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首页> 外文期刊>Infection and immunity >Helicobacter pylori Activates Toll-Like Receptor 4 Expression in Gastrointestinal Epithelial Cells
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Helicobacter pylori Activates Toll-Like Receptor 4 Expression in Gastrointestinal Epithelial Cells

机译：幽门螺杆菌激活胃肠道上皮细胞中的Toll-like受体4表达

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Helicobacter pylori activates the transcription factor NF-κB, leading to proinflammatory cytokine production by gastric epithelial cells. However, the receptors for the initial bacterial interaction with host cells which activate downstream signaling events have not been completely defined. Recently, it has been shown that microbial components activate Toll-like receptors (TLRs), thereby leading to AP-1- and NF-κB-dependent transcription and resulting in the production of proinflammatory cytokines. The aim of this study was to determine whether H. pylori activates TLR4. Reverse transcription-PCR showed that both type I and type II H. pylori clinical isolates induced TLR4 mRNA expression in AGS cells compared with that by uninfected controls. H. pylori upregulated TLR4 protein expression in two gastric epithelial cell lines (AGS and MKN45) and one intestinal epithelial cell line (T84). Monoclonal TLR4 antibody inhibited lipopolysaccharide-induced interleukin-8 secretion from THP-1 macrophages but not from gastric epithelial cells infected with H. pylori. H. pylori demonstrated increased adherence to CHO TLR4-transfected cells compared with that to both CHO TLR2-transfected and nontransfected CHO cells (P < 0.01). These results indicate that H. pylori activates TLR4 expression in epithelial cells and that TLR4 can serve as a receptor for H. pylori binding.
机译：幽门螺杆菌激活转录因子NF-κB，导致胃上皮细胞产生促炎性细胞因子。但是，尚未完全定义与宿主细胞发生初始细菌相互作用的受体，这些受体会激活下游信号传导事件。近来，已显示微生物组分激活Toll样受体（TLR），从而导致AP-1-和NF-κB依赖性转录并导致促炎细胞因子的产生。这项研究的目的是确定是否 H。幽门螺杆菌激活TLR4。逆转录PCR显示I型和II型H。与未感染对照相比，幽门螺杆菌临床分离株能诱导AGS细胞中TLR4 mRNA的表达。 H。幽门螺杆菌上调了两种胃上皮细胞系（AGS和MKN45）和一种肠上皮细胞系（T84）中TLR4蛋白的表达。 TLR4单克隆抗体可抑制脂多糖诱导的THP-1巨噬细胞分泌白介素8分泌，但不能抑制被 H感染的胃上皮细胞分泌。幽门炎。 H。 pylori 证明与CHO TLR2转染的细胞和未转染的CHO细胞相比，对CHO TLR4转染的细胞的粘附性增加（ P <0.01）。这些结果表明 H。幽门螺杆菌激活上皮细胞中TLR4的表达，并且TLR4可以作为 H的受体。幽门螺杆菌结合。

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