Mycobacterium tuberculosis (M. tb) Rv0297-encoded PE_PGRS5 has been known to be expressed at the later stages of infection and in acidified phagosomes during transcriptome and proteomic studies. The possible role of Rv0297 in the modulation of phagosomal maturation and in providing protection against a microbicidal environment has been hypothesized. We show that Rv0297PGRS is involved in modulating the calcium homeostasis of macrophages followed by impedance of the phagolysosomal acidification process. This is evident from the downregulation of the late endosomal markers (Rab7 and cathepsin D) in the macrophages infected with recombinant Mycobacterium smegmatis (rM.smeg)—M.smeg_Rv0297 and M.smeg_Rv0297PGRS—or treated with recombinant Rv0297PGRS protein. Macrophages infected with rM.smeg expressing Rv0297 produce nitric oxide and undergo apoptosis, which may aid in the dissemination of pathogen in the later stages of infection. Rv0297 was also found to be involved in rescuing the bacterium from oxidative and hypoxic stress employed by macrophages and augmented the survivability of the recombinant bacterium. These results attribute to the functional significance of this protein in M.tb virulence mechanism. The fact that this protein gets expressed at the later stages of lung granulomas during M.tb infection suggests that the bacterium possibly employs Rv0297 as its dissemination and survival strategy.

结核分枝杆菌（结核分枝杆菌）已知在转录组和蛋白质组学研究中，Rv0297编码的PE_PGRS5在感染后期和酸化吞噬体中表达。已经假设了Rv0297在吞噬体成熟的调节和提供对杀微生物环境的保护中的可能作用。我们显示Rv0297PGRS参与调节巨噬细胞的钙稳态，随后是吞噬溶酶体酸化过程的阻抗。从重组感染的巨噬细胞中的晚期内体标记（Rab7和组织蛋白酶D）的下调可以明显看出这一点。耻垢分枝杆菌 （r斯麦格）—M.smeg_Rv0297 和 M.smeg_Rv0297PGRS —或用重组Rv0297PGRS蛋白处理。巨噬细胞感染了r斯麦格表达Rv0297的细胞产生一氧化氮并经历凋亡，这可能有助于在感染的后期传播病原体。还发现Rv0297参与拯救细菌免受巨噬细胞利用的氧化和低氧应激，并增强了重组细菌的生存能力。这些结果归因于该蛋白在体内的功能意义。结核菌毒力机制。该蛋白在肺肉芽肿的晚期表达结核菌 感染表明该细菌可能采用Rv0297作为其传播和生存策略。