Host Immune-Metabolic Adaptations Upon Mycobacterial Infections and Associated Co-Morbidities

Mycobacterial diseases are a major public health challenge. Their causative agents include, in order of impact, members of the Mycobacterium tuberculosis complex (causing tuberculosis), Mycobacterium leprae (causing leprosy), and non-tuberculous mycobacterial pathogens including Mycobacterium ulcera...

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Veröffentlicht in:Frontiers in immunology Jg. 12; S. 747387
Hauptverfasser: Llibre, Alba, Dedicoat, Martin, Burel, Julie G., Demangel, Caroline, O’Shea, Matthew K., Mauro, Claudio
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Switzerland Frontiers 23.09.2021
Frontiers Media S.A
Schlagworte:
Adaptation, Physiological - immunology
Adaptation, Physiological / immunology Animals Host-Pathogen Interactions / immunology Humans Macrophages / immunology Macrophages / metabolism Mycobacterium / immunology Mycobacterium Infections / immunology Mycobacterium Infections / metabolism
Animals
host-directed therapies
Host-Pathogen Interactions - immunology
Humans
Immunology
immunometabolism
Life Sciences
macrophage
Macrophages - immunology
Macrophages - metabolism
mycobacteria
Mycobacterium - immunology
Mycobacterium Infections - immunology
Mycobacterium Infections - metabolism
tuberculosis
macrophage
immunometabolism
mycobacteria
host-directed therapies
tuberculosis
ISSN:1664-3224, 1664-3224
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Zusammenfassung:Mycobacterial diseases are a major public health challenge. Their causative agents include, in order of impact, members of the Mycobacterium tuberculosis complex (causing tuberculosis), Mycobacterium leprae (causing leprosy), and non-tuberculous mycobacterial pathogens including Mycobacterium ulcerans. Macrophages are mycobacterial targets and they play an essential role in the host immune response to mycobacteria. This review aims to provide a comprehensive understanding of the immune-metabolic adaptations of the macrophage to mycobacterial infections. This metabolic rewiring involves changes in glycolysis and oxidative metabolism, as well as in the use of fatty acids and that of metals such as iron, zinc and copper. The macrophage metabolic adaptations result in changes in intracellular metabolites, which can post-translationally modify proteins including histones, with potential for shaping the epigenetic landscape. This review will also cover how critical tuberculosis co-morbidities such as smoking, diabetes and HIV infection shape host metabolic responses and impact disease outcome. Finally, we will explore how the immune-metabolic knowledge gained in the last decades can be harnessed towards the design of novel diagnostic and therapeutic tools, as well as vaccines.
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SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
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PMCID: PMC8495197
Reviewed by: Ioannis Mitroulis, Democritus University of Thrace, Greece; David George Russell, Cornell University, United States
These authors have contributed equally to this work
This article was submitted to Molecular Innate Immunity, a section of the journal Frontiers in Immunology
Edited by: Suzie Hingley-Wilson, University of Surrey, United Kingdom
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.747387