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Title:   Author  item
                                            Kogut, Michael

                                                         - *Mike*item
                                            ROTHWELL, LISA - INST OF ANIMAL HEALTHitem
                                            KAISER, PETE - INST OF ANIMAL HEALTH
  Submitted to: International Cytokine Society Annual Meeting
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 9/23/2003
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: The immediate response to invasive pathogens, clearance via the inflammatory response, and activation of appropriate acquired responses are all coordinated by innate host defenses.  Recognition of microbes is accompanied by the induction of multiple cellular processes including the production of pro- and anti-inflammatory cytokines.  Polymorphonuclear leukocytes (PMNs) are vital cellular components of innate response with the primary PMN in poultry being the heterophil.  Priming is the potentiation of the phagocyte activation process by previous exposure to a priming agent.  IFN-g is a pleiotrophic cytokine involved in basically all phases of immune and inflammatory responses that has been shown to prime heterophil functional activities.  In the present experiments, using real-time quantitative RT-PCR, we evaluated the role of recombinant chicken IFN-gamma (rChIFN-g) as a priming mediator to control heterophil responses at the level of gene transcription and expression of the mRNA for proinflammatory  (IL-1b, IL-6, IL-8) and Th1 (IL-18 and IFN-gamma) cytokine genes following stimulation with phagocytosis agonists opsonized and nonopsonized Salmonella enteritidis.  rChIFN-gamma primed the heterophils for an increase in transcription of pro-inflammatory cytokines induced by phagocytic agonists, but also upregulated expression of Th1 cytokine (IL-18 and IFN-gamma) mRNA.  Although rChIFN-gamma priming modulated the expression of cytokine mRNA in heterophils stimulated by different phagocytic agonists, rChIFN-gamma by itself did not directly induce gene expression of either proinflammatory or Th1 cytokines.  The enhanced expression of cytokine mRNA does not appear to be differentially expressed depending on the receptor activated during phagocytosis.  The results from the present experiments suggest that rChIFN-gamma may play a significant role in avian innate immunity against Salmonella infection and may offer an adjunct use in the prevention and treatment of salmonellae infections in newly hatched chickens.


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