不同毒力传染性支气管炎病毒诱导SPF鸡炎症反应的免疫机制

Mechanisms of inflammatory responses to different virulence of infectious bronchitis virus infection in SPF chicken

以specific pathogen-free(SPF)鸡为研究对象,通过滴鼻点眼方式感染传染性支气管炎病毒(Infectious bronchitis virus,IBV)强毒株(CK/CH/LDL/140520)和IBV弱毒株(γCoV/ck/China/I0718/17)。分别在感染后12、36 h和3、7、14 d,采集法氏囊、脾脏、肾脏和气管,运用实时荧光定量PCR法,检测感染不同毒力IBV后,SPF鸡各脏器组织中免疫相关因子表达差异,初步探讨SPF鸡对不同毒力IBV免疫反应机制。结果表明,IBV弱毒株感染早期主要上调Toll样受体15(Toll-like receptors 15,TLR15)基因表达水平,提高白细胞介素(Interleukin,IL-1β)、IL-8基因表达量。法氏囊是介导启动获得性免疫反应的主要器官;脾脏是介导调控获得性免疫反应的主要器官,IBV强毒株在感染后期持续诱导提高TLR7、TLR15、TLR21基因和IL-6基因表达水平。可知,不同毒力IBV诱导SPF鸡炎症反应的免疫活化机制及介导调控获得性免疫反应的器官存在一定差异,为进一步揭示IBV强弱毒株致病性差异及诱导宿主不同免疫反应激活机理提供新的参考依据。

In this study,specific pathogen-free(SPF)chickens was infected with either IBV virulent strain CK/CH/LDL/140520(IBV virulent strain)or IBV attenuated strainγCoV/ck/China/I0718/17(IBV attenuated strain)by a combined intraocular and intranasal route.Bursa of fabricius,spleen,kidney and trachea were collected from each group at 12 h,36 h,3 day,7 day,and 14 days post infection(hpi or dpi).In order to evaluate immune response of SPF chickens to IBV infection,real-time quantitative PCR was used to detect immune-related factors in tissues.The results showed that the expression level of Toll-like receptors 15(TLR15)gene was mainly upregulated in the early stage of IBV attenuated strain infection,and the expression of Interleukin-1β(IL-1β)and IL-8 genes were also increased.Of these tissues investigated,bursa of fabricius was the main organ mediating the initiation of specific immunity response.IBV virulent strain continuously increased gene expressions of TLR7,TLR15,TLR21 and IL-6 in tissues at the late stage of infection.Spleen was the main organ mediating and regulating the specific immunity response.The study showed that there were some differences in the immune activation mechanism of different virulence IBVs inducing inflammatory response in SPF chicken and the organs mediating and regulating specific immunity response,which provided a new reference for further revealing the differences in pathogenicity of virulent and attenuated IBV strains and the activation mechanism of inducing different immunity responses in hosts.