Control of the oxidative burst of human neutrophils by staphylococcal leukotoxins
Control of the oxidative burst of human neutrophils by staphylococcal leukotoxins
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DOI：
10.1128/iai.71.7.3724-3729.2003
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发表时间：
2003-07-01
影响因子：
3.1
通讯作者：
Monteil, H
中科院分区：
文献类型：
--
作者：
Colin, DA;Monteil, H
用荧光分光光度法或流式细胞术研究了葡萄球菌双组分白细胞毒素诱导氧化爆发和/或引发人多形核白细胞（PMNs）的能力。在亚裂解浓度下，白细胞毒素的HlgA-HlgB、HlgA-LukF-PV、LukS-PV-LukF-PV和HlgC-LukF-PV组合，而不是LukS-PV-HlgB和HlgC-HlgB组合，能够诱导H2 O2产生，类似于1 μ M N-甲酰基-Met-Leu-Phe（fMLP）诱导的H2 O2产生。此外，当以亚溶解浓度加入时，所有的白细胞毒素组合都引发了由fMLP诱导的H2 O2产生的PMNs。白细胞毒素的激活依赖于Ca 2+的存在，并抑制渥曼青霉素，磷脂酰肌醇3-激酶的抑制剂，但不是由N-甲基-L-精氨酸，一氧化氮生成的抑制剂，这消除了可能性，NO发挥作用的白细胞毒素的行动。在较高的浓度下，所有的leukotoxins抑制H2 O2的生产由PMNs激活的fMLP，佛波醇12-肉豆蔻酸酯13-乙酸酯（PMA），或leukotoxins本身。这种抑制作用与白细胞毒素诱导的孔形成无关。由fMLP和PMA诱导的细胞内H2 O2释放不被白细胞毒素引发，但被抑制。似乎白细胞毒素抑制H2 O2释放是独立的孔形成，但继发于细胞内的事件，迄今未知，由白细胞毒素触发。
The ability of staphylococcal two-component leukotoxins to induce an oxidative burst and/or to prime human polymorphonuclear cells (PMNs) was studied by using spectrofluorometry or flow cytometry. At sublytic concentrations, the HlgA-HlgB, HlgA-LukF-PV, LukS-PV-LukF-PV, and HlgC-LukF-PV combinations of leukotoxins, but not the LukS-PV-HlgB and HlgC-HlgB combinations, were able to induce H2O2 production similar to the H2O2 production induced by 1 muM N-formyl-Met-Leu-Phe (fMLP). In addition, when added at sublytic concentrations, all of the leukotoxin combinations primed PMNs for H2O2 production induced by fMLP. Leukotoxin activation was dependent on the presence of Ca2+ and was inhibited by wortmannin, an inhibitor of phosphatidylinositol 3-kinase, but not by N-methyl-L-arginine, an inhibitor of NO generation, which eliminates the possibility that NO plays a role in the action of leukotoxins. At higher concentrations, all leukotoxins inhibited H2O2 production by PMNs activated by fMLP, phorbol 12-myristate 13-acetate (PMA), or the leukotoxins themselves. This inhibition was not related to the pore formation induced by leukotoxins. Intracellular release of H2O2 induced by fMLP and PMA was not primed by leukotoxins but was inhibited. It seems that leukotoxin inhibition of H2O2 release is independent of pore formation but secondary to an intracellular event, as yet unknown, triggered by leukotoxins.