Johnson Crystal H, Miao Congrong, Blanchard Elisabeth G, Caidi Hayat, Radu Gertrud U, Harcourt Jennifer L, Haynes Lia M
National Center for Emerging and Zoonotic Infectious Diseases, Division of Scientific Resources, Laboratory Animal Medicine Residency Program, Centers for Disease Control and Prevention (CDC), Atlanta, Georgia, USA.
Comp Med. 2012 Feb;62(1):14-20.
Respiratory syncytial virus (RSV) is the most common cause of serious lower respiratory illness in infants and young children worldwide, making it a high priority for development of strategies for prevention and treatment. RSV can cause repeat infections throughout life, with serious complications in elderly and immunocompromised patients. Previous studies indicate that the RSV G protein binds through a CX3C chemokine motif to the host chemokine receptor, CX3CR1, and modulates the inflammatory immune response. In the current study, we examined the contribution of CX3CR1 to the immune response to RSV infection in mice. CX3CR1-deficient mice showed an impaired innate immune response to RSV infection, characterized by substantially decreased NK1.1(+) natural killer, CD11b(+), and RB6-8C5(+) polymorphonuclear cell trafficking to the lung and reduced IFNγ production compared with those in wildtype control mice. Leukocytes from CX3CR1-deficient mice were poorly chemotactic toward RSV G protein and CX3CL1. These results substantiate the importance of the RSV G CX3C-CX3CR1 interaction in the innate immune response to RSV infection.
呼吸道合胞病毒（RSV）是全球婴幼儿严重下呼吸道疾病的最常见病因，因此制定预防和治疗策略成为当务之急。RSV可在一生中引发反复感染，在老年人和免疫功能低下的患者中会导致严重并发症。先前的研究表明，RSV G蛋白通过一个CX3C趋化因子基序与宿主趋化因子受体CX3CR1结合，并调节炎症免疫反应。在本研究中，我们检测了CX3CR1对小鼠RSV感染免疫反应的作用。与野生型对照小鼠相比，CX3CR1缺陷型小鼠对RSV感染的固有免疫反应受损，其特征为NK1.1(+)自然杀伤细胞、CD11b(+)细胞和RB6-8C5(+)多形核细胞向肺部的迁移显著减少，且IFNγ产生降低。来自CX3CR1缺陷型小鼠的白细胞对RSV G蛋白和CX3CL1的趋化性较差。这些结果证实了RSV G CX3C-CX3CR1相互作用在RSV感染固有免疫反应中的重要性。
