Long non-coding RNA transcripts in Mycobacterium tuberculosis-host interactions

Abstract

Tuberculosis (TB) persists as a significant health threat, affecting millions of people all over the world. Despite years of control measures, the elimination of TB has become a difficult task as morbidity and mortality rates remain unaffected for several years. Developing new diagnostics and therapeutics is paramount to keeping TB under control. However, it largely depends upon understanding the pathogenic mechanisms of Mycobacterium tuberculosis (Mtb), the causative agent of TB. Mtb is an intracellular pathogen capable of subverting the defensive functions of the immune cells, and it can survive and multiply within humans' mononuclear phagocytes. Emerging evidence indicates that long non-coding RNAs (lncRNAs), a class of RNA molecules with limited coding potential, are critical players in this intricate game as they regulate gene expression at transcriptional and post-transcriptional levels and also by chromatin modification. Moreover, they have been shown to regulate cellular processes by controlling the function of other molecules, such as DNA, RNA, and protein, through binding with them. Recent studies have shown that lncRNAs are differentially regulated in the tissues of TB patients and cells infected in vitro with Mtb. Some dysregulated lncRNAs are associated with essential roles in modulating immune response, apoptosis, and autophagy in the host cells, adding a new dimension to TB pathogenesis. In this article, we provide a comprehensive review of the recent literature in this field and the impact of lncRNAs in unraveling pathogenic mechanisms in TB. We also discuss how the studies involving lncRNAs provide insight into TB pathogenesis, especially Mtb-host interactions.