@article{oai:u-ryukyu.repo.nii.ac.jp:02002248,
 author = {Tomimori, Koh and Uema, Eriko and Teruya, Hiromitsu and Ishikawa, Chie and Okudaira, Taeko and Senba, Masachika and Yamamoto, Kazuo and Matsuyama, Toshifumi and Kinjo, Fukunori and Fujita, Jiro and Mori, Naoki},
 issue = {11},
 journal = {Infection and Immunity},
 note = {CCL20 attracts immature dendritic cells and memory T cells, and plays a role on mucosal surfaces in inflammation. However, whether H. pylori infection induces CCL20 in human gastric epithelial cells remains to be determined. The aim of this study was to analyze the molecular mechanism of H. pylori-induced CCL20 expression. Expression of CCL20 mRNA was assessed by reverse transcription-PCR. Five normal and five H. pylori-infected gastric tissue samples were stained immunohistochemically for CCL20. Luciferase assay was used to monitor activation of the CCL20 gene promoter, and electrophoretic mobility shift assay was used to explore the binding of transcription factors to this promoter. CCL20 expression in epithelial cells of H. pylori-positive tissues was higher than in H. pylori-negative tissues. H. pylori induced CCL20 expression in gastric epithelial cell lines, and such induction was dependent on an intact cag pathogenicity island. Activation of the CCL20 promoter by H. pylori occurred through the action of NF-κB. Transfection of dominant negative mutants of IκB kinase and NF-κB-inducing kinase inhibited H. pylori-mediated activation of CCL20. Treatment with inhibitor of Hsp90 suppressed H. pylori-induced CCL20 mRNA due to deactivation of NF-κB. Collectively, these results suggest that H. pylori activates NF-κB through an intracellular signaling pathway that involved IκB kinase and NF-κB-inducing kinase, leading to CCL20 gene transcription, and that Hsp90 is a crucial regulator of H. pylori-induced CCL20 expression, presumably contributing to immune response in H. pylori., 論文},
 pages = {5223--5232},
 title = {Helicobacter pylori Induces CCL20 Expression},
 volume = {75}
}