Calander Ann-Marie, Starckx Sofie, Opdenakker Ghislain, Bergin Philip, Quiding-Järbrink Marianne, Tarkowski Andrej
Department of Rheumatology and Inflammation Research, University of Gothenburg, Guldhedsgatan 10A, S-413 46 Gothenburg, Sweden.
Microbes Infect. 2006 May;8(6):1434-9. doi: 10.1016/j.micinf.2006.01.001. Epub 2006 Mar 29.
Matrix metalloproteinases constitute a family of structurally related endopeptidases that are crucial for the normal turnover of the extracellular matrix. Elevated levels of MMP-9 have been demonstrated in synovial fluids of rheumatoid arthritis patients, and a correlation with the severity of the disease has been described. The aim of this study was to explore the impact of MMP-9 expression on joint inflammation and destruction in a model of bacterially induced septic arthritis. MMP-9 knock-out mice and C57Bl6 congenic controls were inoculated intravenously or intra-articularly with Staphylococcus aureus. Arthritis was evaluated clinically and by means of histology. Zymographic analyses were performed to study ex vivo induction of MMP-9 following exposure to S. aureus. The MMP-9 knock-out mice displayed a significantly higher frequency and severity, but not destructivity, of arthritis than did the wild-type mice. The knock-out mice also proved to harbour an increased number of bacteria locally in joints and systemically in kidneys, possibly by impaired extravasation and recruitment of leukocytes and a deficient early defence against infection. Our findings indicate that deficiency in MMP-9 increases the degree of joint inflammation due to decreased bacterial clearance.
基质金属蛋白酶构成了一类结构相关的内肽酶家族,对细胞外基质的正常更新至关重要。类风湿性关节炎患者的滑液中已证实MMP - 9水平升高,且已描述其与疾病严重程度相关。本研究的目的是在细菌诱导的脓毒性关节炎模型中探讨MMP - 9表达对关节炎症和破坏的影响。将MMP - 9基因敲除小鼠和C57Bl6同基因对照小鼠通过静脉或关节内接种金黄色葡萄球菌。通过临床和组织学方法评估关节炎。进行酶谱分析以研究暴露于金黄色葡萄球菌后MMP - 9的体外诱导情况。与野生型小鼠相比,MMP - 9基因敲除小鼠的关节炎发生率和严重程度显著更高,但关节破坏程度无差异。基因敲除小鼠还被证明在关节局部和肾脏中全身携带的细菌数量增加,这可能是由于白细胞的渗出和募集受损以及早期抗感染防御不足所致。我们的研究结果表明,MMP - 9缺乏会因细菌清除减少而增加关节炎症程度。