Pathophysiology of Helicobacter pylori infection.

Abstract

Helicobacter pylori is now accepted as the major cause of chronic gastritis. The initial response to infection is acute neutrophilic gastritis, which progresses to active chronic gastritis in most people. To confirm the pathogenic role of H. pylori, both the individual histological features of chronic gastritis and its topographical patterns must be shown to be caused by the infection. Surface epithelial degeneration is a probable result of direct tissue injury by bacterial products. Candidates are ammonia or ammonium products, cytotoxins, phospholipases and pro-inflammatory products such as lipopolysaccharide and platelet-activating factor. Neutrophil polymorph and chronic inflammatory cell infiltration are consequences of the mucosal immune response to bacterial antigens. Complement products and interleukin (IL)-8 are polymorph chemotaxins, and monocyte processing of antigens, followed by T helper cell and B lymphocyte responses, explain the presence of these cells in the mucosa. Atrophy may be a consequence of autodestructive products of neutrophil and monocyte activation, such as reactive oxygen metabolites and proteases. Intestinal metaplasia is most probably an adaptive response, possibly to H. pylori infection, exacerbated by other injurious agents such as bile reflux and dietary irritants. Pangastritis is the usual outcome after H. pylori infection. This is followed by multifocal atrophy and intestinal metaplasia. The latter changes weaken mucosal defences further and peptic ulceration may ensue. Patients with an increased parietal cell mass who become infected with H. pylori will exhibit antral restriction of the gastritis because the high acid output protects the corpus mucosa from bacterial adhesion and the inflammatory consequences. Such patients also have acid-induced gastric metaplasia in the proximal duodenum.(ABSTRACT TRUNCATED AT 250 WORDS)