Enhanced disease and pulmonary eosinophilia associated with formalin-inactivated respiratory syncytial virus vaccination are linked to G glycoprotein CX3C-CX3CR1 interaction and expression of substance P
Enhanced disease and pulmonary eosinophilia associated with formalin-inactivated respiratory syncytial virus vaccination are linked to G glycoprotein CX3C-CX3CR1 interaction and expression of substance P
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DOI：
10.1128/jvi.77.18.9831-9844.2003
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发表时间：
2003-09-01
影响因子：
5.4
通讯作者：
Tripp, RA
中科院分区：
文献类型：
--
作者：
Haynes, LM;Jones, LP;Tripp, RA
接种正规的灭活呼吸道合胞病毒（FI-RSV）疫苗或RSV G糖蛋白可导致RSV活感染后肺部疾病增加。增强型肺部疾病以肺嗜酸性粒细胞增多为特征，并伴有明显的炎症反应。我们发现，在FI-RSV疫苗接种或FI-RSV疫苗接种小鼠的RSV攻击期间，或用抗P物质或抗cx3cr1抗体治疗期间，G糖蛋白或G糖蛋白CX3C基序的缺失，减少或消除了增长型肺部疾病，改变了t细胞受体Vbeta的使用，并改变了CC和CXC趋化因子的表达。这些数据表明，G糖蛋白，特别是G糖蛋白CX3C基序，可能是通过诱导P物质增强对FI-RSV疫苗的炎症反应的关键。
Vaccination with formal in-inactivated respiratory syncytial virus (FI-RSV) vaccine or RSV G glycoprotein results in enhanced pulmonary disease after live RSV infection. Enhanced pulmonary disease is characterized by pulmonary eosinophilia and is associated with a substantial inflammatory response. We show that the absence of the G glycoprotein or G glycoprotein CX3C motif during FI-RSV vaccination or RSV challenge of FI-RSV-vaccinated mice, or treatment with anti-substance P or anti-CX3CR1 antibodies, reduces or eliminates enhanced pulmonary disease, modifies T-cell receptor Vbeta usage, and alters CC and CXC chemokine expression. These data suggest that the G glycoprotein, and in particular the G glycoprotein CX3C motif, is key in the enhanced inflammatory response to FI-RSV vaccination, possibly through the induction of substance P.