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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #233008
Title: Gene expression profiling of innate immune response to Campylobacter jejuni infection in the bursa of broilers

Author
item LI, XIANYAO - TEXAS A&M UNIVERSITY
item Swaggerty, Christina - Christi
item Kogut, Michael - Mike
item CHIANG, HSIN-I - TEXAS A&M UNIVERSITY
item YING, WANG - TEXAS A&M UNIVERSITY
item Genovese, Kenneth - Ken
item He, Louis
item KIRITA, VICTOR - UNIVERSITY OF MICHIGAN
item PEVZNER, IGAL - COBB-VANTRESS, INC.
item ZHOU, HUAIJUN - TEXAS A&M UNIVERSITY

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 10/1/2008
Publication Date: 1/10/2009
Citation: Li, X., Swaggerty, C.L., Kogut, M.H., Chiang, H., Ying, W., Genovese, K.J., He, H., Kirita, V.J., Pevzner, I., Zhou, H. 2009. Gene expression profiling of innate immune response to Campylobacter jejuni infection in the bursa of broilers [abstract]. Plant & Animal Genome XVII Conference, January 10-14, 2009, San Diego, California. p. 509.

Interpretive Summary:

Technical Abstract: Campylobacter jejuni (C. jejuni) is a commensal microorganism in chickens, but caused significant health problems in humans. Reduction of C. jejuni colonization in the chicken gut will significantly decrease human campylobacteriosis. To study host response to C. jejuni infection in broilers, both wild-type (wt) and mutant (5 log reduction of C. jejuni colonization in the chicken gut compared to wt) C. jejuni were used to challenge day-one-old broilers. Total RNA were isolated from bursa at 1 and 4 hours post-challenge. Eight biological replicates were used in each group at each time point. The signal intensity of each gene was normalized using the LOWESS method and a mixed model was used to identify differentially expressed genes. There were 908 and 583 genes expressed (P less than 0.01) between mutant C. jejuni infected and non-infected chickens, and between wt C. jejuni infected and non-infected chickens at 1 hour post-challenge, respectively, and 453 and 577 genes at 4 hours post-challenge, respectively. More up-regulated genes than down-regulated genes were found at 1 hour post-challenge in the comparisons of both mutant and wt vs. non-infected controls, while more down-regulated genes than up-regulated genes were detected at 4 hour post-challenge. There was a strong early host response to the mutant strain in the bursa. The results suggest there is a significantly different response caused by different C. jejuni strains within and between time points. These data provide new insights to determine the molecular mechanisms of host immunity to C. jejuni infection in broilers.