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.