|Chiang, Hsin-I - TEXAS A&M UNIVERSITY|
|Dowd, Scot - USDA/ARS|
|Li, Xianyao - TEXAS A&M UNIVERSITY|
|Pevzner, Igal - COBB-VANTRESS, INC., AR|
|Zhou, Huaijun - TEXAS A&M UNIVERSITY|
Submitted to: Biomed Central (BMC) Genomics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 12, 2008
Publication Date: November 6, 2008
Repository URL: http://handle.nal.usda.gov/10113/58137
Citation: Chiang, H., Swaggerty, C.L., Kogut, M.H., Dowd, S.E., Li, X., Pevzner, I.Y., Zhou, H. 2008. Gene expression profiling in chicken heterophils with Salmonella enteritidis stimulation using a chicken 44 K Agilent microarray. Biomed Central (BMC) Genomics. 9:Article 526. Interpretive Summary: Salmonella enteritidis (SE) is a bacterium that causes food poisoning in humans and often results from eating or handling contaminated poultry products. During the first week of life, baby chickens are very susceptible to bacterial infections. Baby chicks have blood cells that can help them prevent these infections. These cells are called heterophils. The objective of this research was to compare heterophils from two lines of chickens (lines A and B) to determine if one is more resistant to SE infections than the other. To make this distinction between lines A and B, we used new technology, called a microarray, to look at the different genes that were turned on following an SE infection. We found there were more immune-related genes that were turned on in line A compared to line B while a lot of genes were actually turned off in line B. Since there were more immune-related genes turned on in line A, this would allow these chickens to fight off infections better than line B chickens. These experiments are important to the commercial poultry breeders because we have identified specific genes that are associated with increased resistance against SE. In doing this, we will be able to select chickens for increased resistance to SE infections. A resistant chicken is going to be stronger and will fight off infections better; therefore, people are less likely to get an infection from eating contaminated poultry.
Technical Abstract: Salmonella enterica serovar Enteritidis (SE) is one of the most common food-borne pathogens that cause human salmonellosis and usually results from the consumption of contaminated poultry products. The mechanism of SE resistance in chickens remains largely unknown. Previously, heterophils isolated from broilers with different genetic backgrounds (SE-resistant [line A] and -susceptible [line B]) have been shown to be important in defending against SE infections. To dissect the interplay between heterophils and SE infection, we used large-scale expression profiling technology: a newly-developed chicken 44K Agilent microarray. The results showed that more differentially expressed genes were found between different lines than between infection (SE-treated) and non-infection (control) samples within line. However, the numbers of expressed immune-related genes between these two comparisons were dramatically different. More genes related to immune function were down-regulated in line B than line A. The analysis of the immune-related genes indicated that SE infection induced a stronger, up-regulated gene expression of line heterophils A than line B, and these genes include several components in the Toll-like receptor (TLR) signaling pathway, and genes involved in T-helper cell activation. Our results showed: (1) A divergent expression pattern of immune-related genes was observed between lines of different genetic backgrounds. The higher expression of immune-related genes might be more beneficial to enhance host immunity in the resistant line; (2) a similar TLR regulatory network might exist in both lines, where a possible MyD88-independent pathway may participate in the regulation of host innate immunity; (3) the genes exclusively differentially expressed in line A or line B with SE infection provided strong candidates for further investigating SE resistance and susceptibility. These findings have laid the foundation for future studies of TLR pathway regulation and cellular modulation of SE infection in chickens.