| Autor: |
Kameoka, Shoichiro, Kameyama, Takeshi, Hayashi, Takaya, Sato, Seiichi, Ohnishi, Naomi, Hayashi, Takeru, Murata-Kamiya, Naoko, Higashi, Hideaki, Hatakeyama, Masanori, Takaoka, Akinori |
| Jazyk: |
angličtina |
| Rok vydání: |
2016 |
| Zdroj: |
Biomedical Research. 37(1):21-27 |
| ISSN: |
0388-6107 |
| Popis: |
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. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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