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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 #269105
Title: Systemic response to Campylobacter jejuni infection by profiling gene transcription in the spleens of two genetic lines of chickens

Author
item LI, X - Texas A&M University
item Swaggerty, Christina - Christi
item Kogut, Michael - Mike
item CHIANG, H - Texas A&M University
item WANG, Y - Texas A&M University
item He, Louis
item Genovese, Kenneth - Ken
item MCCARTHY, FIONA - Mississippi State University
item BURGESS, SHANE - Mississippi State University
item PEVZNER, IGAL - Cobb-Vantress, Inc
item ZHOU, HUAIJUN - Texas A&M University

Submitted to: Immunogenetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/22/2011
Publication Date: 8/20/2011
Citation: Li, X., Swaggerty, C.L., Kogut, M.H., Chiang, H.I., Wang, Y., He, L.H., Genovese, K.J., Mccarthy, F., Burgess, S., Pevzner, I.Y., Zhou, H. 2011. Systemic response to Campylobacter jejuni infection by profiling gene transcription in the spleens of two genetic lines of chickens. Immunogenetics. 64:59-69.

Interpretive Summary: Campylobacter jejuni (C. jejuni) is a leading cause of human food poisoning worldwide, and poultry products are one of the main sources of contamination. We have conducted previous studies using two lines of chickens (A and B) and showed that line A chickens are more resistant to food-borne bacterial infections compared to line B chickens. Day-old chickens from lines A and B were administered a single dose of C. jejuni, and the spleen, an organ associated with the immune response, was removed 7 days later. To further understand the response mechanisms to a C. jejuni infection, RNA was isolated from the spleens and applied to a chicken microarray to compare infected and non-infected chickens within each line and between the two lines A and B. Following infection, there were more genes in the spleen responding to the infection in the resistant line A than in the susceptible line B. These genes were related to defense response to bacteria. Specifically, genes for immune cell activation were up-regulated in the resistant line. Interestingly, in the susceptible line, genes for regulating red blood cells and other RNA biosynthetic processes were all down-regulated. An interaction analysis between genetic line and treatment demonstrated distinct defense mechanisms between lines: the resistant line promoted controlled cell death, whereas the susceptible line responded by down-regulating this function. This was the first time that such defensive mechanisms against C. jejuni infection have been reported. The results of this study have uncovered new mechanisms of host responses to C. jejuni infection in chickens.

Technical Abstract: Campylobacter jejuni (C. jejuni) is a leading cause of human bacterial enteritis worldwide. To understand the systemic molecular response mechanisms to C. jejuni infection in chickens, total splenic RNA was isolated and applied to a whole genome chicken microarray for comparison between infected (I) and non-infected (N) chickens within and between genetic lines A and B. There were more total splenic host genes responding to the infection in the resistant line A than in the susceptible line B. Specifically, genes for lymphocyte activation, differentiation and humoral response, and Ig light and heavy chain were up-regulated in the resistant line. In the susceptible line, genes for regulation of erythrocyte differentiation, hemopoiesis, and RNA biosynthetic process were all down-regulated. An interaction analysis between genetic lines and treatment demonstrated distinct defense mechanisms between lines: the resistant line promoted apoptosis and cytochrome c release from mitochondria, whereas the susceptible line responded with a down-regulation of both functions. This was the first time that such systemic defensive mechanisms against C. jejuni infection have been reported. The results of this study have uncovered novel molecular mechanisms of systemic host responses to C. jejuni infection in chickens that warrant further investigation.