摘要
结核分枝杆菌(Mycobacteria tuberculosis,MTB)是结核病的致病菌,其感染机体后能在细胞内长期生存并在合适的条件下引发疾病.非氧依赖性杀伤是巨噬细胞清除MTB的重要途径,主要表现为细胞内吞体和溶酶体融合,利用细胞自噬作用清除内部细菌.相应的,MTB可利用多种方式顽强抵抗细胞自噬作用,与细胞共存从而逃避宿主免疫杀伤作用. MicroRNA(miRNA)是一种内源性非编码单链小RNA分子,其能在转录后水平沉默相关基因表达,是介导MTB与炎性细胞许多反应的重要分子.近期研究发现,MTB能够通过诱导巨噬细胞特异表达一些miRNA分子并靶向自噬相关基因,阻碍自噬发生、发展,从而实现MTB的抗细胞自噬作用.本文就miRNA在MTB抗细胞自噬中的作用及机制的研究进展作一综述.
Mycobacteria tuberculosis(MTB) is the pathogen responsible for tuberculosis. It can exist in the infected-macrophages for a long time and trigger the disease when the appropriate conditions arise. The primary way to kill intracellular bacteria is via the oxygen-independent route. In this route, macrophages mainly rid themselves of parasites by autophagy where autophagosomes and lysosomes are fused into autophagolysosomes.However, MTB can resist to autophagy and avoid being killed by the immune system of host cells in several ways, thereby co-existing with the host. MicroRNAs(miRNA) are endogenous non-coding single-chain RNA molecules that can silence related genes expression in a post-transcriptional manner. They are crucial molecules for mediating inflammatory reactions between MTB and inflammatory cells. Recent studies found that MTB can induce the expression of certain specific miRNAs in macrophages and target genes related to autophagy and therefore inhibit triggering and progression of autophagy. This mechanism confers resistance to autophagy. The present review summarizes the role of miRNA in the resistance to autophagy by MTB.
作者
张益源
伊正君
付玉荣
ZHANG Yi-Yuan;YI Zheng-Jun;FU Yu-Rong(College Clinical Medicine,Weifang Medical University,Weifang 261053,China;Department of Clinical Laboratory,Weifang Medical University,Weifang 261053,China)
出处
《生物化学与生物物理进展》
SCIE
CAS
CSCD
北大核心
2019年第1期43-50,共8页
Progress In Biochemistry and Biophysics
基金
国家自然科学基金项目(81470001)
山东省自然科学基金项目(ZR2016HM09)~~