摘要
目的探讨幽门螺杆菌(Hp)侵袭内化对细胞AID表达的影响及相关机制。方法选择不同侵袭力的Hp,分别感染AGS细胞,以抗β1整合素抗体抑制侵袭为对照组,经庆大霉素保护性侵袭实验,用real-time RT-PCR和细胞免疫荧光分别检测AID mRNA和蛋白表达水平。用SN-50抑制AGS细胞NF-κB活性,同法检测Hp对AID表达的影响。结果高侵袭力的Hp诱导的AID蛋白和mRNA的表达量均高于低侵袭力的Hp,P<0.05;抗β1整合素抗体处理后各组AID蛋白表达均减少(P<0.05),高侵袭力组mRNA的表达也均减少(P<0.05),低侵袭力组mRNA的表达呈下降趋势;SN-50处理后各组AGS细胞AID蛋白和mRNA表达水平均降低,P<0.05。结论侵入胞内的Hp可刺激AGS细胞诱导AID的异常表达,这种诱导涉及NF-κB信号通路,细菌的诱导能力与内化细菌的数量呈正相关。Hp内化诱导宿主细胞异常表达AID可能是导致Hp相关肿瘤发生的机制之一。
We investigated whether the internalized Helicobacter pylori （Hp） could induce AID expression and explored the corresponding mechanism in this study. Hp strains with different invasiveness invaded AGS cells, respectively. By anti-βl- integrin antibody, the invasion was inhibited as a control. We conducted the gentamiein protection assay, and then we detected the protein and mRNA expression of AID induced by the internalized Hp using immunofluorescence and real-time RT-PCR. U- sing SN-50 to inhibit NF-κB, we detected AID expression by the same ways. The protein and mRNA expression of AID in- duced by high invasiveness strains were found to be stronger than those induced by low invasiveness strains （P〈0.05）. After AGS cells were pretreated with anti-β1-integrin antibody, the protein expression of AID declined in each groups （P〈0.05）; the mRNA declined in high invasiveness groups （P〈0.05） and that was on a declining curve in low invasiveness groups. After AGS cells were pretreated with SN-50, the protein and mRNA expression of AID declined in each groups （P〈0.05）. It is evi- dent that the internalized Hp can induce AID aberrant expression, which may principally involve in NF-κB signal pathway. This induction and amount of the intracellular Hp have positive correlation. AID aberrant expression induced by internalized Hp may contribute to the development of Hp associated neoplasms.
出处
《中国人兽共患病学报》
CAS
CSCD
北大核心
2014年第9期923-928,共6页
Chinese Journal of Zoonoses
基金
国家自然科学基金(No.81271784)
福建省自然科学基金(No.2012J01130)~~
关键词
幽门螺杆菌
侵袭
AID
NF-ΚB
Helicobacter pylor
invasiveness
activation-induced cytidine deaminase
NF-κB
