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Updated: Aug 10, 2026
06:03
Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
Published on: May 9, 2025
Proapoptotic Bid is required for pulmonary fibrosis
G R Scott Budinger1, Gökhan M Mutlu, James Eisenbart
1Department of Medicine, Northwestern University, Chicago, IL 60611, USA.
Summary
The proapoptotic protein Bid is essential for pulmonary fibrosis development. Bid-deficient mice show reduced lung scarring after bleomycin exposure, indicating Bid
Area of Science:
- Pulmonary Medicine
- Molecular Biology
- Cell Death Research
Background:
- Pulmonary fibrosis mechanisms remain unclear.
- Transforming growth factor-beta1 (TGF-β1) activation is crucial for fibrosis.
- The role of Bcl-2 family proteins in this process is not well-defined.
Purpose of the Study:
- To investigate the role of the Bcl-2 family member Bid in bleomycin-induced pulmonary fibrosis.
- To elucidate the molecular mechanisms linking TGF-β1 signaling to fibrosis development.
Main Methods:
- Intratracheal bleomycin instillation in wild-type (WT) and Bid-deficient (bid(-/-)) mice.
- Assessment of pulmonary fibrosis, inflammation, and lung injury.
- In vitro studies using alveolar epithelial cells to evaluate cell death pathways.
Main Results:
- Bid-deficient mice exhibited significantly reduced pulmonary fibrosis compared to WT mice.
- Similar levels of inflammation, lung injury, and active TGF-β1 were observed in both groups.
- Alveolar epithelial cells from bid(-/-) mice were resistant to TGF-β1-induced cell death, but not bleomycin-induced cell death.
Conclusions:
- Bid is a critical regulator of pulmonary fibrosis downstream of TGF-β1 activation.
- Bcl-2 family members play a key role in the pathogenesis of pulmonary fibrosis.
- Targeting Bid may offer a therapeutic strategy for pulmonary fibrosis.
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