Helicobacter pylori induces IL-1ß protein through the inflammasome activation in differentiated macrophagic cells.
Biomed Res
; 37(1): 21-7, 2016.
Article
em En
| MEDLINE
| ID: mdl-26912137
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)-1ß are upregulated in gastric tissues of patients with H. pylori infection. In this study, we investigated the induction mechanism of IL-1ß during H. pylori infection. We found that IL-1ßmRNA and protein were induced in phorbol-12-myristate-13-acetate (PMA)-differentiated THP-1 cells after H. pylori infection. This IL-1ß 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-1ß 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Helicobacter pylori
/
Infecções por Helicobacter
/
Interleucina-1beta
/
Inflamassomos
/
Macrófagos
Tipo de estudo:
Risk_factors_studies
Limite:
Humans
Idioma:
En
Revista:
Biomed Res
Ano de publicação:
2016
Tipo de documento:
Article