Elevated level of renal xanthine oxidase mRNA transcription after nephropathogenic infectious bronchitis virus infection in growing layers

Lin, Huayuan; Huang, Qiqi; Guo, Xiaoquan; Liu, Ping; Liu, Weilian; Zou, Yuelong; Zhu, Shuliang; Deng, Guangfu; Kuang, Jun; Zhang, Caiying; Cao, Huabin; Hu, Guoliang

In the present study, chickens in challenged groups sustained the highest levels of XOD mRNA transcript in kidneys at 8, 15 and 22 dpi (p ＜ 0.01). These results were correlated with the serum activity of XOD between infected and control groups. Previous studies demonstrated that XOD activity or gene transcription could be reinforced by hypoxia and pro-inflammatory cytokines in vitro. Poss et al. [24] showed that hypoxia exposure alone increased XOD activity, but that mRNA transcript levels remained normal in cultured bovine aortic endothelial cells. These results may have occurred because the bovine XOD gene lacks a hypoxia response element for hypoxia-inducible factor-1 [24] . However, Pfeffer et al. [23] demonstrated that cytokines including TNF, IFN-, IL-6, and IL-1 could induce increases in both XOD activity and mRNA transcript levels in bovine renal epithelial cells. Asasi et al. [4] demonstrated that the serum concentration of IFN- increased significantly after IBV infection. Furthermore, Okino et al. [21] showed that the highest relative expression of IL-6, IL-1, and IFN- was correlated with the degree of IBV infection. A previous study also revealed that NIBV infection could induce renal inflammatory responses [33] . Therefore, it is likely that the increase of XOD renal transcription and its serum activity was due to NIBV infection induced by the increase of pro-inflammatory cytokines. However, further study is needed to elucidate the specific mechanism responsible for the increase of XOD renal transcription and its serum activity induced by NBIV infection.