| [ Summary ] |
Salt promotes gastric carcinogenesis in Helicobacter pylori (Hp) infected glandular stomach of Mongolian gerbils (MGs) treated with N-methyl-N-nitrosourea (MNU) in a dose-dependent fashion. Hp infection alone is a much stronger factor than high-salt diet administration in regard to gastric carcinogenesis, salt itself being rather a co-promoter of gastric adenocarcinoma development, especially in combination with Hp. In the present study, salt was found to induce an increase in the surface area of mucous cell type mucins (SMCM) in which Hp is localized, and a decrease in gland mucous cell type mucins (GMCM), which defend against Hp infection. The bacteria induced an increase in MUC 6 mRNA levels, while salt had no influence on MUC 5 AC or MUC 6 mRNA expression in the MG model. Thus, salt alters the mucous microenvironment by increasing the SMCM : GMCM ratio to help Hp colonize and exacerbate inflammation. All glandular stomach carcinomas were classified as gastric phenotype (G type) in non-infected MGs, independent of the histological type, whereas Hp-infected animals harbored all types of cancers including G, gastric-and-intestinal mixed (GI), intestinal (I), and null (N) types. Restriction of salt intake appears to be important for the prevention of stomach cancers in patients with Hp infection. |