结核分枝杆菌脂蛋白Rv1016c增强细菌成膜能力和抑制自噬  

Regulation of autophagy and biofilm formation by Mycobacterium tuberculosis lipoprotein Rv1016c

作　　者：粟海波 彭宝洲 徐英 刘梓健 龚青[1] SU Hai-bo;PENG Bao-zhou;XU Ying;LIU Zi-jian;GONG Qing(Department of Biochemistry,GMU-GIBH Joint School of Life Sciences,Guangzhou Medical University,Guangzhou 511436,Guangdong Province, China)

机构地区：[1]广州医科大学-中科院广州生物医药健康研究院联合生命科学学院生化教研室

出　　处：《微生物学免疫学进展》2019年第4期38-43,共6页Progress In Microbiology and Immunology

基　　金：广东省自然科学基金面上项目(2018A030313560);广东省高校优秀青年创新人才培养计划资助项目(2016KQNCX141);广州市科技计划一般项目(201804010317)

摘　　要：目的研究结核分枝杆菌(Mycobacterium tuberculosis, Mtb)脂蛋白Rv1016c在Mtb感染和结核病发病中的作用和机制。方法将Mtb脂蛋白Rv1016c基因导入野生耻垢分枝杆菌(Mycobacterium smegmatis, MS)构建重组菌株MS-Rv1016c,比较脂蛋白Rv1016c对菌体生长、成膜能力、细菌聚集、毒力等方面的影响,评估重组菌株MS-Rv1016c对自噬的影响。结果 Rv1016c基因的导入,因过表达脂蛋白使得MS的菌落变大、褶皱增加,使菌体聚集度降低,使细菌成膜速度加快、生物被膜产量增加;Rv1016c显著抑制巨噬细胞自噬,促进细菌在细胞内持留。结论 Rv1016c能够促进MS生物被膜形成,抑制细胞自噬,增强细菌毒力。为研究脂蛋白在Mtb致病机理中的作用提供理论依据。Objective To explore the function and mechanism of Mycobacterium tuberculosis lipoproteins Rv1016 c in the pathogenesis of Mycobacterium tuberculosis(Mtb). Methods We constructed the strain MS-Rv1016 c which over-expresses Mtb lipoprotein Rv1016 c in M. smegmatis(MS), and compared it with the wild strain in the growth, biofilm formation, aggregation, virulence of Rv1016 c, and determined the effect of MS-Rv1016 c on autophagy in macrophages. Resul-ts Rv1016 c could increase the size of colonies of MS. Additionally, Rv1016 c reduced the degree of bacterial aggregation, suggesting that Rv1016 c may affect its hydrophobicity. MS-Rv1016 c promoted the rate and production in the biofilm formation. Moreover, MS-Rv1016 c significantly inhibited autophagy in macrophages in comparison with that from the wild type bacteria. Conclusion Rv1016 c could promote the production of biofilm, make its colonies loose, inhibit macrophages autophagy, and enhance the virulence of MS, providing a theoretical basis for exploring the pathogenesis of lipoprotein in Mtb.

关 键 词：结核分枝杆菌 脂蛋白Rv1016c 生物膜 自噬 

分 类 号：R378.911[医药卫生—病原生物学]