Biomedical Research
Online ISSN : 1880-313X
Print ISSN : 0388-6107
ISSN-L : 0388-6107
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Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells
Shoichiro KAMEOKATakeshi KAMEYAMATakaya HAYASHISeiichi SATONaomi OHNISHITakeru HAYASHINaoko MURATA-KAMIYAHideaki HIGASHIMasanori HATAKEYAMAAkinori TAKAOKA
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2016 Volume 37 Issue 1 Pages 21-27

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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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© 2016 Biomedical Research Press
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