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Post-tuberculosis lung disease (PTLD) causes a significant burden of global disease. While a consensus definition of PTLD is still in development, parenchymal cavitation, bronchiectasis, and fibrosis are recognized pathologic features that underlie many symptoms and complications of PTLD. The molecular mechanisms driving development of each feature are largely unknown. To facilitate the mechanistic study of tuberculosis (TB)-associated pathologic tissue remodeling and fibrosis, we adapted a mouse model of infection. The morphologies of fibrosis observed in mice were similar to those observed in human tissue samples. Using Second Harmonic Generation microscopy, we found that fibrillar collagen deposition did not resolve with anti-TB antibiotics. Inflammatory transcriptional signatures were persistently upregulated during chronic infection and did not fully resolve after weeks of anti-TB therapy. 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.