Helicobacter pyloriis causally related to inflammation and ulceration of the stomach and is a risk factor for the development of gastric carcinoma. The mechanisms by which this organism induces cell injury are currently not well understood. Detailed histologic examination of the gastric mucosa support a “leaking roof” model of ulcerogenesis, with progressive focal cellular destruction and exposure of the lamina propria. The cellular damage may result from direct action of soluble factors produced byHelicobacter, such as ammonia and cytotoxin, or indirect stimulation of the inflammatory cascade by activation and degranulation of leukocytes. The immune response againstHelicobactermay damage the gastric mucosa by producing antibodies that cross-react with gastric epithelium. The inflammatory process results in aberrant HLA-DR expression on the epithelial cells.Helicobacteralso increases acid and pepsin secretion by stimulating gastrin and pepsinogen production, which could exacerbate any cellular damage caused by cytotoxins or inflammatory mediators, leading to focal necrosis and ulceration.