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- Title
Overexpression of Helicobacter pylori VacA N-terminal fragment induces proinflammatory cytokine expression and apoptosis in human monocytic cell line through activation of NF-κB.
- Authors
Jing-Jing Luo; Cun-Yan Li; Sheng Liu; Wen Yu; Shuang-Yang Tang; Heng-Ling Cai; Yan Zhang
- Abstract
Vacuolating cytotoxin (VacA) is an important virulence factor in the pathogenesis of Helicobacter pylori-related diseases. The aim of this study was to investigate the function of the amino-terminal 476 residue fragment (p52) of VacA and the possible molecular mechanisms responsible for its induction of proinflammatory cytokines secretion and apoptosis. Human acute monocytic leukemia cell line THP-1 was used as an in vitro model to study proinflammatory cytokines secretion and apoptosis induced by transfection of a recombinant plasmid encoding the amino-terminal 476 residue fragment (p52) of VacA. The results showed that VacA p52 overexpression induced the production of tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), nitric oxide, and reactive oxygen species in THP-1 cells in a time-dependent manner. VacA p52 overexpression also promoted THP-1 cells apoptosis. In addition, VacA p52 triggered the activation of nuclear factor kappa B (NF-κB), indicating a possible mechanism for its induction of proinflammatory cytokines secretion and cell apoptosis. Our study demonstrated that the induction of cytokines secretion and apoptosis by VacA p52 in THP-1 cells could be mediated through activation of nuclear factor kappa B.
- Publication
Canadian Journal of Microbiology, 2013, Vol 59, Issue 8, p523
- ISSN
0008-4166
- Publication type
Academic Journal
- DOI
10.1139/cjm-2013-0021