Activation of sialoadhesin down-regulates the levels of innate antiviral cytokines in porcine alveolar macrophages in vitro.

Porcine sialoadhesin (pSn) is a crucial porcine reproductive and respiratory syndrome virus (PRRSV) receptor mediating the attachment and internalization of virus into its major target cells, porcine alveolar macrophages (PAMs). However, the role of pSn in innate antiviral immune response has not yet been investigated. In this study, our results showed that PRRSV down-regulated significantly the mRNA levels of IFN-α, IFN-β, IFN-γ, IFN-λ1, IFN-λ3 and IFN-λ4 and up-regulated significantly the mRNA levels of IL-10 and pSn in infected PAMs in vitro, suggesting that PRRSV infection inhibited the transcription of innate antiviral cytokines in host cells. Our results also showed that selective activation of pSn down-regulated significantly the mRNA levels of IFN-α, IFN-β, IFN-γ, IFN-λ1, IFN-λ3, IFN-λ4 and TNF-α and up-regulated significantly the mRNA level of IL-10 in PAMs in vitro, suggesting that pSn signaling inhibited the transcription of innate antiviral cytokines. Further results showed that pSn1, pSn2, pSn3, pSn4 and pSn5 domains of pSn were responsible for the inhibition of levels of innate antiviral cytokines. In conclusion, our results suggested that pSn suppressed innate antiviral immune response by down-regulating the levels of innate antiviral cytokines in PAMs. It was possible that PRRSV-pSn interaction may suppress innate antiviral immune response to PRRSV infection by repressing the production of innate antiviral cytokines.