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Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis
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Oropharyngeal Administration of Bleomycin in the Murine Model of Pulmonary Fibrosis

Published on: May 9, 2025

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CCAAT/enhancer binding protein delta (C/EBPδ) deficiency does not affect bleomycin-induced pulmonary fibrosis

Duitman JanWillem1,2, Cong Lin3, Sophie Moog1,2

  • 11 INSERM UMR1152, Medical School Xavier Bichat, Paris, France.

Journal of Clinical and Translational Research
|March 16, 2019
PubMed
Abstract

Insights

The transcription factor CCAAT/enhancer binding protein delta (C/EBPδ) does not appear to influence the development or resolution of experimental pulmonary fibrosis. Targeting C/EBPδ is unlikely to benefit patients with this condition.

Area of Science:

  • Pulmonary Medicine
  • Molecular Biology
  • Fibrotic Diseases

Background:

  • Idiopathic pulmonary fibrosis (IPF) is a severe lung disease with limited treatment options.
  • CCAAT/enhancer binding protein delta (C/EBPδ) is a transcription factor implicated in disease pathophysiology.
  • The role of C/EBPδ in IPF requires further investigation.

Purpose of the Study:

  • To determine the role of C/EBPδ in the development and resolution of experimental pulmonary fibrosis.
  • To validate or refute the suggested importance of C/EBPδ in IPF.

Main Methods:

  • Pulmonary fibrosis was induced in wild-type and C/EBPδ-deficient mice using bleomycin.
  • Fibrosis was assessed using hydroxyproline analysis, histochemistry, and quantitative PCR for fibrotic markers.
  • Macrophage activity was also evaluated.

Main Results:

  • C/EBPδ-deficient mice exhibited similar levels of fibrosis, collagen expression, and fibrotic marker expression compared to wild-type mice.
  • Fibrosis resolution was comparable between the two groups of mice.
  • Macrophage recruitment and differentiation were not significantly different between wild-type and C/EBPδ-deficient mice.

Conclusions:

  • C/EBPδ does not appear to play a significant role in bleomycin-induced experimental pulmonary fibrosis.
  • The findings challenge the importance of C/EBPδ in the context of pulmonary fibrosis.
  • Targeting C/EBPδ is unlikely to be a beneficial therapeutic strategy for IPF patients.
Keywords:
C/EBPδ.IPFPulmonary fibrosistranscription factor

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