Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1
Latent cytomegalovirus infection exacerbates experimental pulmonary fibrosis by activating TGF-β1
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DOI：
10.3892/mmr.2016.5366
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发表时间：
2016-08-01
影响因子：
3.4
通讯作者：
Fei, Guanghe
中科院分区：
文献类型：
--
作者：
Li, Yonghuai;Gao, Jian;Fei, Guanghe
本研究的目的是研究巨细胞病毒（CMV）可能在易感宿主中触发特发性肺纤维化（IPF）和/或CMV的存在可能改变IPF以响应明确的肺纤维化触发因素的假设。建立小鼠巨细胞病毒（MCMV）感染模型，将小鼠分为对照组、博莱霉素组和MCMV+博莱霉素组。测定三组小鼠体重的变化。采用组织病理学方法检测肺纤维化。测量转化生长因子（TGF）-β 1的活性，并使用蛋白质印迹分析确定E-钙粘蛋白、波形蛋白和磷酸化（磷酸化）-小母体抗十肢麻痹（SMAD）2的水平。发现MCMV侵入肺，但它没有引起肺纤维化。与对照小鼠相比，用MCMV+博来霉素处理的小鼠中的纤维化进展更快。在MCMV+博莱霉素组中，波形蛋白和磷酸化SMAD 2的蛋白水平上调，而E-钙粘蛋白的水平下调。结果表明，潜伏MCMV感染加重了小鼠模型的肺纤维化，可能通过激活TGF-β 1。
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)-beta 1 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-beta 1.