دورية أكاديمية

Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.

التفاصيل البيبلوغرافية
العنوان: Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.
المؤلفون: Oliveira MF; Laboratório de Bioquímica de Resposta ao Estresse, Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Medeiros RCA; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Mietto BS; Instituto de Ciências Biológicas, Universidade Federal de Juiz de Fora, Minas Gerais, Brazil., Calvo TL; Laboratório de Hanseníase, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Mendonça APM; Laboratório de Bioquímica de Resposta ao Estresse, Instituto de Bioquímica Médica Leopoldo de Meis, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil., Rosa TLSA; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Silva DSD; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Vasconcelos KGDC; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Pereira AMR; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., de Macedo CS; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.; Centro de Desenvolvimento Tecnológico em Saúde, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Pereira GMB; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Moreira MBP; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Pessolani MCV; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Moraes MO; Laboratório de Hanseníase, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil., Lara FA; Laboratório de Microbiologia Celular, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.
المصدر: Immunological reviews [Immunol Rev] 2021 May; Vol. 301 (1), pp. 193-208. Date of Electronic Publication: 2021 Apr 28.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review
اللغة: English
بيانات الدورية: Publisher: Blackwell Country of Publication: England NLM ID: 7702118 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1600-065X (Electronic) Linking ISSN: 01052896 NLM ISO Abbreviation: Immunol Rev Subsets: MEDLINE
أسماء مطبوعة: Publication: <2002-> : Oxford : Blackwell
Original Publication: Copenhagen, Munksgaard.
مواضيع طبية MeSH: Leprosy* , Mycobacterium leprae*, Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Mitochondria
مستخلص: 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.
(© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
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معلومات مُعتمدة: R01 AI141526 United States AI NIAID NIH HHS
فهرسة مساهمة: Keywords: HIF-1α; LACC1; PKRN; cholesterol; free fatty acid and xenophagy; immunometabolism; inflammasome; leprosy; parkin
تواريخ الأحداث: Date Created: 20210429 Date Completed: 20211025 Latest Revision: 20230412
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC10084840
DOI: 10.1111/imr.12962
PMID: 33913182
قاعدة البيانات: MEDLINE