Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: April 20, 2003
Publication Date: May 9, 2003
Citation: Sonstegard, T.S., Araujo, R.N., Zarlenga, D.S., Padilha, T., Lima, W.S., Nascimento, E., Gasbarre, L.C. 2003. Characterization of immune response gene expression patterns in cattle selected for resistance or suscptibility to gastrointestinal parasites. Meeting Abstract.
Selecting for host resistance offers an alternative method to control disease caused by gastrointestinal (GI) parasites. Recently, a genome scan was performed in a population of linebred Angus cattle divergently selected for resistance to GI parasites that identified putative quantitative trait loci (QTL) related to parasite infection. In an effort to better identify candidate genes for fine mapping that were both relevant in function and position to these putative QTL, expression patterns of 447 immune-related genes were surveyed using mesenteric lymph nodes and small intestine mucosa of animals challenged for six-months on pastures naturally infected with nematodes. Prior to fluorescent probe synthesis, RNA was combined into either the resistant and susceptible pool based on intestinal worm counts, where the difference in the mean value for parasite load between animal pools was over 300-fold. Analysis of glass microarray hybridization results and follow-up validation using real-time RT-PCR indicated resistant animals had significantly higher levels of expression for genes related to humoral immunity. Conversely, susceptible cattle showed increased expression of genes related to the Th (helper) 1 cell response pathway and to tissue damage, inflammation, and immune cell infiltration.. These results imply that in the susceptible animals there may be an inappropriate, delayed type hypersensitivity response to infection that inhibits the development of effective immunity to intestinal parasite infection. These results should aid the identification of genes underlying QTL related to immune response to parasite infection.