When mitophagy dictates the outcome of cellular infection: the case of Brucella abortus

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Résumé

Mitochondria are at the basis of various cellular functions ranging from metabolism and redox homeostasis to inflammation and cell death regulation. Mitochondria therefore constitute an attractive target for invading pathogens to fulfil their infectious cycle. This involves the modulation to their advantage of mitochondrial metabolism and dynamics, including the controlled degradation of mitochondria through mitophagy. Mitophagy might for instance be beneficial for bacterial survival as it can clear bactericidal mitochondrial ROS produced by damaged organelle fragments from the intracellular niche. In the case of the bacterial pathogen Brucella abortus, mitophagy induction has another role in the intracellular lifecycle of the bacteria. Indeed, in our study, we showed that B. abortus triggers an iron-dependent BNIP3L-mediated mitophagy response required for proper bacterial egress and infection of neighboring cells. These results highlight the diversity of mitophagy processes that might be crucial for several stages of cellular infection.

langue originaleAnglais
Pages (de - à)3022-3023
Nombre de pages2
journalAutophagy
Volume19
Numéro de publication11
Date de mise en ligne précoce17 août 2023
Les DOIs
Etat de la publicationPublié - 2023

Financement

J\u00E9r\u00E9my Verbeke was a Research Fellow (2018-2022) of the F.R.S-FNRS (Fonds de la Recherche Scientifique, Belgium). Current address of J\u00E9r\u00E9my Verbeke, Inflammation Research Center (IRC), UGent: [email protected]. This work was also supported by two \u201CCr\u00E9dit de Recherche\u201D grants (CDR 2019-2021: \u201CMITOCHOBRU\u201D grant J.0003.20-AID 35252856 and CDR 2022-2023: \u201CBrucella and BNIP3L-mediated mitophagy\u201D grant J.0003.22 AID 40007965) obtained from the F.R.S-FNRS.

Bailleurs de fondsNuméro du bailleur de fonds
Fonds De La Recherche Scientifique - FNRS
Non ajouté201273
Inflammation Research CenterJ.0003.20-AID 35252856, CDR 2022-2023, J.0003.22 AID 40007965

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