Cuong Duy Tran, Hien Huynh, Fiona Campbell, Peter Coyle, Ross Butler.
Journal of Gastroenterology and Hepatology (2001), Volume 16; Supplement: A122

Asia Pacific Digestive Week 2001 incorporating Australian Gastroenterology Week, 23-27 September 2001, Sydney, Australia

ABSTRACT:

Helicobacter pylori (H. pylon) is recognized as the primary cause of chronic gastritis and gastric diseases, which may be associated with increased reactive oxygen species (ROS). Metallothionein (MT), a ubiquitous, low molecular weight, cysteine-rich metal-binding ligand has been shown to sequester ROS and reduce tissue damage. It is proposed that mice lacking MT expression are more susceptible to gastric damage and exhibit a rapid and florid gastritis. Control (C57BI/ 6; MT +/+) and MT -null (MT-/-) mice were inoculated with 1 x 108 H. pylori/mL (SSI strain) via an oro- gastric gavage and were infected for 4 and 8 weeks. H. pylori load was determined by culturing gastric homogenate and myeloperoxidase (MPO) activity, a marker of neutrophil infiltration, was also determined using gastric homogenate. Gastritis was assessed using a modified Sydney Grading System. Results were analyzed using an unpaired student's t-test and a nonparametric Mann- Whitney U-test. Statistical significance was considered as P < 0.05. At 4 weeks, MT -/- mice have significantly higher H. pylori load compared to MT+/+. However, at 8 weeks there was no difference although MT -/- mice tend to have a higher bacterial load. Neutrophil infiltration was not different between MT+/+ and MT-/- mice at either 4 or 8 weeks however MPO activity was significantly higher in MT-/- compared to MT+/+ mice, irrespective of infection duration. No difference was seen in gastritis score between MT+/+ and MT-/- mice at 4 weeks. At 8 weeks, MT-/- mice showed a significant difference in chronic inflammation of the submucosa of the antrum, the superficial layer of the cardia, the continuous band of inflammatory cells of the basal layer and the submucosa of the transitional zone compared to MT+/+ mice. These findings suggest that mice lacking MT expression are more susceptible to H. pylori colonization and gastric inflammation. In addition, MT, in part may be protective against H. pylori-induced gastritis.