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Article

Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1

  • Authors:
    • Yonghuai Li
    • Jian Gao
    • Guoliang Wang
    • Guanghe Fei
  • View Affiliations / Copyright

    Affiliations: Department of Respiratory Medicine, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China, Pharmaceutical Preparation Section, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China, Department of Pediatrics, Baylor College of Medicine, Feigin Center, Houston, TX 77030, USA
  • Pages: 1297-1301
    |
    Published online on: June 6, 2016
       https://doi.org/10.3892/mmr.2016.5366
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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.
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Copy and paste a formatted citation
Spandidos Publications style
Li Y, Gao J, Wang G and Fei G: Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1. Mol Med Rep 14: 1297-1301, 2016.
APA
Li, Y., Gao, J., Wang, G., & Fei, G. (2016). Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1. Molecular Medicine Reports, 14, 1297-1301. https://doi.org/10.3892/mmr.2016.5366
MLA
Li, Y., Gao, J., Wang, G., Fei, G."Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1". Molecular Medicine Reports 14.2 (2016): 1297-1301.
Chicago
Li, Y., Gao, J., Wang, G., Fei, G."Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1". Molecular Medicine Reports 14, no. 2 (2016): 1297-1301. https://doi.org/10.3892/mmr.2016.5366
Copy and paste a formatted citation
x
Spandidos Publications style
Li Y, Gao J, Wang G and Fei G: Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1. Mol Med Rep 14: 1297-1301, 2016.
APA
Li, Y., Gao, J., Wang, G., & Fei, G. (2016). Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1. Molecular Medicine Reports, 14, 1297-1301. https://doi.org/10.3892/mmr.2016.5366
MLA
Li, Y., Gao, J., Wang, G., Fei, G."Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1". Molecular Medicine Reports 14.2 (2016): 1297-1301.
Chicago
Li, Y., Gao, J., Wang, G., Fei, G."Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1". Molecular Medicine Reports 14, no. 2 (2016): 1297-1301. https://doi.org/10.3892/mmr.2016.5366
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