Chronic helicobacter pylori infection induces SOCS1 expression but not CISH in a murine model of gastric infection

Abstract

Background and Aims Helicobacter pylori infections continue to be a major challenge to the field of gastroenterology. Gastric H. pylori infections is a critical cause of chronic atrophic gastritis and peptic ulcer disease and is one of the leading carcinogens that leads to stomach cancer and MALT lymphoma. Helicobacter pylori infection has been demonstrated to modulate the local inflammatory response in the gastric mucosa. In this study, we examine the role of chronic in vivo H. pylori infection in the modulation of inflam-mation controlled by Supressors of Cytokine Signalling (SOCS), a family of anti-inflammatory regulators that act on various cytokine pathways. Methods C57Bl6 mice were infected at 5 weeks of age with the mouse-adapted H. pylori strain SS1 via oral gavage × 3 inoculations. The mice were culled 20 weeks post-infection and the stomach tissue harvested post-mortem and snap frozen. Total RNA was extracted from these tissues and cDNA produced from the mRNA by reverse transcription. A semi-quantitative real time PCR study was conducted examining Socs1 and Cish relative gene expression in infected ( n = 10) and uninfected controls ( n = 10). Results Mice infected with H. pylori had a significantly increased gene expression of Socs1 ( p Cish gene expression was not signifi-cantly altered upon infection. Conclusions Helicobacter pylori may supress localised inflam-mation via increased expression of SOCS1 in a murine model of chronic infection.