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Let-7b Is Involved in the Inflammation and Immune Responses Associated with Helicobacter pylori Infection by Targeting Toll-Like Receptor 4
Teng, Gui-gen; Wang, Wei-hong; Dai, Yun; Wang, Shu-jun; Chu, Yun-xiang; Li, Jiang
刊名PLOS ONE
2013-02-20
DOI10.1371/journal.pone.0056709
8期:2
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]GASTRIC EPITHELIAL-CELLS ; NF-KAPPA-B ; SIGNALING PATHWAY ; GENE-EXPRESSION ; MICRORNA FAMILY ; CANCER ; LIPOPOLYSACCHARIDE ; INTERLEUKIN-8 ; ACTIVATION ; INDUCTION
英文摘要

Objectives: Toll-like receptors (TLRs) are important initiators in native immune responses to microbial infections. TLR4 is up-regulated in response to H. pylori infection in gastric epithelial cells. However, the regulatory mechanisms for the expression of TLR4 in H. pylori infection have not been clearly defined. The aims of this study are to present the evidence that microRNA let-7b directly regulates TLR4 expression in human gastric epithelial cells, and subsequently influences the activation of NF-kappa B and the expression of the downstream genes in H. pylori infection.

Methods: The expression of let-7b was determined in gastric mucosa specimens and in two gastric epithelial cell lines using quantitative RT-PCR. The expression of TLR4 was determined by immunohistochemistry staining and RT-PCR. The potential target of let-7b was identified by luciferase reporter assay and Western blot. Let-7b mimics and inhibitors were used to examine the effects of let-7b on NF-kappa B activity. The expression of the downstream genes of NF-kappa B was also determined in cells infected with H. pylori 26695.

Results: Let-7b was significantly decreased in gastric mucosa specimens and in gastric epithelial cell lines (AGS, GES-1) infected with H. pylori 26695 (cagA+). Let-7b was complementary to the 3′-UTR of TLR4 mRNA and regulated TLR4 expression via post-transcriptional suppression in gastric epithelium. Infection of H. pylori induced the expression of TLR4 and activated NF-kappa B in AGS and GES-1 cells. Overexpression of let-7b by mimics downregulated TLR4, and subsequently attenuated NF-kappa B, MyD88, NF-kappa B1/p50, RelA/p65. The expression of IL-8, COX-2 and CyclinD1 was inhibited in H. pylori infected cells with let-7b overexpression. Both TAK-242 (TLR4 inhibitor) and SN50 (NF-kappa B inhibitor) significantly inhibited the H. pylori induced downregulation of let-7b.

Conclusions: Let-7b targets at TLR4 mRNA, and regulates the activation of NF-kappa B and the expression of the downstream genes related to the inflammation and immune responses in H. pylori infection.

语种英语
WOS记录号WOS:000315184200148
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被引频次:38[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63849
专题北京大学第一临床医学院_消化科
作者单位Peking Univ, Dept Gastroenterol, Hosp 1, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Teng, Gui-gen,Wang, Wei-hong,Dai, Yun,et al. Let-7b Is Involved in the Inflammation and Immune Responses Associated with Helicobacter pylori Infection by Targeting Toll-Like Receptor 4[J]. PLOS ONE,2013,8(2).
APA Teng, Gui-gen,Wang, Wei-hong,Dai, Yun,Wang, Shu-jun,Chu, Yun-xiang,&Li, Jiang.(2013).Let-7b Is Involved in the Inflammation and Immune Responses Associated with Helicobacter pylori Infection by Targeting Toll-Like Receptor 4.PLOS ONE,8(2).
MLA Teng, Gui-gen,et al."Let-7b Is Involved in the Inflammation and Immune Responses Associated with Helicobacter pylori Infection by Targeting Toll-Like Receptor 4".PLOS ONE 8.2(2013).
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