Modulation of lncRNA NEAT1 overturns the macrophages based immune response in M. tuberculosis infected patients via miR-373 regulation.

There is a lack of studies which explore and clarify the interactions that occur between host macrophage and Mycobacterium tuberculosis with regard to microRNA such as LNCNEAT1 and miR-373. The current study determines the mechanisms involved in the control of M. tuberculosis infection by macrophage using LNCNEAT1 and miR-373. The researchers collected different samples from healthy individuals, pulmonary TB patients, and samples like hMDMs cells and H37Rv infected MTB to determine the concentrations of inflammatory factors. The impact of NEAT1 and miR-373 upon macrophages was analyzed in NEAT1-specific siRNA (si-NEAT1), NEAT1 over-expression vector (pcDNA3.1-NEAT1), miR-373 mimic, miR-373 inhibitor (anti-miR-373), and negative control, and macrophages infected with H37Ra. The results inferred that among pulmonary TB patients, NEAT1 got heavily expressed while the expression level of miR-373 was poor. The number of inflammatory factors with pulmonary TB was notably higher. This got further amplified in macrophages after being infected with H37Ra, while no such observations found for miR-373. During post-transfection, low concentration of inflammatory factors was observed while the cells in si-NEAT1 group got proliferated in low volume compared to both pcDNA3.1-NEAT1 group and NEAT1 negative control group. However, the capability of apoptosis was higher compared to the other two groups (p < 0.05). There was an increase observed in inflammatory factors as well as proliferation in anti-miR-373 group compared to miR-373 mimics and miR-373-negative control group while a significant decline was observed in apoptosis. LNCNEAT1 aggravated the number of inflammatory factors in macrophages that got infected with MTB while on the other end, it mitigated both phagocytosis as well as the cellular immunity of macrophages. In addition to this, it enhanced the proliferation of infected cells and inhibited apoptosis via targeted regulation of miR-373, thus resulting in the development of TB.