title: Helicobacter pylori induces IL-1β protein through the inflammasome activation in differentiated macrophagic cells.
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 Ca(2+) 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 Ca(2+) signaling. These findings may provide therapeutic strategy for the control of gastric cancer in H. pylori-infected patients.
authors.affiliation: Division of Signaling in Cancer and Immunology, Institute for Genetic Medicine, Hokkaido University.
authors.forename: Shoichiro
authors.initials: S
authors.lastname: Kameoka
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kameyama
authors.forename: Takaya
authors.initials: T
authors.lastname: Hayashi
authors.forename: Seiichi
authors.initials: S
authors.lastname: Sato
authors.forename: Naomi
authors.initials: N
authors.lastname: Ohnishi
authors.forename: Takeru
authors.initials: T
authors.lastname: Hayashi
authors.forename: Naoko
authors.initials: N
authors.lastname: Murata-Kamiya
authors.forename: Hideaki
authors.initials: H
authors.lastname: Higashi
authors.forename: Masanori
authors.initials: M
authors.lastname: Hatakeyama
authors.forename: Akinori
authors.initials: A
authors.lastname: Takaoka
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D020013:Calcium Signaling; D020170:Caspase 1 / Q000378:metabolism; D002460:Cell Line; D005110:Extracellular Space / Q000378:metabolism; D016481:Helicobacter Infections / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D016480:Helicobacter pylori / Q000276:immunology; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism*; D053583:Interleukin-1beta / Q000235:genetics / Q000378:metabolism*; D042541:Intracellular Space / Q000378:metabolism; D008264:Macrophages / Q000276:immunology / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D058847:Inflammasomes; D053583:Interleukin-1beta; D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate; D020170:Caspase 1; D011188:Potassium