NF—κB信号通路蛋白和细胞因子在金黄色葡萄球菌PV杀白细胞素相关肺炎症性损伤中的作用

The role of NF-κB signaling pathway protein and cytokines in Staphylococcus aureus Panton-Valen-fine leukocidin-induced lung inflammation and injury

目的探讨NF—κB信号通路蛋白和细胞因子在金黄色葡萄球菌PV杀白细胞毒素（PVL）介导的肺炎症性损伤中的变化和作用。方法取30只新西兰大白兔随机分为2组，每组各15只。rPVL组用重组PVL灌入，正常对照组使用PBS灌入。造模后，于3、6、9h处死兔，每个时间段5只，取肺组织做病理学检查；ELISA方法检测肺组织匀浆IL-6、IL-8、IL-10、TNF—α蛋白含量；免疫组织化学染色检测肺组织中NF—κBp65蛋白。结果rPVL组兔肺组织病理检查显示有弥漫性炎性细胞浸润、出血、水肿等肺损伤表现；肺组织匀浆中IL-6、IL-8、TNF—α含量随感染时间延长逐渐升高，IL-10含量于9h开始升高；NF-κBp65蛋白活化强度随感染时间延长逐渐增强。结论NF-κB信号通路蛋白激活及细胞因子大量释放是PVL相关肺损伤重要的发病机制之一，下调肺内NF-κB激活细胞数量有望成为治疗PVL相关肺损伤的途径。

Objective To explore the role of NF-KB signaling pathway protein and cytokines in Panton-Valentine leukocidin （PVL）-induced acute lung inflammation and injury. Methods Thirty rabbits were distributed randomly into two groups, each group had fifteen rabbits. Group rPVL were directly treated with endotracheal instillation of rPVL, normal control were treated with PBS. Then five rabbits chosen at ran- dom from each group were killed at 3, 6, or 9 h postinfeetion. The lung was removed from the rabbits to determine histopathology studies. ELISA was performed to evaluate levels of IL-6, IL-8, IL-10 and TNF-α. NF-κB p65 protein of the lung tissue was assessed by immunohistochemistry method. Results In group rPVL histopathology study showed symptoms of severe illness： diffuse infiltration of inflammatory cells, hem-orrhage, edema and other manifestations of lung injury. Levels of IL-6, IL-8 and TNF-α were increased gradually, and the level of IL-10 was increased at 9 h postinfeetion. The expression of NF-κB p65 protein was increased gradually with the infection time. Condusion NF-κB activation and cytokines release play an important role in PVL-related lung injury. It may be an important path to down regulate the counts of NF-κB activation.