ArticlePloS one2017
Hypervirulent Mycobacterium tuberculosis strain triggers necrotic lung pathology associated with enhanced recruitment of neutrophils in resistant C57BL/6 mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Immune dysregulation in tuberculosis-diabetes comorbidity: mechanistic and translational insights.Frontiers in immunology · 2026Pooled it
- Association between human genomes and mycobacterial genomes contributes to severity and transmissibility of pulmonary tuberculosis.iScience · 2026Article
- CD39 regulates P2RX7-mediated lung necrotic lesions in severe experimental tuberculosis.Mucosal immunology · 2026Article
- Antimycobacterial and Nitric Oxide Production Inhibitory Activities of Goyazensolide and Centratherin Isolated From Eremanthus crotonoides by High-Speed Countercurrent Chromatography.Chemistry & biodiversity · 2026Article
- Organ-Specific Distribution of Antimycobacterial Neolignans inMolecules (Basel, Switzerland) · 2025Article
- Host-intrinsic and host-extrinsic factors modulate immunity to Mtb infection, reinfection, and noncanonical vaccination routes.Cell reports. Medicine · 2025Review
- Intracellular and Extracellular Efficacy of Homoisoflavone Derivatives Against Mycobacterium Tuberculosis: Progress Toward Novel Antitubercular Agents.ChemMedChem · 2025Article
- The Impact of Animal Models and Strain Standardization on the Evaluation of Tuberculosis Vaccine Efficacy.Vaccines · 2025Review
- Fatty acid metabolism in neutrophils promotes lung damage and bacterial replication during tuberculosis.PLoS pathogens · 2024Article
- Dual neutrophil subsets exacerbate or suppress inflammation in tuberculosis via IL-1β or PD-L1.Life science alliance · 2024Article
- A multifaceted interplay between virulence, drug resistance, and the phylogeographic landscape ofMicrobiology spectrum · 2023Article
- Mouse Models forPathogens (Basel, Switzerland) · 2022Review
- Article
- An In Vivo Model of SeparateInternational journal of molecular sciences · 2022Article
- Extremely lethal and hypervirulentEmerging microbes & infections · 2021Article
- MDR and Pre-XDR ClinicalMicroorganisms · 2021Article
- Immunomodulatory Agents Combat Multidrug-Resistant Tuberculosis by Improving Antimicrobial Immunity.The Journal of infectious diseases · 2021Article
- Harmful Effects of Granulocytic Myeloid-Derived Suppressor Cells on Tuberculosis Caused by Hypervirulent Mycobacteria.The Journal of infectious diseases · 2021Article
- A Murine Model ofFrontiers in microbiology · 2021Article
- Idiosyncratic Biogenesis of Intracellular Pathogens-Containing Vacuoles.Frontiers in cellular and infection microbiology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis (TB) is a chronic infectious disease caused by Mycobacterium tuberculosis (Mtb) that in most cases induces irreversible necrosis of lung tissue as a result of excessive inflammatory reactions. The murine model of TB in resistant C57BL/6 mice infected with reference Mtb strains is widely used in TB studies; however, these mice do not show a necrotic pathology, which restricts their use in studies of irreversible tissue damage. Recently, we demonstrated that necrotic lung lesions could be induced in the C57BL/6 mice by highly virulent Mtb strains belonging to the modern Beijing sublineage. However, the pathogenic mechanisms leading to necrosis in this model were not elucidated. In this study, we investigated the dynamics of lung lesions in mice infected with highly virulent Beijing Mtb strain M299, compared with those infected with laboratory Mtb strain H37Rv. The data demonstrate that necrotic lung lesions in mice infected by the strain M299 were associated with enhanced recruitment of myeloid cells, especially neutrophils, and increased levels of proinflammatory cytokines, consistent with exacerbated inflammation. High levels of IFN-γ production contributed to the control of bacterial growth. Further progression to chronic disease was associated with a reduction in the levels of inflammatory mediators in the lungs, the accumulation of foamy macrophages and partial healing of the necrotic tissue by fibrosis. At a late stage of disease, degradation of foamy cells resulted in the liberation of accumulated lipids and persisting bacilli and further activation of inflammation, which promoted lung consolidation. Overall, our studies show that C57BL/6 mice infected with highly virulent Mtb strain may serve as a TB model reproducing an exacerbated inflammatory response in a resistant host to hypervirulent mycobacteria, leading to irreversible necrotic lung lesions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.