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P53 hemizygous knockout mice but not APC knockout mice enhance gastric mucosal inflammation induced by H pylori


, : P53 hemizygous knockout mice but not APC knockout mice enhance gastric mucosal inflammation induced by H pylori. Gastroenterology. 122(4 Suppl. 1): A-173, Il

H.pyloriplays a critical role in the pathogenesis of peptic ulcers and the chronic inflammatory process which may be linked to gastric cancer, p53 inhibits cell growth through the activation of cell-cycle arrest and apoptosis and most cancers have eitherp53 gene mutation or defects in p53 induction. Mutations in APCgene appear to be responsible not only familial adenomatous polyposis but also sporadic gastric cancer. To determine the role of p53 and APC mutation in the development of gastric carcinogenesis, p53 hemizygous and APC knockout mice were infected with H.pylori. Method: H.pylori strain TN2GF4 which has been reported to induce gastric cancer in Mongolian gerbils was inoculated into both wild type B57 mice an d p53 hemizygous mice. Mice were sacrificed at 6 and 12 months after inoculation. H.pyloriinfection and grade of histological gastritis were assessed. The antibody titer against H.pylori were also examined. APC knockout mice were also studied for up to 6 months. Results: infected animals developed anti-H.pylori serum IgG responses. One year after infection with H.pylori, p53 hemizygous mice showed more active chronic inflammation than wild type mice~ The inflammation score assessed by the updated Sydney System in p53 hemizygous and wild mice were 2.1,1.4, respectively (p

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