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United States Department of Agriculture

Agricultural Research Service

Title: Genetic Control of Disease Resistance in Poultry Diseases

Author
item Lillehoj, Hyun

Submitted to: NE-60 Regional Meeting
Publication Type: Proceedings
Publication Acceptance Date: May 2, 2001
Publication Date: N/A

Interpretive Summary: Coccidiosis, an intestinal infection caused by intracellular protozoan parasites belonging to several different species of Eimeria seriously impairs the growth and feed utilization of livestock and poultry. Due to complex life cycle of organism and intricate host immune responses to Eimeria, coccidia vaccine development has been difficult. Understanding of basic immunobiology of pertinent host-parasite interactions and host immunogenetics involved in the control of coccidiosis susceptibility/resistance is necessary for the development of novel control strategy. Although many chicken DNA markers have been available during the last 10 years, DNA-based marker selection strategy for avian coccidiosis has not been tried. In this report, ARS scientists, in collaboration with other scientists at University of Delaware and Purdue Farms, Inc., carried out preliminary studies to determine the feasibility of using DNA markers to select for the coccidiosis-resistant chickens in broiler meat-type birds. Preliminary findings indicate that a QTL on chromosome 1 is closely related with disease resistant traits associated with coccidiosis. These results will provide necessary knowledge for poultry industry to develop logical genetic-based selection strategy for coccidiosis-resistant chickens. If successful, genetic control strategy will reduce economic loss associated with coccidiosis.

Technical Abstract: The higher resistance of SC chickens may be related to their ability to produce higher levels of antigen-specific antibodies early in infection, their enhanced T cell response to Eimeria antigens and/or greater innate coccidial inhibitory activity. The number of CD4+ cecal tonsil lymphocytes in SC chickens increased at days 4 and 6 ppi whereas those in TK chickens remained consistently low during the same time period. CD8+ cells, on the other hand, were noticeably higher in TK compared to SC chickens following primary infection whereas these cells were significantly higher in SC chickens psi. Although the nature of effector mechanism controlling disease resistance to E. tenella remains to be clarified, it is probable that both CD4+ and CD8+ cells are involved at different phase of host protective immunity. We extended this concept of site-specific immunity to coccidia by quantifying the expression of IFN-g mRNA in various lymphoid tissues where E. tenella undergo intracellular development. Data presented support the hypothesis that local IFN-g production at the sites of parasite infestation is an important component of the host immune response to coccidia. Evidence provided by this study establish that chicken IL-2 is a growth factor for g d T cells and emphasize the important immunoregulatory roles of IL-2 and g d T cells in avian coccidiosis. In this study, IL-2 gene injection into chickens resulted in an increase in splenic g d cells, supporting a role for IL-2 as a growth factor for g d T cells. Further studies will undoubtedly lead to a better understanding of IL-2 mediated immune enhancement in particular and innate immunity against enteric pathogens in general. Results show that the gene encoded by new gene is the homologue of mammalian IL-15 and distinct from chicken IL-2 previously described.

Last Modified: 10/24/2014
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