摘要
目的研究肺炎链球菌表面暴露的毒性表面蛋白C(PspC)促进IL-8分泌的可能机制。方法使用炎症相关的信号分子NF-κB,p38MARK,ERK,JNK的抑制剂预处理人嗜中性粒细胞后,观察PspC对IL-8分泌的影响。从受PspC刺激的人嗜中性粒细胞中分别提取细胞总蛋白和细胞核提取物,用ELISA法测定p38MAPK蛋白的活力和NF-κB的浓度,并且采用Western blot方法验证PspC对p38MAPK和IκB-α蛋白磷酸化水平的影响。结果使用NF-κB及p38MARK的抑制剂预处理人嗜中性粒细胞后,可以扭转PspC促中性粒细胞分泌IL-8的现象;而ERK和JNK的抑制剂无此效果。同时,PspC可以上调中性粒细胞中的P38MAPK蛋白的含量和NF-κB的浓度,也可以提高p38MAPK和NF-κB通路的抑制蛋白IκB-α蛋白磷酸化水平。结论肺炎链球菌PspC诱导人体中性粒细胞释放IL-8受p38MAPK和NF-κB途径的调控。
Interlen-8（IL-8） secreted by neutrophils is an important inflammatory factor.In preliminary experiments,we found that pneumococcal surface protein C（PspC） can promote neutrophil to secrete IL-8.Here,we aim to explore the mechanisms of PspC how to up-regulate chemokine IL-8 in human neutrophils.It was found that NF-κB and p38MARK inhibitors instead of ERK or JNK inhibitors could significantly suppress the release of IL-8 induced by PspC.PspC could also increase the activity of p38 MAPK and the concentration of NF-κB in the neutrophils.Meanwhile,the result of Western blot indicated that PspC could enhance the phosphorylation level of p38MAPK and IκB-α.Together,our results demonstrated that the induction of IL-8 in human neutrophils activated by PspC was regulated by p38 MAPK and NF-κB pathways.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2012年第12期1028-1031,共4页
Immunological Journal
