ArticleThe Journal of infectious diseases2025
Inflammatory Macrophages Associate With Tissue Injury and Fibrosis in a Mouse Model of Tuberculosis.
Article in The Journal of infectious diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Does Tuberculosis Leave a Thromboinflammatory Memory After Cure? A Narrative Review with a Conceptual Framework on Hypercoagulability, Cellular Reservoirs, and Extracellular Vesicle Signaling.International journal of molecular sciences · 2026Review
- Post-TB lung disease: pathogenesis, host-directed therapies, and the C3HeB/FeJ model for pre-clinical advances.Infection and immunity · 2026Review
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Authors and funding
12 authors.
Funding
Abstract
backgroundPost-tuberculosis lung disease causes a significant burden of global disease. While a consensus definition of post-tuberculosis lung disease is still in development, parenchymal cavitation, bronchiectasis, and fibrosis are recognized pathologic features. The molecular mechanisms driving development of each feature are largely unknown.
methodsTo facilitate the mechanistic study of tuberculosis-associated pathologic tissue remodeling and fibrosis, we adapted a mouse model of infection.
resultsThe morphologies of fibrosis observed in mice were similar to those observed in human tissue samples, and fibrillar collagen deposition did not resolve with antituberculosis antibiotics. Inflammatory transcriptional signatures were persistently upregulated during chronic infection and did not fully resolve after weeks of antibiotics. Inflammatory and fibrosis-associated macrophages similarly persisted during treatment. Immunofluorescence microscopy revealed persistent macrophage populations and shifts in abundance and distribution of type 2 alveolar cells at sites of fibrogenesis.
conclusionsA mouse model recapitulates key aspects of tuberculosis-assocaiated fibrosis. Transcriptional and cellular markers of inflammation persist through weeks of antibiotic treatment.
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