical Branch, Galveston 77555-0366.
Scand J Gastroenterol Suppl. 1994;205:22-8. doi: 10.3109/00365529409091405.
Mucosal immune responses are designed to provide local protection against infection, without inducing excessive amounts of inflammation that would alter epithelial integrity or function. It has become clear that the epithelium not only serves as a barrier to exclude pathogens, but also initiates host responses to infection. Gastric epithelial cells infected with Helicobacter pylori can respond within hours to produce inflammatory mediators that recruit and activate neutrophils. The gastric epithelium can also be recognized by local T-cells, resulting in their activation and ability to induce epithelial damage. During infection with H. pylori, there is a remarkable increase in the level of local IgG antibodies, which may also recognize and damage the epithelium. Thus, activated neutrophils, T-cells and auto-antibodies may contribute to a weakened epithelial barrier that allows luminal acid and other factors to contribute to peptic ulceration. The epithelium appears to play a key role in the initiation of the local inflammatory and immune responses that may contribute to the more serious sequelae associated with H. pylori infection.
黏膜免疫反应旨在提供针对感染的局部保护，而不引发会改变上皮完整性或功能的过量炎症。现已明确，上皮不仅作为屏障排除病原体，还启动宿主对感染的反应。感染幽门螺杆菌的胃上皮细胞能在数小时内作出反应，产生招募并激活中性粒细胞的炎症介质。胃上皮也能被局部T细胞识别，导致其活化并具备诱导上皮损伤的能力。在幽门螺杆菌感染期间，局部IgG抗体水平显著升高，这些抗体也可能识别并损伤上皮。因此，活化的中性粒细胞、T细胞和自身抗体可能导致上皮屏障削弱，从而使管腔酸和其他因素促成消化性溃疡。上皮似乎在局部炎症和免疫反应的启动中起关键作用，而这些反应可能导致与幽门螺杆菌感染相关的更严重后遗症。
