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![](https://webarchive.library.unt.edu/eot2008/20081106164631im_/http://www.ars.usda.gov/incme/images/Research_head.gif) |
Research Project:
AVIAN GENOMIC AND IMMUNOLOGIC APPROACHES FOR CONTROLLING MUCOSAL PATHOGENS
Location: Animal Parasitic Diseases
Title: QUANTITATIVE GENETIC AND FUNCTIONAL GENOMICS APPROACHES TO INVESTIGATING PARASITE DISEASE RESISTANCE AND PROTECTIVE IMMUNE MECHANISMS IN AVIAN COCCIDIOSIS
Authors
Submitted to: Developmental Biology
Publication Type:
Peer Reviewed Journal
Publication Acceptance Date: September 9, 2008
Publication Date: September 10, 2008
Citation: Lillehoj, H.S., Hong, Y.H., Kim, C. 2008. Quantitative genetic and functional genomics approaches to investigating parasite disease resistance and protective immune mechanisms in avian coccidiosis. Developmental Biology.132:67-76.
Interpretive Summary: This is the summary of presentation which was given as an invited talk at the international Animal Genomics for Animal Health meeting that was held in Paris, France in October, 2007. In this paper, ARS scientist discusses poultry mucosal immune system and its function in defense against gut pathogens. Intestinal mucosal surfaces are defended against enteric pathogens by the gut-associated lymphoid tissues and the primary effecter cells localized here are intraepithelial lymphocytes (IELs) of the outer mucosal epithelial layer that recognize and destroy pathogens that breach the intestinal epithelium. Thus, IELs play an important role in the host response to avian coccidiosis, an intestinal disease caused by a ubiquitous intestinal protozoa that seriously impairs the growth and feed utilization of infected chickens. This paper summarizes new studies on poultry mucosal immune system and novel genomics methods which are being used to investigate cellular and molecular interactions of host-pathogen. Two major methods described are the quantitative trait loci (QTL) mapping strategies where DNA markers that are associated with growth performance and disease resistance can be identified, and high-throughput gene expression analysis where thousands host genes are interrogated for changes in gene expression and their function. A genome-wide search for markers that control resistance to coccidiosis led to the identification of two QTLs significantly associated with disease resistance to E. maxima. As a supplemental approach, an avian intestinal intraepithelial lymphocyte cDNA array (AVIEA), was constructed from a library of genes expressed by intestinal intraepithelial lymphocytes (IELs) of Eimeria-infected chickens, was used to identify candidate genes affecting gut immune responses to E. maxima infection. These new methods and novel findings will have a major contribution in understanding host immune mechanisms against mucosal pathogens in poultry.
Technical Abstract: A major challenge for the commercial poultry production is controlling enteric disease-causing pathogens in the absence of prophylactic drugs. Although traditional genetic approaches have contributed to enhanced efficiency of poultry production and increased the ability of the industry to provide safe, high quality, and low cost meat products to consumers, economic losses due to enteric diseases remains a significant problem. Therefore, there is a need to develop alternative control strategies against poultry enteric pathogens of economic importance. Recent advances in molecular genetics and functional genomics are now allowing for rapid progress in understanding the molecular mechanisms of disease resistance against major infectious agents of poultry. It is anticipated that identifying the nature of host-pathogen interactions will facilitate the development of novel vaccines and therapeutics. In this paper, recent progress in identifying genes that influence resistance to avian coccidiosis, the most economically important disease of poultry, will be discussed. This work provides an excellent example of how the integration of new molecular genetic and functional genomics tools increases our knowledge of the mechanism of genetic resistance to complex diseases.
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Last Modified: 11/05/2008
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