目的:检测细胞因子信号转导抑制因子1(suppressor of cytokine signaling-1,SOCS-1)和细胞因子信号转导抑制因子3(suppressor of cytokine signaling-3,SOCS-3)在慢性根尖周炎病损组织中的表达水平,探讨SOCS-1、3在慢性根尖周炎发病机...目的:检测细胞因子信号转导抑制因子1(suppressor of cytokine signaling-1,SOCS-1)和细胞因子信号转导抑制因子3(suppressor of cytokine signaling-3,SOCS-3)在慢性根尖周炎病损组织中的表达水平,探讨SOCS-1、3在慢性根尖周炎发病机制中的作用。方法:收集25例慢性根尖周炎病损组织作为病例组,16例健康牙的牙周膜组织作为对照组。对样本中的蛋白表达量采用免疫组织化学法检测,mRNA表达量采用实时定量PCR法检测。采用SPSS13.0软件包对数据进行统计学分析。结果:免疫组织化学结果显示,SOCS-1、3蛋白在慢性根尖周炎病损组织中的表达水平均显著高于对照组(P<0.01);重度炎症组中,SOCS-1、3的蛋白表达显著高于轻中度炎症组(P<0.01)。SOCS-1mRNA在轻中度炎症组、重度炎症组和对照组中的表达量分别为2.620±1.552、2.373±1.083和1.277±1.040,SOCS-3mRNA的表达量分别为9.308±5.901,7.565±3.233和1.232±1.099。SOCS-1、3 mRNA在轻中度炎症组、重度炎症组均显著高于对照组(P<0.01),但不同炎症组之间并无显著差异。结论:SOCS-1、3可能与慢性根尖周炎密切相关。展开更多
Some pathogens can use host suppressor of cytokine signaling I （SOCS-1）, an important negative-feedback molecule, as the main mode of immune evasion. Here we found that group A Streptococcus （GAS） is capable of in...Some pathogens can use host suppressor of cytokine signaling I （SOCS-1）, an important negative-feedback molecule, as the main mode of immune evasion. Here we found that group A Streptococcus （GAS） is capable of inducing SOCS-1 expression in RAW264.7 and BMDM macrophages. IFN-p plays a role in GAS-induced SOCS-1 expression in macrophages following the induction of cytokine expression by GAS, representing the classical pathway of SOCS-1 expression. However, GAS also induced STAT1 activation and SOCS-1 expression when GAS-infected cells were incubated with anti-IFN-p monoclonal antibody in this study. Moreover, upon comparing TLR4-/- BMDM macrophages with wild-type （WT） cells, we found that TLR4 also plays an essential role in the induction of SOCS-1. MyD88, which is an adaptor protein for TLR4, contributes to STAT1 activation and phosphorylation by forming a complex with Janus kinase 1 （JAK1） and signal transducer and activator of transcription 1 （STAT1） in macrophages. GAS-stimulated expression of STAT1 was severely impaired in MyD88-/- macrophages, whereas expression of JAK1 was unaffected, suggesting that MyD88 was involved in STAT1 expression and phosphorylation. Together, these data demonstrated that in addition to IFN-p signaling and MyD88 complex formation, JAK1 and STAT1 act in a novel pathway to directly induce SOCS-1 expression in GAS-infected macrophages, which may be more conducive to rapid bacterial infection.展开更多
文摘目的:检测细胞因子信号转导抑制因子1(suppressor of cytokine signaling-1,SOCS-1)和细胞因子信号转导抑制因子3(suppressor of cytokine signaling-3,SOCS-3)在慢性根尖周炎病损组织中的表达水平,探讨SOCS-1、3在慢性根尖周炎发病机制中的作用。方法:收集25例慢性根尖周炎病损组织作为病例组,16例健康牙的牙周膜组织作为对照组。对样本中的蛋白表达量采用免疫组织化学法检测,mRNA表达量采用实时定量PCR法检测。采用SPSS13.0软件包对数据进行统计学分析。结果:免疫组织化学结果显示,SOCS-1、3蛋白在慢性根尖周炎病损组织中的表达水平均显著高于对照组(P<0.01);重度炎症组中,SOCS-1、3的蛋白表达显著高于轻中度炎症组(P<0.01)。SOCS-1mRNA在轻中度炎症组、重度炎症组和对照组中的表达量分别为2.620±1.552、2.373±1.083和1.277±1.040,SOCS-3mRNA的表达量分别为9.308±5.901,7.565±3.233和1.232±1.099。SOCS-1、3 mRNA在轻中度炎症组、重度炎症组均显著高于对照组(P<0.01),但不同炎症组之间并无显著差异。结论:SOCS-1、3可能与慢性根尖周炎密切相关。
文摘Some pathogens can use host suppressor of cytokine signaling I （SOCS-1）, an important negative-feedback molecule, as the main mode of immune evasion. Here we found that group A Streptococcus （GAS） is capable of inducing SOCS-1 expression in RAW264.7 and BMDM macrophages. IFN-p plays a role in GAS-induced SOCS-1 expression in macrophages following the induction of cytokine expression by GAS, representing the classical pathway of SOCS-1 expression. However, GAS also induced STAT1 activation and SOCS-1 expression when GAS-infected cells were incubated with anti-IFN-p monoclonal antibody in this study. Moreover, upon comparing TLR4-/- BMDM macrophages with wild-type （WT） cells, we found that TLR4 also plays an essential role in the induction of SOCS-1. MyD88, which is an adaptor protein for TLR4, contributes to STAT1 activation and phosphorylation by forming a complex with Janus kinase 1 （JAK1） and signal transducer and activator of transcription 1 （STAT1） in macrophages. GAS-stimulated expression of STAT1 was severely impaired in MyD88-/- macrophages, whereas expression of JAK1 was unaffected, suggesting that MyD88 was involved in STAT1 expression and phosphorylation. Together, these data demonstrated that in addition to IFN-p signaling and MyD88 complex formation, JAK1 and STAT1 act in a novel pathway to directly induce SOCS-1 expression in GAS-infected macrophages, which may be more conducive to rapid bacterial infection.
