CAJ | 학술논문

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灌人.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-κB p65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-κB p65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.
목적 탐토NF-κB신호통로단백화세포인자재금황색포도구균PV살백세포독소(PVL)개도적폐염증성손상중적변화화작용.방법 취30지신서란대백토수궤분위2조,매조각15지.rPVL조용중조PVL관입,정상대조조사용PBS관인.조모후,우3、6、9h처사토,매개시간단5지,취폐조직주병이학검사；ELISA방법검측폐조직균장IL-6、IL-8、IL-10、TNF-α단백함량；면역조직화학염색검측폐조직중NF-κB p65단백.결과 rPVL조토폐조직병리검사현시유미만성염성세포침윤、출혈、수종등폐손상표현；폐조직균장중IL-6、IL-8、TNF-α함량수감염시간연장축점승고,IL-10함량우9h개시승고；NF-κB p65단백활화강도수감염시간연장축점증강.결론 NF-κB신호통로단백격활급세포인자대량석방시PVL상관폐손상중요적발병궤제지일,하조폐내NF-κB격활세포수량유망성위치료PVL상관폐손상적도경.
Objective To explore the role of NF-κB 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 random from each group were killed at 3,6,or 9 h postinfection.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,hemorrhage,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 postinfection.The expression of NF-κB p65 protein was increased gradually with the infection time.Conclusion 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.