Journal
MOLECULAR BIOLOGY REPORTS
Volume 39, Issue 4, Pages 4655-4661Publisher
SPRINGER
DOI: 10.1007/s11033-011-1257-5
Keywords
miR-146a; H. pylori; Proinflammatory cytokines; CagA
Categories
Funding
- Scientific Innovation Research Foundation of Third Military Medical University [2009XQN20]
- Chinese National Natural Science Foundation [30770113]
- State Key Laboratory of Trauma, Burns, and Combined Injury [SKF201012]
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MicroRNAs have been implicated as a central regulator of the immune system. We have previously reported that Helicobacter pylori (H. pylori) was able to increase the expression of miR-146a, and miR-146a may negatively regulate H. pylori-induced inflammation, but the exact mechanism of how H. pylori contribute the induction of miR-146a is not clear. Here, we attempted to assess the role of H. pylori related proinflammatory cytokines including interleukin (IL)-8, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta, and cytotoxin-associated gene A (CagA) virulence factor on the induction of miR-146a. We found that IL-8, TNF-alpha, and IL-1 beta could contribute to the induction of miR-146a in gastric epithelial cell HGC-27 in NF-kappa B-dependent manner, while the induction of miR-146a upon H. pylori stimulation was independent of above proinflammatory cytokines. Furthermore, overexpression of miR-146a reduced H. pylori-induced IL-8, TNF-alpha, and IL-1 beta. However, CagA had no effect on the miR-146a induction. Taken together, our study suggest that proinflammatory cytokines IL-8, TNF-alpha, and IL-1 beta could contribute to the induction of miR-146a during H. pylori infection, while CagA is not necessarily required for miR-146a induction. miR-146a may function as novel negative regulators to modulate the inflammation.
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