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The glucosylation of free cholesterol (FC) byHelicobacter pylori cells has various biological significances for the survival of this bacterium.H. pylori cells with glucosylated FC are capable of evading host immune systems, such as phagocytosis by macrophages and activation of antigen-specific T cells, and surviving in the gastric mucosal tissues for long periods. An additional role of cholesterol glucosylation in the survival ofH. pylori which is distinct from the role of escaping the host immune system, however, has yet to be identified. This study demonstrated that 7-dehydrocholesterol (7dFC), an FC precursor, is a toxic compound fatal toH. pylori cells, but the cell membrane ofH. pylori is capable of absorbing this toxic sterol via glucosylation. In contrast to the case with 7dFC, no toxicity toH. pylori cells was detected from the glucosylated 7dFC. In addition,cgt gene mutantH. pylori cells that cannot glucosylate cholesterols had higher susceptibility to the toxic action of 7dFC than wild-typeH. pylori cells. These results indicate that thecgt gene product ofH. pylori serves to detoxify the sterol fatal to this bacterium and to permit this toxic sterol as a cell membrane lipid component. In summary, this study defined a novel role of cholesterol glucosylation inH. pylori .

Detoxification of 7-Dehydrocholesterol Fatal to Helicobacter pylori Is a Novel Role of Cholesterol Glucosylation