02159nas a2200385   4500000000100000008004100001260001200042653001200054653001000066653000900076653001600085653003400101653002100135653001700156653001200173653001100185100001500196700001700211700001300228700001200241700001600253700001400269700001500283700002100298700001400319700001600333700001600349700001400365700001600379700001300395700001100408245011600419520122400535022001401759       2021                            d  c04/202110aHIF-1α10aLACC110aPKRN10acholesterol10afree fatty acid and xenophagy10aimmunometabolism10ainflammasome10aleprosy10aparkin1 aOliveira M1 aMedeiros RCA1 aMietto B1 aCalvo T1 aMendonça A1 aRosa TLSA1 ada Silva D1 ade Vasconcelos K1 aPereira A1 ade Macedo C1 aPereira GMB1 aMoreira M1 aPessolani M1 aMoraes M1 aLara F00aReduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.3 a<p>Leprosy is a much-feared incapacitating infectious disease caused by Mycobacterium leprae or M lepromatosis, annually affecting roughly 200,000 people worldwide. During host-pathogen interaction, M leprae subverts the immune response, leading to development of disease. Throughout the last few decades, the impact of energy metabolism on the control of intracellular pathogens and leukocytic differentiation has become more evident. Mitochondria play a key role in regulating newly-discovered immune signaling pathways by controlling redox metabolism and the flow of energy besides activating inflammasome, xenophagy, and apoptosis. Likewise, this organelle, whose origin is probably an alphaproteobacterium, directly controls the intracellular pathogens attempting to invade its niche, a feature conquered at the expense of billions of years of coevolution. In the present review, we discuss the role of reduced host cell mitochondrial activity during M leprae infection and the consequential fates of M leprae and host innate immunity. Conceivably, inhibition of mitochondrial energy metabolism emerges as an overlooked and novel mechanism developed by M leprae to evade xenophagy and the host immune response.</p>  a1600-065X