期刊
PATHOGENS AND DISEASE
卷 73, 期 4, 页码 -出版社
OXFORD UNIV PRESS
DOI: 10.1093/femspd/ftu024
关键词
Helicobacter pylori; ROS; NLRP3; inflammasome; IL-1 beta; IL-18
资金
- Construct Program of the Key Discipline in Hunan Province, Hunan Provincial Key Laboratory for Special Pathogen Prevention and Control [Hunan Provincial Science & Technology Department document] [2014-5]
- Construct Program of the Key Discipline in Hunan Province, Hunan Provincial Key Laboratory for Special Pathogen Prevention and Control [Hunan Provincial Education Department document] [2012-312]
- Key Project of Hunan Provincial Education Department [11A103]
- Research Project of Hunan Provincial Science & Technology Department [2013TT2021]
This study investigated whether Helicobacter pylori could activate the nucleotide-binding oligomerization domain-like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) inflammasome in human macrophages and the involvement of reactive oxygen species (ROS) in inflammasome activation. Phorbol-12-myristate-13-acetate (PMA)-differentiated human acute monocytic leukemia cell line THP-1 was infected with H. pylori. The levels of pro-inflammatory cytokines interleukin (IL)-1 beta and IL-18 in supernatant were measured by ELISA. Intracellular ROS level was analyzed by flow cytometry. Quantitative real-time PCR and western blot analysis were employed to determine the mRNA and protein expression levels of NLRP3 and caspase-1 in THP-1 cells, respectively. Our results showed that H. pylori infection could induce IL-1 beta and IL-18 production in PMA-differentiated THP-1 cells in a dose-and time-dependent manner. Moreover, secretion of IL-1 beta and IL-18 in THP-1 cells following H. pylori infection was remarkably reduced by NLRP3-specific small interfering RNA treatment. In addition, the intracellular ROS level was elevated by H. pylori infection, which could be eliminated by the ROS scavenger N-acetylcysteine (NAC). Furthermore, NAC treatment could inhibit NLRP3 inflammasome formation and caspase-1 activation and suppress the release of IL-1 beta and IL-18 from H. pylori-infected THP-1 cells. These findings provide novel insights into the innate immune response against H. pylori infection, which could potentially be used for the prevention and treatment of H. pylori-related diseases.
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