Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells

Kameoka, Shoichiro; Kameyama, Takeshi; Hayashi, Takaya; Sato, Seiichi; Ohnishi, Naomi; Hayashi, Takeru; Murata-Kamiya, Naoko; Higashi, Hideaki; Hatakeyama, Masanori; Takaoka, Akinori

Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells

Kameoka, Shoichiro; Kameyama, Takeshi; Hayashi, Takaya et al.

Biomedical Research, 2016, 37(1), 21-27

Permalink : https://hdl.handle.net/2115/61351

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アクセス権	open access
URI	https://hdl.handle.net/2115/61351
タイトル	Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells
著者	Kameoka, Shoichiro ; Kameyama, Takeshi ; Hayashi, Takaya ; Sato, Seiichi ; Ohnishi, Naomi ; Hayashi, Takeru ; Murata-Kamiya, Naoko ; Higashi, Hideaki ; Hatakeyama, Masanori ; Takaoka, Akinori
著者名 Kameoka, Shoichiro
e-Rad_Researcher 40569505 著者名 Kameyama, Takeshi
著者名 Hayashi, Takaya
著者名 Sato, Seiichi
著者名 Ohnishi, Naomi
著者名 Hayashi, Takeru
著者名 Murata-Kamiya, Naoko
e-Rad_Researcher 20311227 著者名 Higashi, Hideaki
e-Rad_Researcher 40189551 著者名 Hatakeyama, Masanori
e-Rad_Researcher 30323611 著者名 Takaoka, Akinori
言語	英語
発行日	2016-02
出版者	Biomedical Research Press
収録物名	Biomedical Research
巻(号)	37(1)
ページ	21-27
抄録	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.
資源タイプ	学術雑誌論文
出版タイプ	Version of Record
PISSN	0388-6107
関連情報	PMID 26912137
関連情報 (isIdenticalTo)	出版社版DOI https://doi.org/10.2220/biomedres.37.21