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Title: GENE EXPRESSION PROFILING TO STUDY 12 CYTOKINE PRODUCTION AFTER EIMERIA INFECTION

Author
item Min, Wongi
item Lillehoj, Hyun
item KIM, SUNGWON - USDA-ARS,PBESL
item Zhu, James
item Beard, Hunter
item ALKHAROUF, NADIM - USDA-ARS,PSI
item MATTHEWS, BENJAMIN - USDA-ARS,PSI

Submitted to: American Association of Avian Pathologists
Publication Type: Abstract Only
Publication Acceptance Date: 6/1/2003
Publication Date: N/A
Citation: N/A

Interpretive Summary:

Technical Abstract: Avian coccidiosis is caused by several Eimeria strains which infect different regions of the intestine inducing a strain-specific immunity. To investigate host immune response against two major Eimeria spp., we infected SC White-Leghorn chickens with E. acervulina and E. maxima and compared their global transcriptional changes elicited in the intestinal intraepithelial lymphocytes (IELs) using nylon and glass cDNA microarrays. Initially, nylon microarray containing 2600 EST cDNAs selected from the activated T-lymphocyte and macrophage cDNA libraries (http://www.chickest.del.edu) were hybridized with mRNAs extracted from the IELs obtained from E. acervulina- or E. maxima-infected chickens. On the basis of significant changes associated with infection, 419 clones showing at least 1.5-fold changes over the uninfected controls, were selected for cDNA microarray on a glass slide and local host response to Eimeria infection was analyzed at four different time points after primary and secondary infections. In general, E. acervulina infection resulted in greater changes in the local gene expression than E. maxima infection. Both E. acervulina and E. maxima infections induced 37 and 10 genes in the primary and secondary infections, respectively, while repressed 43 and 10 genes in the primary and secondary infections, indicating that the primary infections resulted in a greater change than the secondary infection. The detailed analysis of the local changes in host gene expression following Eimeria infection will enhance our understanding of host-parasite immunobiology leading to protective immunity.