Beck-Speier I, Dayal N, Denzlinger C, Haberl C, Maier K L
GSF-National Research Center for Environment and Health, Institute for Inhalation Biology, Neuherberg/München, Germany.
Z Naturforsch C J Biosci. 1998 Mar-Apr;53(3-4):264-72. doi: 10.1515/znc-1998-3-417.
Air pollutants are supposed to modulate physiological responses of alveolar macrophages (AM). This study was addressed to the question whether at neutral pH sulfur(IV) species in comparison to sulfur(VI) species cause AM to release proinflammatory mediators and which pathways are involved in their generation. Supernatants obtained from canine AM treated with sulfite (0.1 mM to 2 mM) enhanced the respiratory burst of canine neutrophils, measured by lucigenin-dependent chemiluminescence, whereas supernatants derived from AM treated with sulfite (1 mM) did not. The neutrophil-stimulating activity released by sulfite-treated AM consisted of platelet-activating factor (PAF) and leukotriene B4 (LTB4) as shown by desensitization of the corresponding receptors. Inhibitors of phospholipase A2 substantially suppressed release of neutrophil-stimulating activity by sulfite-treated AM. Inhibition of 5-lipoxygenase in sulfite-treated AM also reduced neutrophil-stimulating activity, while inhibition of cyclooxygenase had no effect. In conclusion, sulfite induces AM to release lipid mediators via phospholipase A2- and 5-lipoxygenase-dependent pathways. These mediators activate neutrophils via the receptors for PAF and LTB4.
空气污染物理应会调节肺泡巨噬细胞（AM）的生理反应。本研究旨在探讨在中性pH条件下，与硫（VI）化合物相比，硫（IV）化合物是否会导致AM释放促炎介质，以及其产生涉及哪些途径。用亚硫酸盐（0.1 mM至2 mM）处理犬类AM后获得的上清液，通过基于光泽精的化学发光法测定，增强了犬类中性粒细胞的呼吸爆发，而用亚硫酸盐（1 mM）处理的AM的上清液则没有。如相应受体脱敏所示，亚硫酸盐处理的AM释放的中性粒细胞刺激活性由血小板活化因子（PAF）和白三烯B4（LTB4）组成。磷脂酶A2抑制剂显著抑制了亚硫酸盐处理的AM释放中性粒细胞刺激活性。在亚硫酸盐处理的AM中抑制5-脂氧合酶也降低了中性粒细胞刺激活性，而抑制环氧化酶则没有效果。总之，亚硫酸盐通过磷脂酶A2和5-脂氧合酶依赖性途径诱导AM释放脂质介质。这些介质通过PAF和LTB4受体激活中性粒细胞。
