Hewson Christopher A, Jardine Alice, Edwards Michael R, Laza-Stanca Vasile, Johnston Sebastian L
Department of Respiratory Medicine, National Heart and Lung Institute and Wright Fleming Institute of Infection and Immunity, Imperial College London, Norfolk Place, London W2 1PG, United Kingdom.
J Virol. 2005 Oct;79(19):12273-9. doi: 10.1128/JVI.79.19.12273-12279.2005.
Rhinoviruses (RV) are the major cause of the common cold and acute exacerbations of asthma and chronic obstructive pulmonary disease. Toll-like receptors (TLRs) are a conserved family of receptors that recognize and respond to a variety of pathogen-associated molecular patterns. TLR3 recognizes double-stranded RNA, an important intermediate of many viral life cycles (including RV). The importance of TLR3 in host responses to virus infection is not known. Using BEAS-2B (a human bronchial epithelial cell-line), we demonstrated that RV replication increased the expression of TLR3 mRNA and TLR3 protein on the cell surface. We observed that blocking TLR3 led to a decrease in interleukin-6, CXCL8, and CCL5 in response to poly(IC) but an increase following RV infection. Finally, we demonstrated that TLR3 mediated the antiviral response. This study demonstrates an important functional requirement for TLR3 in the host response against live virus infection and indicates that poly(IC) is not always a good model for studying the biology of live virus infection.
鼻病毒（RV）是普通感冒以及哮喘和慢性阻塞性肺疾病急性加重的主要病因。Toll样受体（TLR）是一类保守的受体家族，可识别多种病原体相关分子模式并作出反应。TLR3可识别双链RNA，这是许多病毒生命周期（包括鼻病毒）的重要中间体。TLR3在宿主对病毒感染的反应中的重要性尚不清楚。利用BEAS-2B（一种人支气管上皮细胞系），我们证明鼻病毒复制会增加细胞表面TLR3 mRNA和TLR3蛋白的表达。我们观察到，阻断TLR3会导致对聚肌胞苷酸（poly(IC)）反应时白细胞介素-6、CXCL8和CCL5减少，但在鼻病毒感染后增加。最后，我们证明TLR3介导了抗病毒反应。本研究证明了TLR3在宿主对活病毒感染的反应中的重要功能需求，并表明聚肌胞苷酸并不总是研究活病毒感染生物学的良好模型。
