ArticlePLoS pathogens2014
Pulmonary infection with hypervirulent Mycobacteria reveals a crucial role for the P2X7 receptor in aggressive forms of tuberculosis.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Systematic review of innate immune responses againstFrontiers in immunology · 2024Pooled it
- Systemic Degree of Perturbation of Plasma Markers Reveals Cumulative Biological Stress Across the Competitive Season in Professional Soccer Players.Sports medicine (Auckland, N.Z.) · 2026Article
- CD39 regulates P2RX7-mediated lung necrotic lesions in severe experimental tuberculosis.Mucosal immunology · 2026Article
- P2X7 receptor: a potential therapeutic target for chronic respiratory diseases.Molecular and cellular biochemistry · 2026Review
- Recent progress in understanding ferroptosis mechanisms in infectious diseases.Frontiers in cellular and infection microbiology · 2026Review
- Genetic Variations in the P2X7 Receptor: Opportunities and Challenges for Drug Development.International journal of molecular sciences · 2025Review
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Intracellular and Extracellular Efficacy of Homoisoflavone Derivatives Against Mycobacterium Tuberculosis: Progress Toward Novel Antitubercular Agents.ChemMedChem · 2025Article
- Toxoplasma gondii soluble antigen (STAg) induces resistance against Mycobacterium tuberculosis in a human monocyte cell line via P2X7 receptor.Molecular biology reports · 2025Article
- Purinergic signaling in the battlefield of viral infections.Purinergic signalling · 2025Review
- Genetic Polymorphisms of P2RX7 but Not of ADORA2A Are Associated with the Severity of SARS-CoV-2 Infection.International journal of molecular sciences · 2024Article
- P2X7 Receptor in Dendritic Cells and Macrophages: Implications in Antigen Presentation and T Lymphocyte Activation.International journal of molecular sciences · 2024Review
- T cell-specific P2RX7 favors lung parenchymal CD4Cell reports · 2023Article
- Co-infection of mice with SARS-CoV-2 andFrontiers in immunology · 2023Article
- Repurposing the Antibacterial Agents Peptide 19-4LF and Peptide 19-2.5 for Treatment of Cutaneous Leishmaniasis.Pharmaceutics · 2022Article
- Physiologic roles of P2 receptors in leukocytes.Journal of leukocyte biology · 2022Review
- Purinergic modulation of the immune response to infections.Purinergic signalling · 2022Review
- Metabolite Dysregulation by Pranlukast inMolecules (Basel, Switzerland) · 2022Article
- Chlamydia evasion of neutrophil host defense results in NLRP3 dependent myeloid-mediated sterile inflammation through the purinergic P2X7 receptor.Nature communications · 2021Article
- P2RX7 at the Host-Pathogen Interface of Infectious Diseases.Microbiology and molecular biology reviews : MMBR · 2021Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The purinergic P2X7 receptor (P2X7R) is a sensor of extracellular ATP, a damage-associated molecule that is released from necrotic cells and that induces pro-inflammatory cytokine production and cell death. To investigate whether the innate immune response to damage signals could contribute to the development of pulmonary necrotic lesions in severe forms of tuberculosis, disease progression was examined in C57BL/6 and P2X7R-/- mice that were intratracheally infected with highly virulent mycobacterial strains (Mycobacterium tuberculosis strain 1471 of the Beijing genotype family and Mycobacterium bovis strain MP287/03). The low-dose infection of C57BL/6 mice with bacteria of these strains caused the rapid development of extensive granulomatous pneumonia with necrotic areas, intense bacillus dissemination and anticipated animal death. In contrast, in P2X7R-/- mice, the lung pathology presented with moderate infiltrates of mononuclear leukocytes without visible signs of necrosis; the disease attenuation was accompanied by a delay in mortality. In vitro, the hypervirulent mycobacteria grew rapidly inside macrophages and induced death by a P2X7R-dependent mechanism that facilitated the release of bacilli. Furthermore, these bacteria were resistant to the protective mechanisms elicited in macrophages following extracellular ATP stimulation. Based on this study, we propose that the rapid intracellular growth of hypervirulent mycobacteria results in massive macrophage damage. The ATP released by damaged cells engages P2X7R and accelerates the necrotic death of infected macrophages and the release of bacilli. This vicious cycle exacerbates pneumonia and lung necrosis by promoting widespread cell destruction and bacillus dissemination. These findings suggest the use of drugs that have been designed to inhibit the P2X7R as a new therapeutic approach to treat the aggressive forms of tuberculosis.
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