@article{95380,
  keywords = {HIF-1α, LACC1, PKRN, cholesterol, free fatty acid and xenophagy, immunometabolism, inflammasome, leprosy, parkin},
  author = {Oliveira M and Medeiros RCA and Mietto B and Calvo T and Mendonça A and Rosa TLSA and da Silva D and de Vasconcelos K and Pereira A and de Macedo C and Pereira GMB and Moreira M and Pessolani M and Moraes M and Lara F},
  title = {Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.},
  abstract = {<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>},
  year = {2021},
  journal = {Immunological reviews},
  month = {04/2021},
  issn = {1600-065X},
  doi = {10.1111/imr.12962},
  language = {eng},
}