Abstract

The infectious bursal disease (IBD) is an acute immunosuppressive viral disease that significantly affects the economics of the poultry industry. The IBD virus (IBDV) was known to infect B lymphocytes and activate macrophage and T lymphocytes, but there are limited studies on the impact of IBDV infection on chicken intraepithelial lymphocyte natural killer (IEL-NK) cells. This study employed an mRNA sequencing approach to investigate the early regulation of gene expression patterns in chicken IEL-NK cells after infection with very virulent IBDV strain UPM0081. A total of 12,141 genes were expressed in uninfected chicken IEL-NK cells, and most of the genes with high expression were involved in the metabolic pathway, whereas most of the low expressed genes were involved in the cytokine-cytokine receptor pathway. A total of 1,266 genes were differentially expressed (DE) at 3 day-post-infection (dpi), and these DE genes were involved in inflammation, antiviral response and interferon stimulation. The innate immune response was activated as several genes involved in inflammation, antiviral response and recruitment of NK cells to the infected area were up-regulated. This is the first study to examine the whole transcriptome profile of chicken NK cells towards IBDV infection and provides better insight into the early immune response of chicken NK cells.

Highlights

  • The infectious bursal disease (IBD) is an acute immunosuppressive viral disease that significantly affects the economics of the poultry industry

  • intraepithelial lymphocyte natural killer (IEL-natural killer (NK)) cells were isolated from duodenum samples collected from uninfected chickens and chickens infected with vvIBDV at 3 dpi

  • The C­ D3−/28.4+ IEL-NK cells were isolated from uninfected chickens and chickens infected with vvIBDV for 3 days

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Summary

Introduction

The infectious bursal disease (IBD) is an acute immunosuppressive viral disease that significantly affects the economics of the poultry industry. The innate immune response was activated as several genes involved in inflammation, antiviral response and recruitment of NK cells to the infected area were up-regulated. The primary physiological role of NK cells is to provide a crucial initial defence against pathological organisms during the time (from day 0 to day 5) that the adaptive immune system is still being m­ ustered[8]. Their major function is to recognize and kill virally infected and neoplastic cells. When the ligand of NK cells interacts with cell-surface receptors, they produce several cytokines such as IFN-γ, which have an immunoregulatory r­ ole[9]

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