Inflammatory Macrophages Associate With Tissue Injury and Fibrosis in a Mouse Model of Tuberculosis.

ABSTRACT:

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 chron

SUBMITTER: Boucau J 

PROVIDER: S-EPMC12718066 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature