|KIM, DUK KYUNG - USDA ARS ANRI APDL
|PARK, DONG WOON - USDA ARS ANRI APDL
|LAMONT, SUSAN - IOWA STATE U, AMES
Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 5/17/2007
Publication Date: 10/20/2007
Citation: Kim, D., Hong, Y.H., Park, D., Lamont, S.J., Lillehoj, H.S. 2007. Differential cytokine gene expression in two genetically disparate chicken lines in response to infection with eimeria maxima. Internation Symposium on Animal Genomics for Animal Health Meeting.Oct 20-27, Paris, France.
Interpretive Summary: Coccidiosis is major parasitic disease of poultry of economic importance and is caused by several distinct species of intracellular protozoa, Eimeria. Current methods such as drugs and live parasite vaccines to control coccidiosis is not cost-effective and has many limitations. Therefore, timely development of alternative control methods for avian coccidiosis is needed. In this paper, ARS scientists collaborated with scientists at Iowa State University to investigate various genetic factors which influence disease resistance to avian coccidiosis using two genetically different chicken strains developed at Iowa State University. The analysis of host response to this parasite indicated that certain genetic elements influence key immune response of chickens to Eimeria parasites. These results provide new insights for parasite survival in chicken host and will lead to the development of better control methods for avian coccidiosis by poultry industry.
Technical Abstract: Coccidiosis is major parasitic disease of poultry causing substantial economic losses to the poultry industry worldwide. This study investigated the immunological basis for the genetic control of host immune response to E. maxima infection. Two highly inbred lines of Fayoumi chickens with different B-haplotypes (MHC) were evaluated for expression of 9 cytokine genes: IFN-', IFN-1', IL-10, IL-15, IL-17, iNOS, LITAF, NK-lysin and TL1A using real time RT-PCR. Gene expression was measured in jejunum intestinal intraepithelial lymphocytes (IEL) and splenocytes at 0, 3, 4 and 5 days post E. maxima infection. Body weight loss and fecal oocyst counts were also examined as parameters of disease progression. Gene expression analysis of jejunum IEL showed that many cytokines differentially expressed between the two Fayoumi lines after E. maxima infection; the M5.1 line, which is the more disease-resistant, expressed higher levels of IFN-', IFN-1', IL-15, IL-17, iNOS and LITAF transcripts and lower NK-lysin and TL1A RNA levels compared with the M15.2 line at 3 days post infection. In the spleen, E. maxima infection down-regulated the expression of IFN-', LITAF and NK-lysin in the M15.2 line. Weight loss following E. maxima infection was more prominent in M15.2 than M5.1 birds, and fecal parasite numbers were higher in M15.2 than in M5.1 birds. These results provide clear evidence that genetically determined disease resistance to E. maxima involves a T-cell-mediated immune mechanism and key cytokines are involved in the induction of protective immunity against E. maxima.