Produção Nacional
Revisado por pares
Reduction of host cell mitochondrial activity as Mycobacterium leprae’s strategy to evade host innate immunity
2021; Wiley; Volume: 301; Issue: 1 Linguagem: Inglês
10.1111/imr.12962
ISSN1600-065X
AutoresMarcus F. Oliveira, Rychelle Clayde Affonso Medeiros, Bruno Siqueira Mietto, Thyago Leal-Calvo, Ana Paula Miranda Mendonça, Thabatta Leal Silveira Andrezo Rosa, Débora Santos da Silva, Karina do Carmo de Vasconcelos Girardi, Antônio Marcos Rodrigues Pereira, Cristiana Santos de Macedo, Geraldo M. B. Pereira, Marcia de Berrêdo Pinho Moreira, María Cristina Vidal Pessolani, Milton Ozório Moraes, Flávio Alves Lara,
Tópico(s)Autophagy in Disease and Therapy
ResumoLeprosy 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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