<i><b>Helicobacter pylori</b></i><b> induces IL-1β protein through the inflammasome activation in differentiated macrophagic </b><b>cells </b>

  • 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
  • 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
  • HAYASHI Takaya
    Research Center for Infection-associated Cancer, Institute for Genetic Medicine, Hokkaido University
  • 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
  • OHNISHI Naomi
    Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University
  • HAYASHI Takeru
    Division of Microbiology, Graduate School of Medicine, University of Tokyo
  • MURATA-KAMIYA Naoko
    Division of Microbiology, Graduate School of Medicine, University of Tokyo
  • HIGASHI Hideaki
    Division of Infection and Immunity, Research Center for Zoonosis Control, Hokkaido University
  • HATAKEYAMA Masanori
    Division of Microbiology, Graduate School of Medicine, University of Tokyo
  • 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.

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