Al-Shujairi Wisam H, Clarke Jennifer N, Davies Lorena T, Alsharifi Mohammed, Pitson Stuart M, Carr Jillian M
Microbiology and Infectious Diseases, School of Medicine, Flinders University, Adelaide, South Australia, Australia.
Centre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia, Australia.
PLoS One. 2017 Jan 17;12(1):e0169814. doi: 10.1371/journal.pone.0169814. eCollection 2017.
We have previously reported that the absence of sphingosine kinase 1 (SK1) affects both dengue virus (DENV) infection and innate immune responses in vitro. Here we aimed to define SK1-dependancy of DENV-induced disease and the associated innate responses in vivo. The lack of a reliable mouse model with a fully competent interferon response for DENV infection is a challenge, and here we use an experimental model of DENV infection in the brain of immunocompetent mice. Intracranial injection of DENV-2 into C57BL/6 mice induced body weight loss and neurological symptoms which was associated with a high level of DENV RNA in the brain. Body weight loss and DENV RNA level tended to be greater in SK1-/- compared with wildtype (WT) mice. Brain infection with DENV-2 is associated with the induction of interferon-β (IFN-β) and IFN-stimulated gene (ISG) expression including viperin, Ifi27l2a, IRF7, and CXCL10 without any significant differences between WT and SK1-/- mice. The SK2 and sphingosine-1-phosphate (S1P) levels in the brain were unchanged by DENV infection or the lack of SK1. Histological analysis demonstrated the presence of a cellular infiltrate in DENV-infected brain with a significant increase in mRNA for CD8 but not CD4 suggesting this infiltrate is likely CD8+ but not CD4+ T-lymphocytes. This increase in T-cell infiltration was not affected by the lack of SK1. Overall, DENV-infection in the brain induces IFN and T-cell responses but does not influence the SK/S1P axis. In contrast to our observations in vitro, SK1 has no major influence on these responses following DENV-infection in the mouse brain.
我们之前曾报道,鞘氨醇激酶1(SK1)的缺失在体外会影响登革病毒(DENV)感染和先天免疫反应。在此,我们旨在确定DENV诱导疾病的SK1依赖性以及体内相关的先天反应。缺乏对DENV感染具有完全正常干扰素反应的可靠小鼠模型是一项挑战,在此我们使用免疫活性小鼠脑内DENV感染的实验模型。将DENV-2颅内注射到C57BL/6小鼠中会导致体重减轻和神经症状,这与脑中高水平的DENV RNA相关。与野生型(WT)小鼠相比,SK1基因敲除小鼠的体重减轻和DENV RNA水平往往更高。DENV-2脑感染与干扰素-β(IFN-β)和干扰素刺激基因(ISG)表达的诱导有关,包括viperin、Ifi27l2a、IRF7和CXCL10,WT小鼠和SK1基因敲除小鼠之间没有任何显著差异。DENV感染或SK1的缺失不会改变脑中SK2和1-磷酸鞘氨醇(S1P)的水平。组织学分析表明,DENV感染的脑中存在细胞浸润,CD8的mRNA显著增加,但CD4的mRNA没有增加,这表明这种浸润可能是CD8+而非CD4+ T淋巴细胞。T细胞浸润的增加不受SK1缺失的影响。总体而言,脑内DENV感染会诱导IFN和T细胞反应,但不会影响SK/S1P轴。与我们在体外的观察结果相反,SK1对小鼠脑内DENV感染后的这些反应没有重大影响。