Micro managing survival the Mycobacterium tuberculosis way

Abstract

Tuberculosis is an ancient disease which has scourged humanity since thousands of years. Mycobacterium tuberculosis, its causative agent was discovered in 1884 and drugs against it are available since 1940’s, but this disease still killed around 1.5 million people worldwide in 2015. This alludes to the remarkable ability of this pathogen to adapt and survive in its host over a long period of time despite the presence of effective medications. The evolutionary adaptation of the pathogen to survive in lethal immune cells of the host during adverse situations and its ability to grow under favorable circumstances, hints at the extent of manipulation exercised by Mycobacterium tuberculosis. The pathogen outmaneuvers host’s immune mechanisms by modulating key defensive pathways like autophagy and phago-lysosomal fusion. MicroRNAs are an emerging class of molecules known to affect gene regulation by degrading the mRNA or blocking its translation. Insights into interactions between microRNAs and immune cells are unraveling novel strategies adapted by Mycobacterium tuberculosis to micro manage its survival. Classically, the pathogen down-modulate inflammatory pathways of the host as one of its strategy for survival. Recent studies have revealed the role of several microRNAs in inflammation modulation and metabolic regulation. Variation(s) of microRNAs in latency and active disease are also beginning to emerge. Further, the active role of microRNAs in granuloma and its temporal variations during transition from acute disease to chronic latency and vice-versa are fascinating areas that are anticipated to yield insightful findings. In this editorial, we present recent studies referring to multiple approaches adopted by Mycobacterium tuberculosis to alter gene expression of critical targets by manipulating microRNAs for its survival. The information will be helpful in formulating future strategies for preventing tuberculosis.