Abstract

BackgroundSalmonella 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 utilized large-scale gene expression profiling.ResultsThe results showed 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.ConclusionWe found: (1) A divergent expression pattern of immune-related genes 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.

Highlights

  • 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 results from this study demonstrate that higher expression of immune-related genes is more beneficial to enhance the host response against SE infection

  • The immune deficiency in the susceptible line is likely due to suppressed functions in recovering from cellular changes induced by SE infection

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Summary

Introduction

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. It has been reported that a large influx of heterophils is observed in the intestines of SE-infected chickens, indicating an increase in heterophils to the infection site contributes to defending against microbial infection [9,10] Both studies of in vivo and in vitro SE-infected heterophils from different chicken lines revealed that the up-regulated mRNA expression levels of interleukin (IL)-1β, IL-6, IL-8 ( known as CXCLi2), IL-18, and anti-inflammatory cytokines transforming growth factor-β4 (TGF-β4) might be responsible for determining overall immune competence [11,12]. The data indicate differences in heterophil function and innate responsiveness are under genetic control

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