Pulmonary tuberculosis (PTB) infection is a chronic inflammatory response caused by Mycobacterium tuberculosis (Mtb). The purpose of this study was to confirm the value of Long non-coding RNA (LncRNA) non-coding activated by DNA damage (NORAD) in the diagnosis of PTB and to explore its mechanism in Mtb-infected macrophages. NORAD serum levels were estimated by qRT-PCR in 90 PTB patients and 85 healthy individuals. ROC curves were employed to assess the diagnostic value of NORAD for PTB. Human and murine macrophages were infected with Mtb strain H37Rv. CCK-8 and ELISA detected macrophages viability and inflammatory cytokine secretion. A dual-luciferase reporter assay was performed to analyze the targeting relationship between NORAD and microRNA (miR)-618. NORAD was significantly elevated in patients with PTB, and its positivity was correlated with inflammatory cytokines IL-1 β (r = 0.854), TNF-α (r = 0.617), IL-6 (r = 0.585). With an AUC of 0.918, and sensitivity and specificity of 80.0% and 89.4%, respectively, NORAD remarkedly identified PTB patients from healthy individuals. Furthermore, Mtb infection significantly increased NORAD levels in THP-1 and RAW264.7 and increased their viability and inflammation (P <0.001). However, this increased effect was weakened by reduced NORAD. Dual-luciferase reporter assay confirmed that miR-618 in macrophages was a target miRNA for NORAD and can be negatively regulated by it. Moreover, elevated miR-618 suppressed macrophage viability and inflammation in Mtb infection. NORAD is a potential diagnostic biomarker for PTB and is involved in Mtb infected macrophage activity and inflammation by targeting miR-618. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.