Food Animal Health Research Program, Ohio Agricultural Research and Development Center, The Ohio State University, 1680 Madison Avenue, Wooster, OH 44691, USA.
Vet Res. 2011 Jul 12;42(1):85. doi: 10.1186/1297-9716-42-85.
Infectious bursal disease (IBD) is an important immunosuppressive disease of chickens. The causative agent, infectious bursal disease virus (IBDV), consists of two serotypes, 1 and 2. Serotype 1 consists of classic IBDV (cIBDV) and variant IBDV (vIBDV). Both of these strains vary in antigenicity and pathogenesis. The goal of this study was to compare the immunopathogenesis of cIBDV and vIBDV. Three-week-old specific pathogen free chickens were inoculated intraocularly with standard challenge strain (STC) (cIBDV) and a variant strain Indiana (IN) (vIBDV). The cIBDV produced more pronounced bursal damage, inflammatory response and infiltration of T cells as compared to vIBDV. There were significant differences in the expression of innate (IFN-α and IFN-β), proinflammatory cytokine and mediator (IL-6 and iNOS) in cIBDV- and vIBDV-infected bursas. The expression of chemokines genes, IL-8 and MIP-α was also higher in cIBDV-infected chickens during the early phase of infection. The expression of Toll like receptor 3 (TLR3) was downregulated at post inoculation days (PIDs) 3, 5, and 7 in the bursas of vIBDV-infected chickens whereas TLR3 was upregulated at PIDs 3 and 5 in cIBDV-infected bursas. In vIBDV-infected bursa, TLR7 expression was downregulated at PIDs 3 and 5 and upregulated at PID 7. However, TLR7 was upregulated at PIDs 3 and 7 in cIBDV-infected bursas. The expression of MyD88 was downregulated whereas TRIF gene expression was upregulated in cIBDV- and vIBDV-infected bursa. These findings demonstrate the critical differences in bursal lesions, infiltration of T cells, expression of cytokines, chemokines and TLRs in the bursa of cIBDV-and vIBDV-infected chickens.
传染性法氏囊病（IBD）是一种重要的鸡免疫抑制性疾病。病原体传染性法氏囊病病毒（IBDV）由两个血清型 1 和 2 组成。血清型 1 包括经典传染性法氏囊病病毒（cIBDV）和变异传染性法氏囊病病毒（vIBDV）。这两种毒株在抗原性和发病机制上有所不同。本研究的目的是比较 cIBDV 和 vIBDV 的免疫发病机制。将 3 周龄无特定病原体鸡通过眼内接种标准攻毒株（STC）（cIBDV）和变异株印第安纳（IN）（vIBDV）进行接种。与 vIBDV 相比，cIBDV 导致更明显的法氏囊损伤、炎症反应和 T 细胞浸润。在 cIBDV 和 vIBDV 感染的法氏囊中，先天（IFN-α 和 IFN-β）、促炎细胞因子和介质（IL-6 和 iNOS）的表达存在显著差异。趋化因子基因 IL-8 和 MIP-α 的表达在感染早期也在 cIBDV 感染的鸡中更高。在 vIBDV 感染的法氏囊中，Toll 样受体 3（TLR3）的表达在接种后第 3、5 和 7 天（PID）下调，而在 cIBDV 感染的法氏囊中 TLR3 在 PID 第 3 和 5 天上调。在 vIBDV 感染的法氏囊中，TLR7 的表达在 PID 第 3 和 5 天下调，在 PID 第 7 天上调。然而，在 cIBDV 感染的法氏囊中，TLR7 在 PID 第 3 和 7 天上调。MyD88 的表达下调，而 TRIF 基因的表达在 cIBDV 和 vIBDV 感染的法氏囊中上调。这些发现表明，cIBDV 和 vIBDV 感染的鸡法氏囊的法氏囊病变、T 细胞浸润、细胞因子、趋化因子和 TLR 的表达存在显著差异。
