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Title:   Author  item
                                            Lillehoj, Hyunitem
                                            LILLEHOJ, ERIK - UNIV OF MARYLANDitem
                                            LEE, SUNG - VIST. SY BA
  Submitted to: Veterinary Immunology and Immunopathology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 1/20/2007
                                    Publication  Date: 4/2/2007
                                    Citation: Hong, Y.H., Lillehoj, H.S., Lillehoj, E.P., Lee, S.H. 2007. Changes in immune-related gene rxpression and intestinal lymphocyte subpopulations following Eimeria maxima infection of chickens. Veterinary Immunology and Immunopathology. 114:259-272.Interpretive Summary: Coccidiosis is an intestinal parasitic disease caused by several distint species of Eimeria parasites. Drugs have been traditionally used to control coccidiosis. However, with increasing concerns by the consumers on the development of drug resistance, alternative control strategies against avian coccidiosis is needed. In this paper, ARS scientists in collaboration with non-ARS scientists report indepth studies on mucosal host immune response to coccidiosis using molecular genomics technology. The results show thst coccidia parasites elicit complex host immune responses in the gut which involve many different types of lymphocytes and chemokines. Understadning how different intestinal cells interact with coccidia parasites to elicit protective immune response will facilitate the development of new control strategy against this infection and vaccine discovery.
                                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 were measured in intestinal intraepithelial lymphocytes (IELs) after Eimeria maxima infection.  In addition, changes in IEL numbers were quantified following E. maxima infection.  Transcripts of the pro-inflammatory and Th1 cytokines IFN-g, IL-1b, IL-6, IL-12, IL-15, IL-17, and IL-18 were increased 66- to 8x107-fold following primary parasite infection.  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-?, TGF-b4, and K60 transcripts showed no increased expression, and only the level of the Th2 cytokine IL-13 was increased following secondary E. maxima infection.  Increases in intestinal T cell subpopulations following E. maxima infection also were detected.  CD3+, CD4+, and CD8+ cells were significantly increased at days 8, 6, and 7 post-primary infection respectively, 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.


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