| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Research Abstract |
It has not been determined how cholesteryl alpha-glucosyltransferase (aCgT), which forms cholesteryl alpha-glucosides (aCGs), functions in the pathogenesis of H. pylori infection. We show that the activity of aCgT from H. pylori clinical isolates is highly correlated with the degree of gastric atrophy. We investigated the role of aCGs in various aspects of the immune response. aCGs were recognized by invariant natural killer T (iNKT) cells, eliciting an immune response in vitro and in vivo. Following inoculation of H. pylori harboring highly active aCgT into iNKT cell-deficient (Ja18 KO) or wild-type mice, bacterial recovery significantly increased in Ja18 KO compared to wild-type mice. Moreover, cytokine production characteristic of Th1 and Th2 cells dramatically decreased in Ja18 KO compared to wild-type mice. These findings demonstrate that aCGs play critical roles in H. pylori-mediated gastric inflammation and precancerous atrophic gastritis.
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