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Induction of Mouse Lung Injury by Endotracheal Injection of Bleomycin
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Rapamycin Regulates Bleomycin-Induced Lung Damage in SP-C-Deficient Mice.

Satish K Madala1, Melissa D Maxfield, Cynthia R Davidson

  • 1Division of Pulmonary Medicine, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229-3039, USA.

Pulmonary Medicine
|June 11, 2011
PubMed
Summary

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Rapamycin did not improve lung fibrosis in mice lacking surfactant protein C (SP-C). This study suggests new therapies are needed for SP-C deficient interstitial lung disease.

Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Toxicology

Background:

  • Distal respiratory epithelium injury is linked to idiopathic lung diseases.
  • Mutations in surfactant protein C (SP-C) cause interstitial lung disease (ILD) and pulmonary fibrosis (PF).
  • SP-C deficient mice (Sftpc(-/-)) model human SP-C related lung disease.

Purpose of the Study:

  • To investigate if rapamycin could reduce bleomycin-induced lung fibrosis in Sftpc(-/-) mice.
  • To evaluate rapamycin's efficacy in both preventative and therapeutic settings.
  • To assess rapamycin's impact on lung function and inflammatory markers.

Main Methods:

  • Bleomycin-induced lung injury model in Sftpc(+/+) and Sftpc(-/-) mice.
  • Administration of rapamycin either prophylactically or therapeutically post-injury.

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  • Assessment of lung fibrosis, survival rates, weight loss, airway resistance, and lung compliance.
  • Analysis of Th2 cytokine and INF-γ expression.

    • Main Results:

    • Rapamycin treatment worsened weight loss and decreased survival in both genotypes.
    • Rapamycin did not reduce lung fibrosis in either preventative or rescue experiments.
    • Rapamycin increased airway resistance and decreased lung compliance in Sftpc(-/-) mice.
    • Rapamycin elevated profibrotic Th2 cytokines and reduced INF-γ expression.

    Conclusions:

    • Rapamycin is ineffective and potentially harmful for treating bleomycin-induced lung fibrosis in SP-C deficient mice.
    • Novel therapeutic strategies are necessary for treating SP-C deficient ILD/IPF.
    • The study highlights the complex role of immune responses in SP-C related lung fibrosis.