Journal Article 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

37 ( 1 )  , pp.21 - 27 , 2016-02 , Biomedical Research Press
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.

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