ArticleScientific reports2013
Characterizing virulence-specific perturbations in the mitochondrial function of macrophages infected with Mycobacterium tuberculosis.
Article in Scientific reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed.
- Mycobacterium tuberculosis curli pili (MTP) facilitates pathogenicity by modulating oxidative phosphorylation and carbon flux during early infection of A549 epithelial cells.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Legionella effector LpPIP recruits protein phosphatase 1 to the mitochondria to induce dephosphorylation of outer membrane proteins.PLoS biology · 2025Article
- Mitophagy: A Potential Therapeutic Target for Tuberculosis Immunotherapy.ImmunoTargets and therapy · 2025Review
- Predictive biomarkers for latent Mycobacterium tuberculosis infection.Tuberculosis (Edinburgh, Scotland) · 2024Article
- Apoptosis and its pathways as targets for intracellular pathogens to persist in cells.Parasitology research · 2023Review
- Impaired mitophagy induces antimicrobial responses in macrophages infected with Mycobacterium tuberculosis.Cell & bioscience · 2023Article
- A Mycobacterium tuberculosis Effector Targets Mitochondrion, Controls Energy Metabolism, and Limits CytochromeMicrobiology spectrum · 2023Article
- Tuberculosis-Associated Immune Reconstitution Inflammatory Syndrome-An Extempore Game of Misfiring with Defense Arsenals.Pathogens (Basel, Switzerland) · 2023Review
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- Characteristics ofFrontiers in cellular and infection microbiology · 2023Article
- Role of MHC class I pathways inFrontiers in cellular and infection microbiology · 2023Review
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- System-wide identification of myeloid markers of TB disease and HIV-induced reactivation in the macaque model of Mtb infection and Mtb/SIV co-infection.Frontiers in immunology · 2022Article
- Mitochondria as a Cellular Hub in Infection and Inflammation.International journal of molecular sciences · 2021Review
- Mitochondrial Fusion Mediated by Mitofusin 1 Regulates Macrophage Mycobactericidal Activity by Enhancing Autophagy.Infection and immunity · 2021Article
- Effect of Reactive Oxygen Species on the Endoplasmic Reticulum and Mitochondria during Intracellular Pathogen Infection of Mammalian Cells.Antioxidants (Basel, Switzerland) · 2021Review
- Mycobacterium tuberculosis Infection Drives Mitochondria-Biased Dysregulation of Host Transfer RNA-Derived Fragments.The Journal of infectious diseases · 2021Article
- A Mitocentric View of the Main Bacterial and Parasitic Infectious Diseases in the Pediatric Population.International journal of molecular sciences · 2021Review
- Article
- Mycobacterial Control of Host Mitochondria: Bioenergetic and Metabolic Changes Shaping Cell Fate and Infection Outcome.Frontiers in cellular and infection microbiology · 2020Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To probe how the pathogen Mycobacterium tuberculosis controls host cellular death pathways, we compared mitochondrial responses in human macrophages infected either with the avirulent mycobacterial strain H37Ra, or its virulent counterpart H37Rv. Following H37Ra infection, induction of the apoptotic response was foreshadowed by the early suppression of stress-induced mitochondrial activity. In contrast, mitochondria in H37Rv-infected cells displayed robust activity with increased membrane potential and ATP synthesis. An examination of the mitochondrial proteome revealed that attenuation of mitochondrial function was also coupled with the vigorous activation of bactericidal mechanisms in H37Ra-infected cells. In contrast, augmentation of mitochondrial activity by H37Rv enabled manipulation of host cellular mechanisms to inhibit apoptosis on the one hand, while ensuring fortification against anti-microbial pathways on the other. These results thus provide novel insights into the molecular interplay that facilitates adaptation of virulent mycobacteria within the hostile intracellular milieu of the host macrophage.
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