Beck-Speier I, Dayal N, Maier K L
GSF-National Research Centre for Environment and Health, Institute for Inhalation Biology, Neuherberg/Munich, Germany.
J Biolumin Chemilumin. 1998 Mar-Apr;13(2):91-9. doi: 10.1002/(SICI)1099-1271(199803/04)13:2<91::AID-BIO476>3.0.CO;2-P.
Alveolar macrophages (AM) were studied for their capability to release mediators involved in modulation of neutrophil (PMN) functions. Initial responses were induced by sulphite. Supernatants obtained from canine, human and rat AM pre-treated with sulphite in concentrations of 0.1-2 mmol/L enhanced the respiratory burst of canine, human and rat PMN, measured by lucigenin-dependent chemiluminescence (CL). This PMN-stimulating activity exhibited platelet-activating factor (PAF)-like properties, as indicated by desensitization of the PAF receptor, inhibition with PAF antagonists WEB 2086 and CV 3988, and the kinetic CL response like PAF after chloroform extraction of supernatants inhibitable by PAF antagonist CV 3988. These results indicate that AM are triggered by sulphite to release mediators that activate the respiratory burst of PMN, primarily via the PAF receptor.
研究了肺泡巨噬细胞（AM）释放参与调节中性粒细胞（PMN）功能的介质的能力。初始反应由亚硫酸盐诱导。用浓度为0.1 - 2 mmol/L的亚硫酸盐预处理的犬、人和大鼠AM获得的上清液，通过基于光泽精的化学发光（CL）测量，增强了犬、人和大鼠PMN的呼吸爆发。这种PMN刺激活性表现出类似血小板活化因子（PAF）的特性，这通过PAF受体脱敏、PAF拮抗剂WEB 2086和CV 3988的抑制作用以及上清液经氯仿萃取后类似PAF的动力学CL反应（可被PAF拮抗剂CV 3988抑制）得以表明。这些结果表明，亚硫酸盐触发AM释放介质，主要通过PAF受体激活PMN的呼吸爆发。
