The Serum Cytokine Profiles Of Piglets Atfer A PRRS MLV Vaccination And/or An Experimental Infection With A Virulent PRRSV Strain

Porcine reproductive and respiratory syndrome （PRRS） is the most significantinfectious disease currently affecting swine industry worldwide. Since2006, thehighly pathogenic PRRS virus （HP-PRRSV） caused hundred billions US dollarseconomic losses in China. PRRSV-infected pigs more vulnerable to infection ofbacterial pathogens and other viral pathogens. It is high mortality.To reveal the PRRSV induce cellular immune mechanisms, in this study, naivesusceptible specific pathogen-free piglets were used to establish PRRSVimmunization and experimental infection model, and serum immune cytokinesparameters at different time points were assayed.In vivo study,14pigs （age,3weeks） blood samples were obtained from acommercial herd. PRRSV Ag/Ab, CSFV、PRV and PCV2negative piglets weredetected. They were randomly three groups, immunized group （5piglets）, challengegroup （6piglets） and control group（3piglets）. Piglets in the challenged group wereinfected by the oro-nasal route with10^5.5TCID₅₀of a highly virulent PRRSV strainTJM-F5. Immunized group inoculated10⁶TCID₅₀of the PRRSV TJM-F92strain. Thecontrol group inoculated with1ml saline. Piglets of control and immunized groupswere challenged to TJM-F5strain with2×10^5.5TCID₅₀/ml at28days postinfection（d.p.i.）. And these groups were renamed control/challenged group andimmunized/challenged group respectively. All animals bled at1,2,3,4,7,14,21,28,35and42d.p.i. for PRRSV-Ab titer and the concentration of cytokines （IFN-α/β, IL-2,IL-10, IL-12p40and TNF-α） analysis. Statistical analyses were performed using SPSS13.0software for analysis of variance （one-way ANOVA）, LSD and T-test.Results show that piglets of challenged group serum IFN-β concentration rose.But immunized group IFN-β concentration continued to be lower than piglets of thecontrol and challenged group. Immunized/challenged group IFN-β concentration waslower than control/challenged group, but the concentration increased gradually. The serum IL-10levels increased significantly in challenged group （p<0.01） at14d.p.i.. There was no obvious difference on the serum IL-10concentration in theimmunized group （p>0.05）. There was no obvious difference on the IL-10level in theimmunized/challenged group. Piglets of the control/challenged group serum IL-10concentration increased significantly （p<0.01） at7d.p.i., and than it decreased belowthe initial level.The immunized group serum IL-12p40increased and continued to28d.p.i.. Butthe difference was not statistically significant （p>0.05）. The challenged group pigletsserum IL-12p40concentration was lower than the control group and immunized group.But the difference was not statistically significant. The immunized/challenged grouppiglets serum IL-12p40decreased slowly at28d.p.i. But the difference was notsignificant （p>0.05）.The serum IFN-α level in the immunized group was no different from that of thechallenged group （p>0.05）. And the levels were lower than the control group. Theserum IFN-α level in the immunized group increased at28d.p.i.. The immunizedgroup were challenged with virulent strain. And than, the cytokine concentration wasdecreased significantly （p<0.01）. The challenged group IFN-α concentration did notchange significantly （p>0.05）. Control/challenged group IFN-α showed a remarkabletransient rise after28d.p.i.（p<0.01）.The concentration of the immunized group IL-2did not change substantiallyduring21d.p.i. Serum IL-2concentration of the challenged group rose rapidly. Whilethat of the immunized/challenged group did not change remarkably. Although it washigher than that of the control/challenged group.The concentration of the immunized group TNF-α did not change substantiallyduring21d.p.i.. But the concentration was significantly higher than in the other twogroups （p<0.01）. TNF-α concentration of the challenged group was lower than thecontrol group. And the lowest point was at21d.p.i.. The immunized/challenged groupserum TNF-α began to decline at28d.p.i. And the concentration change wasremarkable at35d.p.i.（p<0.01）. Control/challenged group TNF-α showed aremarkable transient rise after28d.p.i.（p<0.01）.Based on these data we could conclude that PRRSV TJ-F5strain can promote host production of IFN-β and IL-10, but the TJM-F92strain can inhibit IFN-β andIL-10expression; TJM-F92strain can increase IL-10expression. It suggested thatTJM-F92strain can resist HP-PRRSV immunosuppressive, and activated the specificcellular immune response. And resultantly it plays the anti-infection effects. However,It is not yet clear that the role of IL-2, TNF-α and IFN-α during PRRSV TJM-F92regulating immune response.In order to in-depth study that the cytokine network of PRRS-specific cellularimmune mechanism and its response characteristics, it is the first time to establishPRRS MLV vaccination and/or an experimental infection with a virulent PRRSVstrain mode for the specific pathogen-free susceptible animals. Through the serumcytokine profiles, PRRSV TJM-F92strain induced higher cellular immune responses.These results laid the foundation to clarify the PRRS special cellular immunemechanism, and also for the prevention and control of HP-PRRSV.