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Metallothionein is a crucial protective factor against Helicobacter pylori-induced gastric erosive lesions in a mouse model

¹Laboratory Animal Research Center and ²Department of Public Health and Molecular Toxicology, School of Pharmaceutical Sciences, Kitasato University, Tokyo, Japan; ³Laboratory of Pharmaceutical Health Sciences, School of Pharmacy, Aichi Gakuin University, Nagoya, Japan; ⁴Department of Veterinary Pathology, Faculty of Agriculture, Tottori University, Tottori, Japan; ⁵Center for Genetic Studies of Integrated Biological Functions, School of Medicine, Kitasato University, Sagamihara, Japan; ⁶Environmental Health Sciences Division, National Institute for Environmental Studies, Tukuba, Japan; ⁷Department of Health Chemistry, School of Pharmaceutical Sciences, Showa University, Tokyo, Japan; and ⁸Laboratory of Molecular Nutrition and Toxicology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan

Submitted 6 June 2007 ; accepted in final form 10 January 2008

Infection with the gastric pathogen Helicobacter pylori (H. pylori) causes chronic gastritis, peptic ulcer, and gastric adenocarcinoma. These diseases are associated with production of reactive oxygen species (ROS) from infiltrated macrophages and neutrophiles in inflammatory sites. Metallothionein (MT) is a low-molecular-weight, cysteine-rich protein that can act not only as a metal-binding protein, but also as a ROS scavenger. In the present study, we examined the role of MT in the protection against H. pylori-induced gastric injury using MT-null mice. Female MT-null and wild-type mice were challenged with H. pylori SS1 strain, and then histological changes were evaluated with the updated Sydney grading system at 17 and 21 wk after challenge. Although the colonization efficiency of H. pylori was essentially the same for MT-null and wild-type mice, the scores of activity of inflammatory cells were significantly higher in MT-null mice than in wild-type mice at 17 wk after challenge. Histopathological examination revealed erosive lesions accompanied by infiltration of inflammatory cells in the infected MT-null mice but not in wild-type mice. Furthermore, activation of NF-B and expression of NF-B-mediated chemokines such as macrophage inflammatory protein-1 and monocytes chemoattractant protein-1 in gastric cells were markedly higher in MT-null mice than in wild-type mice. These results suggest that MT in the gastric mucosa might play an important role in the protection against H. pylori-induced gastric ulceration.

gastric ulcer; reactive oxygen species; NF-B; chemokine

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