ArticlePloS one2011
Mycobacterium tuberculosis induces an atypical cell death mode to escape from infected macrophages.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed.
- Characterization of programmed cell death pathways activated in Mycobacterium tuberculosis-infected human macrophages.Cell death discovery · 2026Article
- Identification ofMicrobiology spectrum · 2025Article
- Distinguishing multiple roles of T cell and macrophage involvement in determining lymph node fates during Mycobacterium tuberculosis infection.PLoS computational biology · 2025Article
- Zinc-limitedInfection and immunity · 2025Article
- IL-27 attenuated macrophage injury and inflammation induced by Mycobacterium tuberculosis by activating autophagy.In vitro cellular & developmental biology. Animal · 2025Article
- Pathogenic role for CD101-negative neutrophils in the type I interferon-mediated immunopathogenesis of tuberculosis.Cell reports · 2025Article
- BACH1 promotes tissue necrosis and Mycobacterium tuberculosis susceptibility.Nature microbiology · 2024Article
- Mmu-let-7a-5p inhibits macrophage apoptosis by targeting CASP3 to increase bacterial load and facilities mycobacterium survival.PloS one · 2024Article
- Virulence Factors ofPathogens (Basel, Switzerland) · 2023Review
- High Bacillary Burden and the ESX-1 Type VII Secretion System Promote MHC Class I Presentation by Mycobacterium tuberculosis-Infected Macrophages to CD8 T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Bag it, tag it: ubiquitin ligases and host resistance to Mycobacterium tuberculosis.Trends in microbiology · 2022Review
- Article
- Targeting ferroptosis as a vulnerability in pulmonary diseases.Cell death & disease · 2022Review
- Chemical-genetic interaction mapping links carbon metabolism and cell wall structure to tuberculosis drug efficacy.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A Dual Role of Heme Oxygenase-1 in Tuberculosis.Frontiers in immunology · 2022Review
- The Flp type IV pilus operon ofFrontiers in cellular and infection microbiology · 2022Article
- The role of necroptosis in common respiratory diseases in children.Frontiers in pediatrics · 2022Review
- An investigation of tuberculosis progression revealing the role of macrophages apoptosis via sensitivity and bifurcation analysis.Journal of mathematical biology · 2021Article
- Type I interferon signaling mediates Mycobacterium tuberculosis-induced macrophage death.The Journal of experimental medicine · 2021Article
- Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors.
Funding
Abstract
backgroundMacrophage cell death following infection with Mycobacterium tuberculosis plays a central role in tuberculosis disease pathogenesis. Certain attenuated strains induce extrinsic apoptosis of infected macrophages but virulent strains of M. tuberculosis suppress this host response. We previously reported that virulent M. tuberculosis induces cell death when bacillary load exceeds ∼20 per macrophage but the precise nature of this demise has not been defined. METHODOLOGY/PRINCIPAL
findingsWe analyzed the characteristics of cell death in primary murine macrophages challenged with virulent or attenuated M. tuberculosis complex strains. We report that high intracellular bacillary burden causes rapid and primarily necrotic death via lysosomal permeabilization, releasing hydrolases that promote Bax/Bak-independent mitochondrial damage and necrosis. Cell death was independent of cathepsins B or L and notable for ultrastructural evidence of damage to lipid bilayers throughout host cells with depletion of several host phospholipid species. These events require viable bacteria that can respond to intracellular cues via the PhoPR sensor kinase system but are independent of the ESX1 system. CONCLUSIONS/SIGNIFICANCE: Cell death caused by virulent M. tuberculosis is distinct from classical apoptosis, pyroptosis or pyronecrosis. Mycobacterial genes essential for cytotoxicity are regulated by the PhoPR two-component system. This atypical death mode provides a mechanism for viable bacilli to exit host macrophages for spreading infection and the eventual transition to extracellular persistence that characterizes advanced pulmonary tuberculosis.
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