Cunha F Q, Moss D W, Leal L M, Moncada S, Liew F Y
Wellcome Research Laboratories, Beckenham, U.K.
Immunology. 1993 Apr;78(4):563-7.
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.
在γ干扰素（IFN-γ）存在的情况下，用杀死的革兰氏阳性菌金黄色葡萄球菌或其膜成分体外刺激的小鼠腹腔巨噬细胞表达高水平的一氧化氮（NO）合酶，并以剂量依赖的方式产生大量NO。这不是由于革兰氏阴性内毒素的污染，因为多粘菌素B的添加不影响刺激活性。糖皮质激素地塞米松或NO合成的特异性抑制剂L-N-亚氨基乙基鸟氨酸（L-NIO）可抑制用中毒性休克综合征毒素-1（TSST）、脂磷壁酸（LTA）或杀死的完整金黄色葡萄球菌与IFN-γ一起刺激的巨噬细胞中NO合酶的表达和NO的合成。外毒素与IFN-γ一起还激活巨噬细胞以杀死细胞内寄生虫硕大利什曼原虫。L-NIO完全抑制了杀利什曼原虫活性。
