Journal
IMMUNOLOGICAL REVIEWS
Volume 301, Issue 1, Pages 193-208Publisher
WILEY
DOI: 10.1111/imr.12962
Keywords
cholesterol; free fatty acid and xenophagy; HIF‐ 1α immunometabolism; inflammasome; LACC1; leprosy; parkin; PKRN
Categories
Funding
- National Institute of Allergy and Infectious Diseases of the National Institutes of Health [R01AI141526-01A1, R01AI129835]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq) [310155/2017-7, 432434/2018-6, 313657/2018-1, 4000170/2017-2, 303044/2017-9, 313633/2017-7]
- Fundacao de Amparo do Estado do Rio de Janeiro (FAPERJ) [E_09/2019, E_34/2014, E-26/203.043/2016, E-26/211.087/2019, E-26/202.667/2019]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [001]
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Leprosy is an incapacitating infectious disease caused by Mycobacterium leprae or M lepromatosis, affecting roughly 200,000 people worldwide annually. Mitochondria play a key role in regulating immune signaling pathways, and M leprae evades host immune response by reducing host cell mitochondrial activity.
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.
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