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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。
Objective To investigate the possible mechanism by which surface-exposed toxic surface protein C (PspC) of Streptococcus pneumoniae promotes the secretion of IL-8. Methods The effect of PspC on the secretion of IL-8 was observed after pretreatment of human neutrophils with inhibitors of NF-κB, p38MARK, ERK and JNK. Cell total protein and nuclear extracts were extracted from PspC-stimulated human neutrophils, p38MAPK protein activity and NF-κB concentration were measured by ELISA, and p38MAPK and IκB-α Effect of protein phosphorylation level. Results Pretreatment of human neutrophils with inhibitors of NF-κB and p38MARK reversed the effect of PspC-induced neutrophils secreting IL-8, whereas ERK and JNK inhibitors did not. At the same time, PspC up-regulated the content of P38MAPK protein and the concentration of NF-κB in neutrophils, and also increased the phosphorylation of IκB-α, a protein of p38MAPK and NF-κB. Conclusion Streptococcus pneumoniae PspC induces the release of IL-8 from human neutrophils by the p38MAPK and NF-κB pathway.