S1PR1 expression correlates with inflammatory responses to Newcastle disease virus infection |
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| Institution: | 1. National and Regional Joint Engineering Laboratory for Medicament of Zoonosis Prevention and Control, China;2. Key Laboratory of Animal Vaccine Development, Ministry of Agriculture, China;3. College of Veterinary Medicine, South China Agricultural University, 483 Wushan Road, Guangzhou 510642, China;1. Peking University Clinical Research Institute, Peking University First Hospital, Beijing, China;2. Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA;3. Changzhi Medical College, Shanxi, China;4. Xi''an Jiaotong University, Shaanxi, China;5. Hohhot Center for Disease Control and Prevention, Hohhot, Inner Mongolia, China;6. Yangcheng Ophthalmology Hospital, Shanxi, China;7. Department of Epidemiology and Biostatistics, Peking University School of Public Health, Beijing, China;8. China Center for Health Development Studies, Peking University, Beijing, China;9. The George Institute for Global Health, Australia, Sydney, Australia;10. The University of Sydney, Sydney, Australia;11. National Center for Food Safety Risk Assessment, Beijing, China |
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| Abstract: | Newcastle disease virus (NDV) is the causative agent of Newcastle disease, which is characterized by inflammatory pathological changes in the organs of chickens. The inflammatory response to this disease has not been well characterized. Previous reports showed that the sphingosine-1-phosphate-1 receptor (S1PR1), a G protein-coupled receptor, is important to the activation of inflammatory responses. To understand better the viral pathogenesis and host inflammatory response, we analyzed S1PR1 expression during NDV infection. We observed a direct correlation between chicken embryo fibroblast (CEF) cellular inflammatory responses and S1PR1 expression. Virulent NDV-infected CEF cells also had elevated levels of pro-inflammatory cytokines (IL-1β, IL-6 and IL-18). When S1PR1 was inhibited by using the specific antagonist W146, pro-inflammatory cytokine production declined. Overexpression of S1PR1 resulted in increased virus-induced IL-1β production. S1PR1 expression levels did not impact significantly NDV replication. These findings highlight the important role of S1PR1 in inflammatory responses in NDV infection. |
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