Haynes Lia M, Jones Les P, Barskey Albert, Anderson Larry J, Tripp Ralph A
Division of Viral and Rickettsial Diseases, National Center of Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, GA 30333, USA.
J Virol. 2003 Sep;77(18):9831-44. doi: 10.1128/jvi.77.18.9831-9844.2003.
Vaccination with formalin-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.
用福尔马林灭活的呼吸道合胞病毒(FI-RSV)疫苗或呼吸道合胞病毒G糖蛋白进行疫苗接种后,在感染活的呼吸道合胞病毒后会导致肺部疾病加重。肺部疾病加重的特征是肺部嗜酸性粒细胞增多,并伴有大量炎症反应。我们发现,在对FI-RSV疫苗接种的小鼠进行FI-RSV疫苗接种或攻击时,若缺少G糖蛋白或G糖蛋白CX3C基序,或者用抗P物质或抗CX3CR1抗体进行治疗,可减轻或消除肺部疾病加重的情况,改变T细胞受体Vβ的使用,并改变CC和CXC趋化因子的表达。这些数据表明,G糖蛋白,尤其是G糖蛋白CX3C基序,在对FI-RSV疫苗接种的炎症反应增强中起关键作用,可能是通过诱导P物质实现的。