Helicobacter pylori infection and inflammation

Abstract

Helicobacter pylori infection and chronic active gastritis are inextricably linked, and this organism is almost certainly responsible for inducing the resulting inflammatory changes. Acute ingestion studies have confirmed that H. pylori infection causes acute gastritis, and the progression to chronic gastritis has been documented. Duodenitis and H. pylori infection often occur concurrently, but colonization is restricted to those with significant gastric metaplasia. The association between H. pylori-induced inflammation and symptoms is at present unclear. In some treatment studies H. pylori eradication has been associated with a symptomatic response, whereas the acute inflammatory response appears frequently to subside H. pylori infection of the gastroduodenal mucosa is associated with both mucosal and systemic antibody responses. The mucosal response occurs both within the stomach and locally in the duodenum in patients with duodenitis. Mucosal cellular responses also appear active in patients with H. pylori gastritis. Cytokines are produced locally, which could have significant pathophysiologic effects. The concurrent use of non-steroidal anti-inflammatory agents in patients with H. pylori-induced gastritis may modify the subsequent inflammatory response. Although H. pylori is a major and consistent stimulus for inflammation within the gastroduodenal mucosa, our understanding of the development of these responses is far from complete. Inflammatory mediators are released during infection and probably play a major role in modulating the subsequent mucosal immune responses.