Author: Khan, Samiullah; Roberts, Juliet; Wu, Shu-Biao
Title: Regulation of Immunity-Related Genes by Infectious Bronchitis Virus Challenge in Spleen of Laying Chickens. Cord-id: 63w0n6mc Document date: 2020_1_27
ID: 63w0n6mc
Snippet: Understanding of host pathogen interactions is important in planning strategies for effective control of the pathogen. The present study investigated the regulation of genes involved in the activation of splenic immune system in mature laying chickens challenged with T strain of infectious bronchitis virus (IBV). Among all the genes studied, the relative expression levels of Fas cell surface death receptor (FAS), interleukin 7 (IL7), IL18, proteasome subunit alpha 3 (PSMA3), major histocompatibi
Document: Understanding of host pathogen interactions is important in planning strategies for effective control of the pathogen. The present study investigated the regulation of genes involved in the activation of splenic immune system in mature laying chickens challenged with T strain of infectious bronchitis virus (IBV). Among all the genes studied, the relative expression levels of Fas cell surface death receptor (FAS), interleukin 7 (IL7), IL18, proteasome subunit alpha 3 (PSMA3), major histocompatibility complex, class II (MHCII), interferon alpha (IFNα), immunoglobulin A (IgA), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) were significantly (p < 0.05) upregulated, while Toll-like receptor 7 (TLR7) and TLR5 were significantly downregulated in the challenge compared with the control group. Genes such as vascular cell adhesion molecule 1 (VCAM1), FK506-binding protein 1B (FKBP1B), transforming growth factor-beta 3 (TGFB3), NLR family pyrin domain containing 3 (NLRP3), TYRO3 protein tyrosine kinase (TYRO3), TNF receptor-associated factor 3 (TRAF3), C-X-C motif chemokine receptor 4 (CXCR4), macrophage inflammatory protein-3 (MIP3A), TLR2-1, TLR3, and TLR21 were not altered in mRNA expression levels between the challenge and control groups. In conclusion, the splenic immune response to IBV infection involved the regulation of cytokines, TLRs and NF-κB.
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