Mycobacterium tuberculosis (Mtb)-induced apoptosis of alveolar macrophages plays an important role in the pathogenesis of tuberculosis. Previous studies indicated that massive LncRNAs could deteriorate MTB invasion or latent infection by regulating macrophage’s apoptosis. However, whether LincRNA-Cox2 is involved in apoptosis of macrophage infected with Mtb is unclear. In this study, we found Bacillus Calmette-Guerin(BCG)infection induced cell apoptosis with a increasing LincRNA-Cox2 expression in RAW264.7 cells. Furthermore, the activation of TLR signal pathway elevated the expression of lincRNA-Cox2. In this regard, we used small interfering RNA to explore the role of LincRNA-Cox2 on regulating apoptosis of RAW264.7 cells infected with BCG. The results showed that si-LincRNA-Cox2 was capable of increased the expression of apoptosis-associated proteins and accumulation of ROS in BCG-infected RAW264.7 cells. Mechanically, si-LincRNA-Cox2 facilitated BCG-induced macrophage apoptosis by activating the intrinsic apoptotic pathway as well as increased the genes expression of PERK/eIF2α/CHOP. These results provide novel insights into host-pathogen interactions and highlight the potential role of LincRNA-Cox2 in regulating apoptosis induced by BCG-infection.

结核分枝杆菌（Mtb）诱导的肺泡巨噬细胞凋亡在结核病的发病机理中起重要作用。先前的研究表明，大量的LncRNA可通过调节巨噬细胞的凋亡来恶化MTB的侵袭或潜在的感染。但是，尚不清楚LincRNA-Cox2是否参与感染Mtb的巨噬细胞的凋亡。在这项研究中，我们发现卡介苗芽孢杆菌（BCG）感染诱导RAW264.7细胞中LincRNA-Cox2表达增加的细胞凋亡。此外，TLR信号途径的激活提高了lincRNA-Cox2的表达。在这方面，我们使用小干扰RNA来探索LincRNA-Cox2在调节被BCG感染的RAW264.7细胞凋亡中的作用。结果表明，si-LincRNA-Cox2能够增加BCG感染的RAW264.7细胞凋亡相关蛋白的表达和ROS的积累。在机械上，si-LincRNA-Cox2通过激活内在的凋亡途径促进BCG诱导的巨噬细胞凋亡，并增加了PERK /eIF2α/ CHOP的基因表达。这些结果提供了对宿主-病原体相互作用的新颖见解，并突出了LincRNA-Cox2在调节BCG感染诱导的细胞凋亡中的潜在作用。