Galdiero Massimiliano, Vitiello Mariateresa, Sanzari Emma, D'Isanto Marina, Tortora Annalisa, Longanella Anna, Galdiero Stefania
Istituto di Microbiologia, Facoltà di Medicina e Chirurgia, Seconda Università degli Studi di Napoli, 80138 Naples, Italy.
Infect Immun. 2002 Feb;70(2):558-68. doi: 10.1128/IAI.70.2.558-568.2002.
In this study we examined the ability of Salmonella enterica serovar Typhimurium porins to activate activating protein 1 (AP-1) and nuclear factor kappaB (NF-kappaB) through the mitogen-activated protein kinase (MAPK) cascade, and we identified the AP-1-induced protein subunits. Our results demonstrate that these enzymes may participate in cell signaling pathways leading to AP-1 and NF-kappaB activation following porin stimulation of cells. Raf-1 was phosphorylated in response to the treatment of U937 cells with porins; moreover, the porin-mediated increase in Raf-1 phosphorylation is accompanied by the phosphorylation of MAPK kinase 1/2 (MEK1/2), p38, extracellular-signal-regulated kinase 1/2, and c-Jun N-terminal kinase. We used three different inhibitors of phosphorylation pathways: 2'-amino-3'-methoxyflavone (PD-098059), a selective inhibitor of MEK1 activator and the MAPK cascade; 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)1H-imidazole (SB203580), a specific inhibitor of the p38 pathway; and 7beta-acetoxy-1alpha,6beta,9alpha-trihydroxy-8,13-epoxy-labd-14-en-11-one (forskolin), an inhibitor at the level of Raf-1 kinase. PD-098059 pretreatment of cells decreases AP-1 and NF-kappaB activation by lipopolysaccharide (LPS) but not by porins, and SB203580 pretreatment of cells decreases mainly AP-1 and NF-kappaB activation by porins; in contrast, forskolin pretreatment of cells does not affect AP-1 and NF-kappaB activation following either porin or LPS stimulation. Our data suggest that the p38 signaling pathway mainly regulates AP-1 and NF-kappaB activation in cells treated with S. enterica serovar Typhimurium porins. Antibody electrophoretic mobility shift assays showed that JunD and c-Fos binding is found in cells treated with porins, in cells treated with LPS, and in unstimulated cells. However, by 30 to 60 min of stimulation, a different complex including c-Jun appears in cells treated with porins or LPS, while the Fra-2 subunit is present only after porin stimulation. These data suggest different molecular mechanisms of activation induced by porins or by LPS.
在本研究中,我们检测了鼠伤寒沙门氏菌孔蛋白通过丝裂原活化蛋白激酶(MAPK)级联反应激活活化蛋白1(AP-1)和核因子κB(NF-κB)的能力,并鉴定了AP-1诱导的蛋白质亚基。我们的结果表明,这些酶可能参与细胞信号通路,在孔蛋白刺激细胞后导致AP-1和NF-κB活化。用孔蛋白处理U937细胞后,Raf-1发生磷酸化;此外,孔蛋白介导的Raf-1磷酸化增加伴随着MAPK激酶1/2(MEK1/2)、p38、细胞外信号调节激酶1/2和c-Jun氨基末端激酶的磷酸化。我们使用了三种不同的磷酸化途径抑制剂:2'-氨基-3'-甲氧基黄酮(PD-098059),一种MEK1激活剂和MAPK级联反应的选择性抑制剂;4-(4-氟苯基)-2-(4-甲亚磺酰基苯基)-5-(4-吡啶基)-1H-咪唑(SB203580),p38途径的特异性抑制剂;以及7β-乙酰氧基-1α,6β,9α-三羟基-8,13-环氧-labd-14-烯-11-酮(福斯可林),一种Raf-1激酶水平的抑制剂。用PD-098059预处理细胞可降低脂多糖(LPS)诱导的AP-1和NF-κB活化,但不影响孔蛋白诱导的活化;用SB203580预处理细胞主要降低孔蛋白诱导的AP-1和NF-κB活化;相反,用福斯可林预处理细胞不影响孔蛋白或LPS刺激后AP-1和NF-κB的活化。我们的数据表明,p38信号通路主要调节鼠伤寒沙门氏菌孔蛋白处理的细胞中AP-1和NF-κB的活化。抗体电泳迁移率变动分析表明,在用孔蛋白处理的细胞、用LPS处理 的细胞以及未刺激的细胞中均发现JunD和c-Fos结合。然而,在刺激30至60分钟后,在用孔蛋白或LPS处理的细胞中出现了一种不同的复合物,包括c-Jun,而Fra-2亚基仅在孔蛋白刺激后出现。这些数据表明孔蛋白或LPS诱导活化的分子机制不同。