摘要
目的:分析鲍曼不动杆菌标准株ATCC 19606(Acinetobacter baumannii ATCC 19606)外膜蛋白A(outer membrane protein A,Omp A)对RAW264. 7细胞的自噬诱导作用。方法:建立Omp A刺激RAW264. 7细胞的模型,通过细胞免疫荧光染色、Western blot和透射电子显微镜检测Omp A对RAW264. 7细胞自噬的影响。结果:Omp A可以引起自噬蛋白LC3B-II表达升高,并抑制Akt/mTOR/p70S6K的磷酸化水平;雷帕霉素可以进一步降低mTOR和p70S6K磷酸化,并提高Omp A引起的LC3B-II表达升高。结论:鲍曼不动杆菌Omp A通过Akt/mTOR/p70S6K信号通路引起RAW264. 7细胞自噬。这为将来进一步研究鲍曼不动杆菌引起自噬的分子机制及找到对抗其感染的新方法提供理论依据。
AIM:To analyze the effects of outer membrane protein A(OmpA)from Acinetobacter baumannii ATCC19606on the autophagy of RAW264.7cells.METHODS:The RAW264.7cell model stimulated by OmpA was established.The effects of OmpA on the autophagy of RAW264.7cells were detected by immunofluorescence,Western blot and transmission electron microscopy.RESULTS:The OmpA increased the expression of LC3B-Ⅱand reduced the phosphorylation levels of Akt,mTOR and p70S6K.Rapamycin further reduced the phosphorylation levels of mTOR and p-70S6K,and increased the expression of LC3B-Ⅱinduced by OmpA.CONCLUSION:The OmpA of Acinetobacter baumannii induces autophagy via Akt/mTOR/p70S6K signaling pathway in the RAW264.7cells.This work provides a basis for further research on the molecular mechanism of autophagy induced by Acinetobacter baumannii to find a new method against the infection of Acinetobacter baumannii.
作者
安志远
丁文一
郑春明
黄骁舾
AN Zhi-yuan;DING Wen-yi;ZHENG Chun-ming;HUANG Xiao-xi(Medical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China;Department of Clinical Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China)
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2018年第12期2267-2270,2276,共5页
Chinese Journal of Pathophysiology
基金
国家自然科学基金资助项目(No.81300049)
