Interactions between inducible nitric oxide and other inflammatory mediators during Helicobacter pylori infection.

Abstract

Recent studies in both humans and animal models strongly suggest the contribution of the host immune response to Helicobacter pylori-related disease. Inducible nitric oxide synthase has been shown to be up-regulated in the gastric epithelium during H. pylori gastritis, suggesting a role in inflammation. C57BL/6 wild-type and inducible nitric oxide synthase gene knockout mice were infected with H. pylori strain SS1. Expression of macrophage inflammatory protein-2 (MIP-2), interleukin-1 beta (IL-1 beta), Th1 (IL-2 and gamma interferon) and Th2 (IL-4 and IL-10) cytokines, and inducible cyclooxygenase mRNA in mice was determined in mouse gastric tissues and quantified using either competitive reverse transcription-polymerase chain reaction or competitive polymerase chain reaction following reverse transcription. The Th1 cytokine gamma interferon was only detected in wild-type and inducible nitric oxide synthase gene knockout infected mice, while a Th2 (IL-4) response was not detected. H. pylori induced MIP-2 and IL-1 beta mRNA in mice. Because similar levels of inflammatory mediators were noted in both wild-type and nitric oxide synthase gene knockout infected mice, our data suggest that inducible nitric oxide synthase does not influence expression of these inflammatory mediators in the early stages of H. pylori infection in mice.