Zhao Y X, Ljungdahl A, Olsson T, Tarkowski A
University of Göteborg, Sweden.
Arthritis Rheum. 1996 Jun;39(6):959-67. doi: 10.1002/art.1780390613.
To investigate patterns of synovial and systemic cytokine messenger RNA (mRNA) expression in mice with superantigen-mediated Staphylococcus aureus arthritis.
Mice were inoculated intravenously with 1 x 10(7) colony-forming units of toxic shock syndrome toxin-1-producing S aureus LS-1. Synovial tissues and spleens were obtained at varying time intervals after bacterial inoculation, and examined for mRNA expression of interleukin-1beta (IL-1beta), IL-4, IL-10, IL-12, tumor necrosis factor alpha (TNFalpha), TNFbeta, interferon-gamma (IFN-gamma), transforming growth factor beta, and perforin, by an in situ hybridization technique.
In situ hybridization revealed early synovial up-regulation of TNFalpha and IL-1 beta mRNA expression. Peak frequencies of these proinflammatory cytokines were observed at the second and third week of the infection. Expression of T cell-derived cytokine mRNAs was detected later, and in a relatively low frequency. Notably, induction and peak numbers of Th2 cytokine (IL-4 and IL-10) mRNA expression preceded Th1 cytokine (IFNgamma and TNFbeta) mRNAs. In comparison with synovial tissues, peak spleen cytokine mRNA expression of IL-1beta, TNFalpha, TNFbeta, IL-12, and IFNgamma occurred earlier, but displayed a clearly lower magnitude of expression.
These findings demonstrate synovial and systemic up-regulation of cytokine mRNA expression during S aureus arthritis, indicating that both monocyte/macrophage and T cell-derived products are involved in the pathogenesis of this disease.
研究超抗原介导的金黄色葡萄球菌关节炎小鼠滑膜和全身细胞因子信使核糖核酸(mRNA)的表达模式。
给小鼠静脉注射1×10⁷个产中毒性休克综合征毒素-1的金黄色葡萄球菌LS-1菌落形成单位。在细菌接种后的不同时间间隔获取滑膜组织和脾脏,采用原位杂交技术检测白细胞介素-1β(IL-1β)、IL-4、IL-10、IL-12、肿瘤坏死因子α(TNFα)、TNFβ、干扰素-γ(IFN-γ)、转化生长因子β和穿孔素的mRNA表达。
原位杂交显示滑膜中TNFα和IL-1β mRNA表达早期上调。这些促炎细胞因子的峰值频率在感染的第二和第三周观察到。T细胞衍生的细胞因子mRNA表达检测较晚,且频率相对较低。值得注意的是,Th2细胞因子(IL-4和IL-10)mRNA表达的诱导和峰值数量先于Th1细胞因子(IFNγ和TNFβ)mRNA。与滑膜组织相比,脾脏中IL-1β、TNFα、TNFβ、IL-12和IFNγ的细胞因子mRNA峰值表达出现得更早,但表达量明显较低。
这些发现表明金黄色葡萄球菌关节炎期间滑膜和全身细胞因子mRNA表达上调,表明单核细胞/巨噬细胞和T细胞衍生产物均参与了该疾病的发病机制。