Toll样受体4通路在幽门螺杆菌致病机制中的作用

Role of Toll-like receptor 4 pathway in pathogenesis of Helicobacter pylori infection

目的:比较Toll样受体4(TLR4)及MyD88在幽门螺杆菌(Hp)感染的BALB/c小鼠胃黏膜内表达含量随时间的变化,探讨TLR4通路在Hp致病机制中的作用。方法:70只BALB/c小鼠随机分为7组,分别于感染Hp的第0天、第3天、第7天、第14天、抗生素三联疗法治疗的第3天、第7天、第14天取得各组小鼠的胃黏膜标本,用RT-PCR和Western blotting的方法半定量检测TLR4、MyD88在基因和蛋白水平上的表达。结果:(1)小鼠TLR4、MyD88在感染Hp后均迅速升高,在治疗后迅速回落,但仍高于正常水平。(2)小鼠TLR4、MyD88的表达含量与病理严重程度无相关性。结论:TLR4信号通路参与了Hp的致病机制,但与炎症反应的严重程度无相关性。

Objective To compare the mRNA and protein changes of Toll-like receptor 4 （TLR4） and myeloid differentiation primary response gene 88 （MyD88） in gastric mucosa of Helicobacter pylori （Hp） infected BALB/c mice, and to explore the role of TLR4 signal pathway in the pathogenesis of Hp. Methods Seventy BALB/ c mice were randomly divided into 7 groups, specimens of gastric mucosa of each group mice were respectively obtained at day O,days 3,days 7,days 14 of Hp infection and at days 3,days 7,days 14 of triple therapy of antibiotics. RT-PCR and Western blotting methods were used to detect mRNA and protein expression of TLR4 and MyD88. Results The expression of TLR4 and MyD88 increased rapidly after Hp infection and decreased rapidly after the treatment, but was still higher than normal. No correlation was found between the severity of pathology and the expression level of TLR4 and MyD88. Conclusions TLR4 signaling pathway may he involved in the pathogenesis of Hp, but there was no correlation between TLR4, MyD88 and severity of inflammation.