Submitted to: Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 3/1/2007
Publication Date: 7/14/2007
Citation: Lillehoj, H.S., Hong, Y.H. 2007. Changes in Immune-Related Chicken Cytokine and Chemokine Gene Expression Following Eimeria Infection. Proceedings of Association of Avian Veterinary Pathologists Meetings, July 14-18, Washington DC. P 118. Interpretive Summary: Coccidiosis is the major parasitic disease of poultry with significant economic loss. With increasing concerns over the use of drugs in animal production and increasing incidence of drug resistant strains of field coccidia associated with commonly used drugs, discovery of new method for coccidiosis control is urgently needed. In this report, ARS scientists studied host intestinal immune response to coccidiosis using molecular genomics tools. Results of gene expression of cytokines and chemokines in the gut provided new insughts on the nature of inflammatory response associated with parasite infecton. This information will enhance our basic understanding of host-parasite interactions in avian coccidiosis that will aid in the development of new strategy for coccidiosis control.
Technical Abstract: The expression levels of mRNAs encoding a panel of 28 chicken cytokines and chemokines were quantified in intestinal lymphocytes following E. acervulina, E. tenella and E. maxima primary and secondary infections. Transcripts of the pro-inflammatory, Th1 and Th1 regulatory cytokines IFN- , IL-1 , IL-6, IL-12, IL-15, IL-17, and IL-18 were uniformly increased after E. acervulina and E. maxima primary infection, but either unchanged (IL-15, IL-16, IL-18), increased (IFN- , IL-10, IL-12), or decreased (IL-2) following E. tenella primary infection. Following secondary infection, Th1 cytokines mRNA levels were relatively unchanged. Similarly, mRNA levels of the Th2 or Th2 regulatory cytokines IL-3 and GM-CSF were increased following primary or secondary infection with three parasites. The chemokines IL-8, lymphotactin, and MIP-1 revealed significant increase following primary infection, but not secondary infection. We conclude that coccidiosis induces a diverse and robust primary cytokine/chemokine response, but a more subdued secondary response.