【摘 要】
：
Helicobacter pylori (H. Pylori) persistently colonizes the gastric mucosa despite a vigorous immune response. Vacuolating cytotoxin secreted by H. Pylori has tu
【机 构】
：
Department of Medical Microbiology and Parasitology, Present ddress:Infectious Disease Division,part
【基金项目】
：
上海市自然科学基金;the Foundation for Excellent Young Investigator of Shanghai Jiao Tong University, School of Medicine, the National Key Program for Infectious Diseases of China;The Program of Shanghai Subjec
论文部分内容阅读
Helicobacter pylori (H. Pylori) persistently colonizes the gastric mucosa despite a vigorous immune response. Vacuolating cytotoxin secreted by H. Pylori has turned out to be a potent immunomodulatory toxin, but the signal trausduction pathways involved has not been studied in macrophages. We observed in this study that vacA-deficient H. Pylori induced significantly higher expression of integrin-linked kinase (ILK) and endothelial nitric oxygen synthase (eNOS), and significantly more production of reactive oxygen species (ROS) in monocyte/macrophage-like U937 cells, as compared with isogenic vacA~ H. Pylori. The expression of eNOS mRNA in U937 cells overexpressing ILK was markedly increased compared with those transfected with empty vectors. Thus, vacA-deficient H. Pylori appears to upregnlate ILK expression, which modulates the expression of eNOS and as a result, stimulates the production of ROS. It is VacA that prevents such a process by inhibiting ILK expression, helping H. Pylori escape host immunoreaction. This mechanism explains, at least in part, persistent infection of H. Pylori in the stomach. Cellular & Molecular Immunology. 2009;6(3):191-197.
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