Richards I M, Griffin R L, Oostveen J A, Morris J, Wishka D G, Dunn C J
Hypersensitivity Diseases Research, Upjohn Company, Kalamazoo, Michigan 49001.
Am Rev Respir Dis. 1989 Dec;140(6):1712-6. doi: 10.1164/ajrccm/140.6.1712.
The selective leukotriene B4 (LTB4) antagonist, U-75302, 6-(6-(3-hydroxy-1E,5Z-undecadien-1-yl)-2-pyridinyl)-1,5-hexa nediol) was examined for its ability to inhibit the "late-phase" bronchopulmonary eosinophilia that occurs 6 to 24 h after inhalation of specific antigen in sensitized guinea pigs. Groups of 6 male guinea pigs, sensitized with ovalbumin, were pretreated with U-75302, 1.0, 10.0, or 30.0 mg/kg, or vehicle 1 h before and 7 h after antigen inhalation. Twenty-four hours after antigen provocation, the lungs were lavaged for the enumeration of inflammatory cell populations. Doses of U-75302 (1.0, 10.0 and 30.0 mg/kg) administered orally produced 12.2%, (p greater than 0.05), 43.2% (p less than 0.05), and 61.1% (p less than 0.05) inhibition, respectively, of the antigen-induced influx of eosinophils into the bronchial lumen. Neutrophil populations were not significantly affected by treatment with U-75302. In a separate study, we compared the histopathological changes that occurred following antigen challenge in U-75302-treated or vehicle-treated guinea pigs. Vehicle-treated, sensitized animals exhibited marked changes in the airway at 8 min, 6 h, and 24 h after antigen challenge. U-75302 treatment produced a significant reduction in eosinophil adherence to peribronchial/peribronchiolar capillaries followed by a dramatic and specific reduction of peribronchial eosinophil infiltration (81% reduction at 6 h and 79% reduction at 24 h). Neutrophil migration appeared unaffected. These data implicate LTB4 as a mediator of antigen-induced bronchopulmonary eosinophilia in the guinea pig.
研究了选择性白三烯B4(LTB4)拮抗剂U-75302(6-(6-(3-羟基-1E,5Z-十一碳二烯-1-基)-2-吡啶基)-1,5-己二醇)抑制致敏豚鼠吸入特异性抗原后6至24小时出现的“迟发性”支气管肺嗜酸性粒细胞增多的能力。将6只经卵清蛋白致敏的雄性豚鼠分为几组,在抗原吸入前1小时和吸入后7小时,分别用1.0、10.0或30.0mg/kg的U-75302或赋形剂进行预处理。抗原激发24小时后,对肺进行灌洗以计数炎症细胞群体。口服给予U-75302的剂量(1.0、10.0和30.0mg/kg)分别对抗原诱导的嗜酸性粒细胞流入支气管腔产生12.2%(p>0.05)、43.2%(p<0.05)和61.1%(p<0.05)的抑制作用。中性粒细胞群体未受到U-75302治疗的显著影响。在另一项研究中,我们比较了U-75302治疗组或赋形剂治疗组豚鼠抗原激发后发生的组织病理学变化。用赋形剂治疗的致敏动物在抗原激发后8分钟、6小时和24小时气道出现明显变化。U-75302治疗使嗜酸性粒细胞对支气管周围/细支气管周围毛细血管的黏附显著减少,随后支气管周围嗜酸性粒细胞浸润显著且特异性减少(6小时减少81%,24小时减少79%)。中性粒细胞迁移似乎未受影响。这些数据表明LTB4是豚鼠抗原诱导的支气管肺嗜酸性粒细胞增多的介质。