The role of the local immune response in the pathogenesis of peptic ulcer formation.

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.