The Mechanism Of Omega-3 Fatty Acids Affect Vaccine Inducing Immune Response

Rabies virus(RV)and Japanese encephalitis virus(JEV)are major causative agents of zoonosis.The first step of those viruses entering into host is fighting with host immune system.However,when the host immune system was downregulated,the virus infection would upregulate and the vaccine immune would be abortive.Recently,some researches have reported that dietary omega-3 fatty acids(ω-3)depress immune cell activation and impair the immune response against pathogens infection,but the ω-3 could whether affect virus infection has not been study.Interestingly,our results also have demonstrated that imcreasing of intestinal florain bovine.In the recent study,we have found that the dendritic cells(DCs)isolating from ω-3 over expressing mouse have low immune sensitization and poor RV and JEV control.Therefore,the hypothesis is ω-3 play a key role in regulating the immune evasion of RV and JEV.To demonstrate that,we use DCs in vitro culture system,flow cytometry and immunofluorescence assay to study the singling pathway of ω-3 regulating DCs activation and ant-viral immune response.Furthermore,we analyed the poliferration of DCs,T cells and B cells in spleens and lymps nodes from FAD3/WT mouse.Finally we detected DCs activation level after blocking with GPR120 stimulant or antagonist.The results showed that the CD86 on DCs from FAD3 mouse were 2 fold lower than WT mouse and the memory T cells from FAD3 mouse were 5%lower than WT mouse.It seems that DHA can decrease the vitality of immune cells in mouse.Furthermore,the activation of DCs can return by blocking GPR120 after treatment of DHA.And the DCs which is high expression GPR120 would not be sensitive to RV and JEV infection.Interestingly,GPR120 expression was reverse related to DCs activation which indicated GPR120 is not only a receptor of DHA but also a regulator of DCs.Our researches firstly demonstrate that co-3 hijack the DCs by down regulating the immune system to suppress the vaccine immunity.Those results illustrate a noval immune suppression mechanism that promote viral infection.