Vascular endothelial growth factor induction by rhinovirus infection
Vascular endothelial growth factor induction by rhinovirus infection
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DOI：
10.1002/jmv.20591
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发表时间：
2006-05-01
影响因子：
12.7
通讯作者：
Bardin, PG
中科院分区：
文献类型：
--
作者：
De Silva, D;Dagher, H;Bardin, PG
鼻病毒感染急性后果的一个突出特征是表现为流鼻涕（鼻液溢）的血管参与。血管内皮生长因子（VEGF）是一种血管生成因子，也可诱导血管通透性的有效增加;它是鼻病毒感染引起鼻漏的候选介质，也有助于鼻病毒相关哮喘急性发作中血管渗漏的增强。已经显示鼻病毒诱导原代气道成纤维细胞中VEGF蛋白和mRNA的显著增加[Ghildyal等人（2005）：J Med Virol 75：608-6151。目前的研究评估了原代培养气道上皮、上皮细胞和成纤维细胞系以及鼻病毒感染的鼻分泌物中VEGF对鼻病毒的反应。分别用鼻病毒血清型16和VEGF蛋白及其亚型感染上皮细胞和成纤维细胞，通过ELISA和RT-PCR评估。上皮细胞和成纤维细胞系以及培养的原代气道上皮细胞均释放VEGF蛋白，但鼻病毒感染后VEGF蛋白没有增加。在细胞系和原代培养细胞中产生编码六种已知VEGF同种型中的四种或五种的PCR产物（121、145、165和183和/或189个氨基酸），但没有特异性同种型与鼻病毒感染相关。鼻VEGF也在一组经证实的鼻病毒和呼吸道合胞病毒（RSV）感染的哮喘患者中进行了测量。单独鼻病毒感染后VEGF没有升高，但如果同时存在RSV感染，则VEGF显著升高。这些数据表明，成纤维细胞，而不是上皮细胞可能发挥关键作用，在VEGF介导的血管反应后鼻病毒感染。这可能有助于炎症细胞的募集，并导致气道炎症和支气管阻塞。(c)2006 Wiley-Liss，Inc.
Vascular participation manifested by a runny nose (rhinorrhea) is a prominent feature of the acute consequences of rhinovirus infection. Vascular endothelial growth factor (VEGF) is an angiogenic factor that also induces potent increases in vascular permeability; it is a candidate mediator of rhinorrhea in response to rhinovirus infection as well as contributing to enhanced vascular leakage in rhinovirus-linked asthma exacerbations. It has been shown that rhinovirus induces significant increases in both VEGF protein and mRNA in primary airway fibroblasts [Ghildyal et al. (2005): J Med Virol 75:608-6151. The current studies assessed VEGF responses to rhinovirus in primary culture airway epithelium, in epithelial and fibroblast cell lines and in rhinovirus-infected nasal secretions. Epithelial and fibroblast cells were infected with rhinovirus serotype 16 and VEGF protein and isoforms assessed by ELISA and RT-PCR, respectively. VEGF protein was released by both epithelial and fibroblast cell lines and primary airway epithelial cells in culture but was not increased following rhinovirus infection. PCR products coding for four or five of the six known VEGF isoforms were produced (121, 145, 165 and 183, and/or 189 amino acids) in cell lines and primary culture cells, but no specific isoform was linked to rhinovirus infection. Nasal VEGF was also measured in a cohort of asthmatics with verified rhinovirus and respiratory syncytial virus (RSV) infection. VEGF was not raised following rhinovirus infection alone, but was increased significantly if concomitant RSV infection was present. The data suggest that fibroblasts rather than the epithelium may play a key role in VEGF mediated vascular responses after rhinovirus infection. This may aid recruitment of inflammatory cells and contribute to airway inflammation and bronchial obstruction. (c) 2006 Wiley-Liss, Inc.