LINC00870 regulates Th1/Th2 via the JAK/STAT pathway in peripheral blood mononuclear cells infected with Mycobacterium tuberculosis

Long, noncoding RNAs reportedly play vital roles in tuberculosis (TB). For example, upregulation of LINC00870 has been observed in tuberculosis, though its role and underlying mechanism remains unclear. In this study, we investigated the expression and effect of LINC00870 in Mycobacterium tuberculosis (MTB) infection by comparing MTB-infected peripheral blood mononuclear cells (PBMCs) with controls. The results showed LINC00870 was significantly increased in MTB infected PBMCs. Additionally, LINC00870 overexpression inhibited Th1-secreted cytokines while promoted Th2-secreted cytokine in MTB-infected PBMCs. Furthermore, LINC00870 promoted p-STAT5 and p-JAK2 protein expression, thus activating JAK/STAT signaling in MTB-infected PBMCs. Sputum and plasma samples were obtained from TB, latent tuberculosis infection (LTBI) patients and healthy controls. The qRT-PCR results showed higher levels of LINC00870 in the sputum and plasma from TB and LTBI patients compared to healthy controls. In addition, LINC00870 were decreased in both TB and LTBI patients after three month of therapy, respectively. The results showed a correlation between LINC00870 inhibition and Th1/Th2, as well as JAK/STAT signaling pathway in PBMCs from active TB patients. In conclusion, higher levels of LINC00870 in tuberculosis might be associated with Th1/Th2-related immune responses by activating JAK/STAT signaling. LINC00870 thus may be a novel biomarker for diagnosing and treating tuberculosis.