Noonan T C, Gundel R H, Desai S N, Stearns C, Barton R W, Rothlein R, Letts L G, Piper P J
Boehringer Ingelheim Pharmaceuticals Inc., Ridgefield, CT 06877.
Agents Actions. 1991 Sep;34(1-2):211-3. doi: 10.1007/BF01993282.
Aerosol ovalbumin challenge (OA) of sensitized guinea pigs induced airway hyperreactivity (AH) to i.v. acetylcholine (Ach) and serotonin (5-HT) 24 hr post OA. Bronchoalveolar lavage fluid 24 hrs after OA showed increased leukocytes compared to unsensitized unchallenged animals. Treatment with monoclonal antibody R15.7 (3 mg/kg i.v.,) 1 hr prior and 4 hours after OA prevented the induction of AH to Ach but not to 5-HT and reduced influx of leukocytes. We conclude: 1) antigen inhalation induces an increase in AH with an increase in proinflammatory cell influx and 2) treatment with anti-CD18 antibody inhibits cell influx and airway hyperreactivity.
对致敏豚鼠进行雾化卵清蛋白激发试验（OA），在激发后24小时可诱导气道对静脉注射乙酰胆碱（Ach）和5-羟色胺（5-HT）产生高反应性（AH）。与未致敏且未激发的动物相比，OA后24小时支气管肺泡灌洗液中的白细胞增多。在OA前1小时和后4小时静脉注射单克隆抗体R15.7（3mg/kg）可预防对Ach产生AH，但不能预防对5-HT产生AH，并减少白细胞流入。我们得出结论：1）抗原吸入可诱导AH增加，同时促炎细胞流入增加；2）用抗CD18抗体治疗可抑制细胞流入和气道高反应性。
