Long non-coding RNA SNHG16 silencing inhibits proliferation and inflammation in Mycobacterium tuberculosis-infected macrophages by targeting miR-140-5p expression.

Abstract

The study investigated the clinical diagnostic value of long non-coding RNA (LncRNA) small nucleolar RNA host gene 16 (SNHG16) and explored its underlying molecular mechanism through Mycobacterium tuberculosis (M. tuberculosiinfection of macrophages. RT-qPCR analysis of the serum SNHG16 levels of the 66 healthy individuals, 67 latent TB (LTB) patients, and 67 active TB (ATB) patients. The receiver-operating characteristic (ROC) curve to detect the clinical diagnostic value of SNHG16 in TB patients. In vitro, M. tuberculosis-infected macrophages, CCK-8 and ELISA to detect cell proliferation and inflammatory factor levels. Luciferase reported assay was performed to analyze the targeting relationship between SNHG16 and miR-140-5p. SNHG16 was significantly elevated in TB patients, and among them, ATB patients were higher than LTB patients. ROC confirmed that SNHG16 could distinguish LTB patients from healthy controls, and ATB patients from LTB patients, and can be used as a good diagnostic biomarker for TB. M. tuberculosis infection increased SNHG16 levels and promoted the proliferation and inflammation in macrophages. However, SNHG16 silencing significantly reversed the effect of infection. miR-140-5p, a direct target miRNA of SNHG16, was down-regulated in TB patients and was negatively correlated with SNHG16. When miR-140-5p was inhibited, the alleviating effect of SNHG16 silencing on M. tuberculosis infection proliferation and inflammation was significantly reversed. The present results suggested that SNHG16 may be a new diagnostic biomarker for TB patients and SNHG16 silencing may alleviate TB by inhibiting the proliferation of macrophages in TB by regulation miR-140-5p.