Application of functional genomics, immunology and molecular biology tools to explore host immune response to Eimeria.

Lillehoj1, H. S., Dalloul1, R. A., Hong1, Y. H., Bliss2, T. W., Keeler2, C. L., Ben Chouikha1, I., Park1, D.W., and Han3, J.Y. Animal Parasitic Diseases Laboratory1, Animal and Natural Resources Institute, U.S. Department of Agriculture, Beltsville, MD. 20705, Department of Animal and Food Sciences2, University of Delaware, Newark, DE., School of Agricultural Biotechnology3, Seoul National University, Seoul 151-742, Korea (email address of presenting author: hlilleho@anri.barc.usda.gov)

Avian coccidiosis is caused by several different Eimeria species which infect different regions of the intestine inducing a specie-specific immunity. Coccidiosis usually stimulates a number of immunological defense mechanisms, namely antibody- and cell-mediated. Recent technological advance in molecular genomics is opening a novel way for the discovery of molecular/cell biological pathways associated with complex biological phenomenon and is facilitating the development of an alternative strategy to combat coccidiosis. Using high-throughput molecular genomics approaches, we have identified host genes involved in the disease process and resistance. Since intraepithelial lymphocytes (IELs) play a critical role in protective immune response to Eimeria, a list of genes expressed by intestinal IEL of Eimeria-infected chickens was compiled using the expressed sequence tag (EST) strategy. The 14,409 ESTs consisted of 1,851 clusters and 7,595 singletons, which revealed 9,446 unique genes in the data set. This EST library will be a valuable resource for profiling global gene expression in normal and pathogen-infected chickens for the identification of host immune-related genes. We have also carried out fine mapping of quantitative trait locus (QTL) which control coccidiosis resistance and identified a QTL on chromosome 1 that significantly affects Eimeria oocyst shedding and three QTLs that influence body weight of chickens during coccidiosis. These results provide the foundation for further investigation to validate the QTL. In addition, we have investigated local host immunity to Eimeria using tissue-specific cDNA microarrays. The results of these studies clearly indicate that the intricate and complex interactions of host local innate immune response and parasites determine the outcome of host response to coccidiosis.