Immunosuppression mediated by porcine FcγRIII in PRRSV infection to PAMS
Li Na
Abstract
Li Na
Abstract
Objective: To study immunosuppression mediated by the porcine FcγRⅢ in porcine reproductive and respiratory syndrome virus( PRRSV) infection to pulmonary alveolar macrophages( PAMS). Methods: In this study pulmonary alveolar macrophages cells were treated with containing 200 TCID50 PRRSV,lipopolysaccharide( LPS)( 100 ng /ml) and purified mouse antipig FcγR Ⅲ IgG( 550 μg /ml) separately,simultaneously,PAM cells treated with purified mouse anti-pig FcγR Ⅲ IgG( 550 μg /ml)was infected by 200 TCID50 PRRSV,untreated PAM cells as the control group. Each group were post-cultured 12,24,36,48,60,72 h,the cells and the supernatant were collected. The dynamic variation of PRRSV RNA copies in inoculation group were detected by using real-time fluorescence quantitative PCR method. mRNA level of IFN-α and TNF-α in each group were detected by using relative fluorescence quantitative PCR. Results: The result showed that mRNA level of IFN-α was improved during PRRSV infection to PAMS12-24 h,and mRNA level of IFN-α was inhibited during 36-72 h,then mRNA level of IFN-α recovered normally; mRNA level of TNF-α was increased slightly post-infection 12-72 h. IFN-α and TNF-α mRNA levels of PAM cells treated with LPS were both up-regulated,using the purified mouse anti-pig FcγRⅢ IgG to treat the PAM cells,selective activation of porcine FcγRⅢ in the PAM cells down-regulated significantly mRNA levels of IFN-α and TNF-α. PRRSV infection assay mediated by selective activation FcγRⅢof the PAM cells inhibited antiviral cytokine( IFN-α and TNF-α) mRNA levels. Conclusion: The results show selective activation of FcγRⅢinhibited significantly mRNA levels of the antiviral cytokine IFN-α and TNF-α of host cells,and innate antiviral immune response to PRRSV infection.
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Objective: To study immunosuppression mediated by the porcine FcγRⅢ in porcine reproductive and respiratory syndrome virus( PRRSV) infection to pulmonary alveolar macrophages( PAMS). Methods: In this study pulmonary alveolar macrophages cells were treated with containing 200 TCID50 PRRSV,lipopolysaccharide( LPS)( 100 ng /ml) and purified mouse antipig FcγR Ⅲ IgG( 550 μg /ml) separately,simultaneously,PAM cells treated with purified mouse anti-pig FcγR Ⅲ IgG( 550 μg /ml)was infected by 200 TCID50 PRRSV,untreated PAM cells as the control group. Each group were post-cultured 12,24,36,48,60,72 h,the cells and the supernatant were collected. The dynamic variation of PRRSV RNA copies in inoculation group were detected by using real-time fluorescence quantitative PCR method. mRNA level of IFN-α and TNF-α in each group were detected by using relative fluorescence quantitative PCR. Results: The result showed that mRNA level of IFN-α was improved during PRRSV infection to PAMS12-24 h,and mRNA level of IFN-α was inhibited during 36-72 h,then mRNA level of IFN-α recovered normally; mRNA level of TNF-α was increased slightly post-infection 12-72 h. IFN-α and TNF-α mRNA levels of PAM cells treated with LPS were both up-regulated,using the purified mouse anti-pig FcγRⅢ IgG to treat the PAM cells,selective activation of porcine FcγRⅢ in the PAM cells down-regulated significantly mRNA levels of IFN-α and TNF-α. PRRSV infection assay mediated by selective activation FcγRⅢof the PAM cells inhibited antiviral cytokine( IFN-α and TNF-α) mRNA levels. Conclusion: The results show selective activation of FcγRⅢinhibited significantly mRNA levels of the antiviral cytokine IFN-α and TNF-α of host cells,and innate antiviral immune response to PRRSV infection.
Key concepts: Porcine reproductive and respiratory syndrome virus, Biology, Immunosuppression, Messenger RNA, Lipopolysaccharide, Molecular biology, Tumor necrosis factor alpha, Real-time polymerase chain reaction