Differential expression of the Toll-like receptor pathway and related genes of chicken bursa after experimental infection with infectious bursa disease virus
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Infectious bursa disease virus causes an acute infection in bursal B cells. The Toll-like receptor (TLR) signaling pathway plays a key role in innate immunity during virus infection. In this study, an Agilent microarray was used to investigate different transcriptional profiles of the TLR pathway and related genes of chicken bursa at 48 h after infection with IBDV, compared with simulated infection. Expression of >58 genes changed significantly. Forty-six genes associated with chicken bursa proinflammatory effects, chemotactic effects, and T-cell stimulation were upregulated, which meant enhancement of these features. Twelve genes that are related to proliferation and differentiation of bursal cells were downregulated, implying suppression of these features. These results revealed that genes of the TLR pathway play an important role in the pathogenicity of IBDV infection. The findings are helpful for understanding the molecular basis of viral pathogenesis and the underlying mechanism of the host antiviral response.
KeywordsInterferon Regulatory Factor Imiquimod Negative Regulatory Factor Host Antiviral Response Bursal Tissue
This work was supported by grants from National Twelve-Five Technological Supported Plan of China (No. 2011BAD34B01) and public service sectors agriculture research projects (No. 201003060-9/10). We are thankful for the help from the members of China Agricultural University & Beijing University of Agriculture Traditional Chinese Veterinary Medicine (CAU-BUA TCVM) teaching and research team. This study was approved by the Beijing Administration Office of Laboratory Animals, and all of our experiments were operated at Veterinary Laboratory Biosafety Level 2. Special thanks to Advanced Throughput Inc. for their assistance with the chip experiments and data analysis.
Conflict of interest
None of the authors has a financial or personal relationship with other people or organizations that could inappropriately influence or bias the content of this paper.
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