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Systemic response to Campylobacter jejuni infection by profiling gene transcription in the spleens of two genetic lines of chickens
- Li, Xianyao, Swaggerty, Christina L., Kogut, Michael H., Chiang, Hsin I, Wang, Ying, Genovese, Kenneth J., He, Haiqi, McCarthy, Fiona M., Burgess, Shane C., Pevzner, Igal Y., Zhou, Huaijun
- Immunogenetics 2011 v.64 pp. 59
- Campylobacter jejuni, RNA, apoptosis, bacterial enteritis, cell differentiation, chickens, cytochrome c, digestive tract, disease resistance, erythrocytes, gene expression regulation, genes, genetic lines, genetic resistance, hematopoiesis, humans, humoral immunity, lymphocyte proliferation, microarray technology, mitochondria, poultry products, resistance mechanisms, spleen, transcription (genetics)
- Campylobacter jejuni (C. jejuni) is a leading cause of human bacterial enteritis worldwide with poultry products being a major source of C. jejuni contamination. The chicken is the natural reservoir of C. jejuni where bacteria colonize the digestive tract of poultry, but rarely cause symptoms of disease. 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 resistant line A than in susceptible line B. Specifically, genes for lymphocyte activation, differentiation and humoral response, and Ig light and heavy chain were upregulated in the resistant line. In the susceptible line, genes for regulation of erythrocyte differentiation, hemopoiesis, and RNA biosynthetic process were all downregulated. 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 downregulation 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 revealed novel molecular mechanisms of the systemic host responses to C. jejuni infection in chickens that warrant further investigation.