期刊
MICROBES AND INFECTION
卷 12, 期 11, 页码 854-863出版社
ELSEVIER
DOI: 10.1016/j.micinf.2010.06.002
关键词
Helicobacter pylori; miR-146a; Post-transcriptional regulation; Inflammation; IRAK1; TRAF6
资金
- Chinese National Natural Science Foundation [30770113]
- National Basic Research Program of China (973 Program) [2009CB522606]
- National High Technology Research and Development Program of China (863 Program) [2006AA02A208]
- Major National Science & Technology Specific Projects of China [2008ZX09101-033]
Helicobacter pylori (H. pylori) is a major human pathogenic bacterium in gastric mucosa. However, the regulatory mechanism of H. pylori-induced immune response is not clear. MicroRNAs (miRNAs) have recently emerged as key post-transcriptional regulators of gene expression, and their role in H. pylori infection is just beginning to be explored. Here, we first reported that H. pylori infection up-regulated the expression of miR-146a in gastric epithelial cells as well as in gastric mucosal tissues in NF-kappa B-dependent manner. In turn, miR-146a may downregulate the expression of target genes, interleukin-1 receptor-associated kinase 1 (IRAK1) and TNF receptor-associated factor 6 (TRAF6). Furthermore, miR-146a negatively regulated H. pylori-triggered interleukin (IL)-8, growth-related oncogene (GRO)-alpha, and macrophage inflammatory protein (MIP) -3 alpha through diminishing NF-kappa B activity. In conclusion, H. pylori-induced miR-146a plays a potential role in a negative feedback loop to modulate the inflammation by targeting IRAK1 and TRAF6. (C) 2010 Institut Pasteur. Published by Elsevier Masson SAS. All rights reserved.
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