Induction of macrophage parasiticidal activity by Staphylococcus aureus and exotoxins through the nitric oxide synthesis pathway.
Induction of macrophage parasiticidal activity by Staphylococcus aureus and exotoxins through the nitric oxide synthesis pathway.
复制标题
金黄色葡萄球菌和外毒素通过一氧化氮合成途径诱导巨噬细胞杀寄生虫活性。
作者：
F. Cunha;D. Moss;L. Leal;S. Moncada;F. Liew
在存在干扰素-γ (IFN-γ) 的情况下，用灭活的革兰氏阳性菌金黄色葡萄球菌或其膜成分体外刺激小鼠腹膜巨噬细胞，表达高水平的一氧化氮 (NO) 合酶，并以剂量依赖性方式产生大量 NO。这不是由于革兰氏阴性内毒素的污染，因为刺激活性不受添加多粘菌素B的影响。用中毒性休克综合征毒素-1(TSST)、脂磷壁酸(LTA)刺激或杀死整个金黄色葡萄球菌与IFN-γ一起刺激的巨噬细胞的NO合成酶的表达和NO的合成被糖皮质激素、地塞米松或NO合成的特异性抑制剂抑制， L-N-iminoethyl-ornithine (L-NIO).外毒素与 IFN-γ 一起还激活巨噬细胞以杀死细胞内寄生虫大型利什曼原虫。 L-NIO 完全抑制杀利什曼病活性。
Murine peritoneal macrophages stimulated in vitro with killed Gram-positive bacteria Staphylococcus aureus or its membrane components in the presence of interferon-gamma (IFN-gamma) expressed high levels of nitric oxide (NO) synthase and produced large amounts of NO in a dose-dependent manner. This is not due to the contamination by Gram-negative endotoxin because the stimulatory activity was not affected by the addition of polymyxin B. The expression of the NO synthase and the synthesis of NO by macrophages stimulated with toxic shock syndrome toxin-1 (TSST), lipoteichoic acid (LTA) or killed whole S. aureus together with IFN-gamma was inhibited by the glucocorticoid, dexamethasone or by the specific inhibitor of NO synthesis, L-N-iminoethyl-ornithine (L-NIO). The exotoxins together with IFN-gamma also activated macrophages to kill the intracellular parasite Leishmania major. The leishmanicidal activity was completely inhibited by L-NIO.