Open AccessLatent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1
Author(s) -
YongHuai Li,
Jian Gao,
Guoliang Wang,
Guanghe Fei
Publication year - 2016
Publication title -
molecular medicine reports
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2016.5366
Subject(s) - bleomycin , pulmonary fibrosis , smad , fibrosis , transforming growth factor , vimentin , biology , immunology , idiopathic pulmonary fibrosis , pathology , lung , cancer research , medicine , immunohistochemistry , endocrinology , chemotherapy
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.