Tuberculosis is initiated by the entry of Mycobacterium tuberculosis (Mtb) into macrophages in the lungs. A study of the cellular factors responsible for the entry of Mtb into host cells will potentially benefit the development of therapeutic treatments or preventive agents against Mtb infection. Using human THP1-derived macrophages as a model, we found that infection of Mtb H37Ra transiently reduced the level of ASAP1, an ADP ribosylation factor (Arf)-GTPase activating protein. Furthermore, knockdown of ASAP1 increased the efficiency of H37Ra entry into the cell and altered the status of actin remodeling as indicated by the enhanced aggregation of F-actin and the increased numbers of vinculin- and paxillin-rich puncta. Collectively, the results in this report identified ASAP1 as a regulator controlling the entry of Mtb H37Ra into macrophage by remodeling actin cytoskeleton.

结核病是由结核分枝杆菌进入引起的(Mtb) 进入肺中的巨噬细胞。对导致 Mtb 进入宿主细胞的细胞因子的研究可能有利于开发针对 Mtb 感染的治疗方法或预防剂。使用人类 THP1 衍生的巨噬细胞作为模型，我们发现感染 Mtb H37Ra 会暂时降低 ASAP1 的水平，ASAP1 是一种 ADP 核糖基化因子 (Arf)-GTPase 激活蛋白。此外，ASAP1 的敲低提高了 H37Ra 进入细胞的效率，并改变了肌动蛋白重塑的状态，如 F-肌动蛋白的聚集增强和富含纽蛋白和桩蛋白的斑点数量增加所示。总的来说，本报告中的结果将 ASAP1 确定为通过重塑肌动蛋白细胞骨架来控制 Mtb H37Ra 进入巨噬细胞的调节剂。