Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.
Marcus Fernandes OliveiraRychelle Clayde Affonso MedeirosBruno Siqueira MiettoThyago Leal CalvoAna Paula Miranda MendonçaThabatta Leal Silveira Andrezo RosaDébora Santos da SilvaKarina Girardi do Carmo de VasconcelosAntonio Marcos Rodrigues PereiraCristiana Santos de MacedoGeraldo Moura Batista PereiraMarcia de Berrêdo Pinho MoreiraMaria Cristina Vidal PessolaniMilton Ozório MoraesFlavio Alves LaraPublished in: Immunological reviews (2021)
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.