摘要
目的:研究PspA促人类单核细胞分泌炎性细胞因子和趋化因子的机制。方法:使用炎症相关的信号分子JNK、pI3K、JAK的抑制剂及NF-κB抑制蛋白IκB-α磷酸化的抑制剂预处理人类单核细胞后,观察PspA对细胞因子分泌作用的影响。然后利用流式细胞术和Western blot方法检测PspA对人单核细胞中各信号分子磷酸化水平的影响。结果:IκB-α或JNK的抑制剂预处理人类单核细胞后,可以抑制PspA促细胞分泌IL-6、IL-8、CCL2、CCL4、CCL5的现象;而ERK和JNK的抑制剂无此效果。流式细胞术和Western blot方法均证实PspA可以上调人类单核细胞中的IκB-α和JNK蛋白的磷酸化水平。结论:NF-κB和JNK通路参与肺炎链球菌PspA诱导人类单核细胞分泌炎性细胞因子和趋化因子的过程。
Objective：To indicate that the Streptococcus pneumococcal surface protein A （PspA） could promote human mono- cytes secreting IL-6, IL-8, CCL2,CCL4, CCL5 ;and to further explored its molecular mechanisms. Methods： The inhibitors of signaling molecules including ERK, p38MARK, pI3K and JAK was added into the medium of human monocytes respectively and their effects on the cytokines secretion induced by PspA were evaluated by ELISA assay. And then the phosphocylation levels of signaling molecule af- ter PspA added in the medium was detected by flow cytometry and Western blot. Results： ELISA assay manifests demonstrated that only the inhibitors of IKB-α and JNK could significantly suppress human monocytes secreting cytokines which was induced by PspA. And PspA could improve the phosphorylation level of IKB-c~ and JNK by flow cytometry and Western blot analysis. Conclusion： Human monocytes secreting cytokines induced by PspA is regulated by NF-KB and JNK pathway.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2014年第4期464-467,共4页
Chinese Journal of Immunology
关键词
肺炎链球菌
人类单核细胞
细胞因子
Streptococcus pneumoniae
Human monocytes
NF-KB
JNK
Cytokines
