Modulation of host pathways by Mycobacterium tuberculosis for survival

Mycobacterium tuberculosis (Mtb) is an extremely pathogenic bacterium which is responsible for causing tuberculosis. M. tuberculosis generally causes infection in lungs and other organs, can survive different physiological conditions inside the host and can also cause latent infection. Mtb, for its survival and pathogenesis, has to modulate various host pathways. The common pathways that are altered by Mtb include modulation of glycolytic flux, endoplasmic reticulum (EPR) stress, mitochondrial metabolism, apoptosis, and necrosis, inhibition of phagosome maturation and autophagy. Mtb harbors various mechanisms to evade host defense pathways for its survival. There are several types of antiinflammatory microRNA-21 which can help in cadence of glycolytic flux and also regulate the levels of phosphofructokinase by decreasing the biosynthetic precursors which are required for inflammatory responses. Further, the EPR stress pathway can be modulated by Mtb with the help of unfolded protein response–inducible transcription factor C/EBP homologous protein. The necrosis is regulated by inhibiting reactive oxygen species (ROS) production with the help of prostaglandin E2. With the help of extracellular regulated kinase 1/2, signal transducer and activator of transcription 3, and mitogen-activated protein kinase p38, interleukin -10 executes apoptosis pathway. Further, autophagy modulation synthesizes phenolic glycolipid with the help of polyketide synthase, encoded by intact pks 1–15 and by manipulating Ca2+ signaling.