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Title:   Author  item
                                            Solano-Aguilar, Gloriaitem
                                            Beshah, Ethiopiaitem
                                            VENGROSKI, K - USDA ARS IDRLitem
                                            Zarlenga, Danteitem
                                            JAUREGUI, L - USDA ARS IDRLitem
                                            COSIO, M - USDA ARS IDRLitem
                                            DOUGLASS, L - U MD COLLEGE PARKitem
                                            Dubey, Jitenderitem
                                            Lunney, Joan
  Submitted to: International Immunology Congress
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 6/15/2001
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: A major strategy for the prevention of Toxoplasmosis in swine is the understanding of the immune response against Toxoplasma gondii infection by defining specific responding cells and cytokines which may induce definitive protection. The phenotype of PBMC and the kinetics of IFN-g, IL- 12 and IL-10 transcriptional changes were characterized in T. gondii oocyst tinfected NIH miniature swine. An increase in expression of activation markers CD25 and SLA-DQ was detected in the first week of infection. A significant increase in % of CD8+ cells was observed in week 2. Relative competitive RT-PCR analysis indicated an increase in IFN-gamma RNA as well as a reduction in IL-10 mRNA during week 2 post infection.  An increase in IL-12 transcription was not observed until the fourth week of infection. The ability of the pigs to respond to T. gondii infection by simultaneously inducing pro-inflammatory cytokines early and anti-  inflammatory cytokines later is a likely indication of the requirement to strike a balance between controlling parasite growth and avoiding cytokine toxicity.


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