AVIAN GENOMIC AND IMMUNOLOGIC APPROACHES FOR CONTROLLING MUCOSAL PATHOGENS
Title: IMMUNE-RELATED GENE EXPRESSION IN TWO GENETICALLY DISPARATE FAYOUMI CHICKEN LINES FOLLOWING EIMERIA MAXIMA INFECTION
| Kim, Duk Kyung - VIS SCI, APDL, ARS, USDA |
| Hong, Yeong |
| Park, Dong Woon - VIS SCI, APDL, ARS, USDA |
| Lamont, Susan - IA STATE U., AMES, IA |
| Han, Jae Yong - SEOUL NAT UNIV, KOREA |
| Lillehoj, Erik - UNIV MD, SCH OF MED, BALT |
Submitted to: International Journal of Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 9, 2008
Publication Date: July 20, 2008
Citation: Kim, D., Lillehoj, H.S., Hong, Y.H., Park, D., Lamont, S.J., Han, J., Lillehoj, E.P. 2008. Immune-related gene expression in two genetically disparate fayoumi chicken lines following eimeria maxima infection. International Journal of Poultry Science. 87:433-443.
Interpretive Summary: Coccidiosis is the major parasitic disease of poultry caused by protozoa belonging to the genus Eimera. Avian coccidiosis causes significant economic losses to the world poultry industry due to reduction in production efficiency as a result of mortality, nutrient malabsorption, retarded growth rate, and decreased egg production. Conventional disease control strategies have relied on prophylactic chemotherapy and vaccination, but both are not without serious drawbacks, and drug-resistant parasites and consumer apprehension concerning chemical residues in food hamper the use of coccidiostats, while the risk of clinical disease induced by live parasite vaccination is increasing. Accordingly, numerous studies have been performed to identify alternative methods to control avian coccidiosis. Genetic selection of disease resistance in commercial broiler chickens is considered by many as one of the best ways to achieve this goal and ultimately lead to the elimination of drugs in commercial poultry production. In this paper, ARS scientists collaborated with scientists at the Iowa State University, Seoul National University and University of Maryland to identify host genes which control coccidiosis susceptibility and to identify genetic basis for disease susceptibility differences in different chicken breeds. In this study, the Fayoumi breeds, which originated in Egypt, showed different disease resistance to coccidiosis. Investigation of their immune response at the molecular level demonstrated that the two Fayoumi lines show different gene expression of immune-related cytokines and chemokines following experimental infection with E. maxima. The results of this study establish different host response of Fayoumi lines to coccidiosis challenge for the first time and provide experimental basis for future studies on the mechanisms of disease resistance in these chicken lines.
To investigate the influence of genetic differences in the major histocopatibility complex (MHC) on susceptibility to avian coccidiosis, M5.1 and M15.2 B-haplotype congenic Fayoumi chickens were orally infected with live Eimeria maxima oocysts and body weight gain, fecal oocyst production, and expression of a panel of immune-related genes were determined as parameters of protective immunity. Weight loss was reduced and fecal parasite numbers were lower in M5.1 compared with M15.2 line birds. Intestinal intraepithelial lymphocytes from M5.1 chickens expressed higher levels of transcripts encoding interferon-' (IFN-'), interleukin-1ß (IL-1ß), IL-6, IL-8, IL-12, IL-15, IL-17A, inducible nitric oxide synthase (iNOS), and lipopolysaccharide-induced tumor necrosis factor-a factor (LITAF) and lower levels of mRNAs for IFN-a, IL-10, IL-17D, NK-lysin, and tumor necrosis factor superfamily 15 (TNFSF15), compared with the M15.2 line. In the spleen, E. maxima infection was associated with higher expression levels of IFN-', IL-15, and IL-8 and lower levels of IL-6, IL-17D, and IL-12 in M5.1 vs. M15.2 birds. These results suggest that genetic determinants within the chicken MHC influence resistance to E. maxima infection by controlling the local and systemic expression of immune-related cytokine and chemokine genes.