Mycobacterium tuberculosis (Mtb) is an intracellular pathogen known to persist in host cells. The apoptotic response of macrophages serves as a defense mechanism to inhibit the growth of intracellular bacteria, the failure of which can favor the spread of the pathogen to new cells. However, the mycobacterial components that regulate cell death and the related underlying mechanisms remain poorly understood. In this study, we investigated protein Rv3261, isolated from an Mtb culture filtrate, for its apoptotic potential using multidimensional fractionation. Rv3261 was found to induce macrophage apoptosis through the caspase-3/-9-dependent pathway. Furthermore, the ROS-dependent JNK activation pathway was found to be critical in Rv3261-mediated apoptosis. Rv3261 inhibited the growth of intracellular Mtb, which was significantly abrogated by pre-treatment with the ROS scavenger N-acetylcysteine (NAC), suggesting that Rv3261-mediated apoptosis may act as a host defense response. These findings suggest that Rv3261 is involved in the apoptotic modulation of Mtb-infected macrophages.

结核分枝杆菌（Mtb）是已知在宿主细胞中持续存在的细胞内病原体。巨噬细胞的凋亡反应是抑制细胞内细菌生长的防御机制，其失败可以促进病原体向新细胞的扩散。但是，调节细胞死亡的分枝杆菌成分和相关的潜在机制仍然知之甚少。在这项研究中，我们调查了多维分离法从Mtb培养滤液中分离出的Rv3261蛋白的凋亡潜力。发现Rv3261通过caspase-3 / -9依赖性途径诱导巨噬细胞凋亡。此外，发现ROS依赖的JNK激活途径在Rv3261介导的凋亡中至关重要。Rv3261抑制细胞内Mtb的生长，N-乙酰半胱氨酸（NAC），表明Rv3261介导的凋亡可能充当宿主防御反应。这些发现表明Rv3261参与了感染Mtb的巨噬细胞的凋亡调控。