Acute inflammatory response induced by Helicobacter pylori in the rat air pouch.

Infection by Helicobacter pylori elicits persistent neutrophil infiltration in the gastric mucosa and stimulates the release of substances that may contribute to the establishment of gastritis. In this study, we used the rat air pouch model to evaluate the acute inflammatory response to H. pylori, in vivo. A pronounced neutrophil infiltration was observed 6 h and 12 h after the injection of H. pylori into the air pouch. Strains with different genotypes were able to induce cellular influx. This response was dependent upon the amount of bacteria injected and still occurred when heat-killed bacteria were employed. An increase in prostaglandin E(2) levels was observed, indicating that H. pylori induced cyclooxygenase 2 in this model. The production of interleukin-1 beta and tumor necrosis factor-alpha by leukocytes was also enhanced, suggesting that this model may be useful for studying the direct activation of neutrophils by H. pylori in vivo.