| セッション情報 |
The 2nd JSGE International Topic Conference Poster Session
Upper GI：Basic Approach
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| タイトル |
IT-P-08：Increased Interleukin-32 Expression in Gastric Inflammation Induced by Helicobacter pylori
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| 演者 |
Sakitani Kosuke（Department of Gastroenterology, The University of Tokyo, Japan） |
| 共同演者 |
Hirata Yoshihiro（Department of Gastroenterology, The University of Tokyo, Japan）, Serizawa Takako（Department of Gastroenterology, The University of Tokyo, Japan）, Takahashi Ryota（Department of Gastroenterology, The University of Tokyo, Japan）, Yoshida Haruhiko（Department of Gastroenterology, The University of Tokyo, Japan）, Koike Kazuhiko（Department of Gastroenterology, The University of Tokyo, Japan） |
| 抄録 |
Levels of interleukin（IL）-32, a recently described inflammatory cytokine, are increased in various inflammatory diseases, such as rheumatoid arthritis and Crohn’s disease, and in malignancies, including gastric cancer. We examined IL-32 expression in human gastric disease. In immunohistochemistry, IL-32 expression was detected in 50%（2/4）of normal gastric tissues, 100%（4/4）of gastritis tissues, and 44%（7/16）of gastric cancer tissues. IL-32 protein levels in ELISA analysis increased depending on the pathology. H. pylori-induced IL-32 expression in human gastric epithelial cell line, AGS was dependent on the bacterial cagPAI genes. IL-32 levels were reduced by siRNAs for JNK1, JNK2, and IKKβ. H. pylori-induced NF-κB, and mitogen activated kinases（MAPKs；JNK, p38, and ERK）activation was decreased in IL-32-knockdown cells compared to a control AGS cell line. We also found that expression of chemokines, CXCL1, CXCL2, and IL-8, were decreased in IL-32-knockdown AGS cell lines. These results suggest that IL-32 is involved in the inflammation-cancer process through the amplification of signaling pathways and up-regulation of its targets. |
| 索引用語 |
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