<i><b>Helicobacter pylori</b></i><b> induces IL-1β protein through the inflammasome activation in differentiated macrophagic </b><b>cells </b>
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- KAMEOKA Shoichiro
- Division of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University
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- KAMEYAMA Takeshi
- Division of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University
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- HAYASHI Takaya
- Research Center for Infection-associated Cancer, Institute for Genetic Medicine, Hokkaido University
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- SATO Seiichi
- Division of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University
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- OHNISHI Naomi
- Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University
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- HAYASHI Takeru
- Division of Microbiology, Graduate School of Medicine, University of Tokyo
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- MURATA-KAMIYA Naoko
- Division of Microbiology, Graduate School of Medicine, University of Tokyo
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- HIGASHI Hideaki
- Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University
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- HATAKEYAMA Masanori
- Division of Microbiology, Graduate School of Medicine, University of Tokyo
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- TAKAOKA Akinori
- Division of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University Molecular Medical Biochemistry Unit, Biological Chemistry and Engineering Course, Graduate School of Chemical Sciences and Engineering, Hokkaido University
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Abstract
More than 50% of people in the world are infected with Helicobacter pylori (H. pylori), which induces various gastric diseases. Especially, epidemiological studies have shown that H. pylori infection is a major risk factor for gastric cancer. It has been reported that the levels of interleukin (IL)-1β are upregulated in gastric tissues of patients with H. pylori infection. In this study, we investigated the induction mechanism of IL-1β during H. pylori infection. We found that IL-1βmRNA and protein were induced in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells after H. pylori infection. This IL-1β production was inhibited by a caspase-1 inhibitor and a ROS inhibitor. Furthermore, K+ efflux and Ca2+ signaling were also involved in this process. These data suggest that NOD-like receptor (NLR) family, pyrin domain containing 3 (NLRP3) and its complex, known as NLRP3 inflammasome, are involved in IL-1β production during H. pylori infection because it is reported that NLRP3 inflammasome is activated by ROS, K+ efflux and/or Ca2+ signaling. These findings may provide therapeutic strategy for the control of gastric cancer in H. pylori-infected patients.
Journal
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- Biomedical Research
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Biomedical Research 37 (1), 21-27, 2016
Biomedical Research Press
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Details 詳細情報について
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- CRID
- 1390282679879167232
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- NII Article ID
- 130005128374
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- ISSN
- 1880313X
- 03886107
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- HANDLE
- 2115/61351
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- PubMed
- 26912137
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- Text Lang
- en
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- Data Source
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- JaLC
- IRDB
- Crossref
- PubMed
- CiNii Articles
- KAKEN
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- Abstract License Flag
- Disallowed