2025/07/07 by Julie Boucau, Jennie Ruelas Castillo, Threnesan Naidoo +9 · 1 voice
Immunology and Microbiology · Medicine · #Immune cells in cancer #Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis #Tuberculosis Research and Epidemiology
paper · doi:10.1093/infdis/jiaf361
openalex publication_date 2025/07/07 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
BACKGROUND: Post-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. METHODS: To facilitate the mechanistic study of tuberculosis-associated pathologic tissue remodeling and fibrosis, we adapted a mouse model of infection. RESULTS: The 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. CONCLUSIONS: A mouse model recapitulates key aspects of tuberculosis-assocaiated fibrosis. Transcriptional and cellular markers of inflammation persist through weeks of antibiotic treatment.