Imunosuppression by a corticosteroid fails to exacerbate Helicobacter pylori infection in a mouse model of gastric colonization.

Helicobacter pylori can colonize the human stomach for prolonged periods of time, and this colonization uniformly leads to the development of chronic active gastritis. In a small percentage of individuals, gastric pathology progresses to peptic ulceration or more rarely certain gastric cancers. In addition to non-specific inflammation, specific systemic and local immunity develops in response to gastric colonization by this pathogen. However, these responses combined appear inadequate for eliminating H. pylori from the gastric mucosa. This is also the case in a mouse model of gastric colonization by H. pylori. In the present study, we attempted to determine whether the mammalian host response to infection with H. pylori exerts any overt antibacterial effects. To this end we examined H. pylori colonization in normal mice, and mice immunosuppressed by treatment with a corticosteroid. Despite obvious suppression of the immune response in the latter mice, H. pylori burdens remained similar in both groups after three months of colonization. This suggests that the murine host response, at least, exerts little obvious protection against H. pylori colonization.