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Updated: Mar 19, 2026
Refined Murine Model of Idiopathic Pulmonary Fibrosis
Published on: June 17, 2025
Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1
Yonghuai Li1, Jian Gao2, Guoliang Wang3
1Department of Respiratory Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China.
Abstract:
The aim of the present study was to investigate the hypotheses that cytomegalovirus (CMV) may trigger idiopathic pulmonary fibrosis (IPF) in a susceptible host and/or that the presence of CMV may alter IPF in response to a well-defined trigger of pulmonary fibrosis. A mouse model of murine CMV (MCMV) infection was established, and the mice were divided into a control group, bleomycin group and an MCMV+bleomycin group. Changes in the weights of the mice were determined in the three groups. Pulmonary fibrosis was detected using a histopathological method. The activity of transforming growth factor (TGF)‑β1 was measured, and the levels of E‑cadherin, Vimentin and phosphorylated (phospho)‑small mothers against decapentaplegic (SMAD)2 were determined using western blot analysis. MCMV was found to invade the lungs, however, it did not cause pulmonary fibrosis. The progression of fibrosis in the mice treated with MCMV+bleomycin was more rapid, compared with that in the control mice. The protein levels of Vimentin and phospho-SMAD2 were upregulated, whereas the level of E‑cadherin was downregulated in the MCMV+bleomycin group,. The results suggested that latent MCMV infection aggravated pulmonary fibrosis in the mouse model, possibly through the activation of TGF-β1.
Insights
Latent cytomegalovirus (CMV) infection did not cause pulmonary fibrosis but aggravated its progression in a mouse model. This suggests CMV may worsen idiopathic pulmonary fibrosis (IPF) through transforming growth factor-beta 1 activation.
Area of Science:
- Virology
- Pulmonology
- Pathology
Background:
- Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with unknown triggers.
- Cytomegalovirus (CMV) is a common virus that may be implicated in IPF pathogenesis.
Purpose of the Study:
- To investigate if cytomegalovirus (CMV) triggers idiopathic pulmonary fibrosis (IPF) or exacerbates it.
- To explore the role of latent CMV infection in pulmonary fibrosis development.
Main Methods:
- Established a mouse model using murine CMV (MCMV) and bleomycin to induce pulmonary fibrosis.
- Assessed pulmonary fibrosis via histopathology, body weight changes, and Western blot analysis.
- Measured transforming growth factor-beta 1 (TGF-β1) activity and protein levels of E-cadherin, Vimentin, and phospho-SMAD2.
Main Results:
- Murine CMV (MCMV) infected lungs but did not independently cause pulmonary fibrosis.
- Mice co-exposed to MCMV and bleomycin showed accelerated fibrosis progression compared to controls.
- Upregulation of Vimentin and phospho-SMAD2, and downregulation of E-cadherin were observed in the MCMV+bleomycin group.
Conclusions:
- Latent MCMV infection exacerbates pulmonary fibrosis in a susceptible host.
- CMV may worsen IPF progression potentially via activation of the TGF-β1 signaling pathway.
