ARS | Publication request: KINETIC CHANGES IN IMMUNE-RELATED GENE EXPRESSION AND INTESTINAL LYMPHOCYTE SUBPOPULATIONS FOLLOWING E. MAXIMA INFECTION

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: July 31, 2006
Publication Date: October 21, 2006
Citation: Hong, Y.H., Lillehoj, H.S., Lee, S.H., Dalloul, R. 2006. Kinetic changes in immune-related gene expression and intestinal lymphocyte subpopulations following e. maxima infection. Proceedings of International Avian Immunology Research Group Meeting. Oct 21-24, Paris, France. P 64.

Technical Abstract: Coccidiosis, a major intestinal parasitic disease of poultry, induces a cell-mediated immune response against the etiologic agent of the disease, Eimeria. In the current study, the expression levels of gene transcripts encoding pro-inflammatory, Th1, and Th2 cytokines, as well as chemokines and intestinal intraepithelial lymphocyte subpopulations, were quantified following E. maxima infection. Transcripts of the pro-inflammatory and Th1 cytokines IFN-gamma, IL-1 beta, IL-6, IL-12, IL-15, IL-17, and IL-18 were increased 66- to 80,000,000-fold following primary coccidiosis. Similarly, mRNA levels of the Th2 cytokines IL-3, IL-10, IL-13, and GM-CSF were up-regulated 34- to 8,800-fold, and the chemokines IL-8, lymphotactin, MIF, and K203 were increased 42- to 1,756-fold. In contrast, IFN-alpha, TGF-beta4, and K60 transcripts showed no increased expression, and only the level of the Th2 cytokine IL-13 was increased following secondary E. maxima infection. Intestinal T cell subpopulations CD3+, CD4+, and CD8+ cells were significantly increased at days 8, 6, and 7 days post primary E. maxima infection, but only CD4+ cells remained elevated following secondary infection. TCR1+ cells exhibited a biphasic pattern following primary infection, whereas TCR2+ cells displayed a single peak in levels. Taken together, these data indicate a global chicken intestinal immune response is produced following experimental Eimeria infection involving multiple cytokines, chemokines, and T cell subsets.