• Zhen Liu, Bin Xiao, Bin Tang, Bosheng Li, Na Li, Endong Zhu, Gang Guo, Jiang Gu, Yuan Zhuang, Xiaofei Liu, Honglei Ding, Xiaoyan Zhao, Hong Guo, Xuhu Mao, and Quanming Zou.
• Department of Clinical Microbiology and Immunology, College of Medical Laboratory Science, Third Military Medical University, Chongqing 400038, China.
• Microbes Infect. 2010 Oct 1; 12 (11): 854-63.

AbstractHelicobacter 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-κB-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)-α, and macrophage inflammatory protein (MIP) -3α through diminishing NF-κB 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.Copyright © 2010 Institut Pasteur. Published by Elsevier SAS. All rights reserved.

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