The effects of an inhaled corticosteroid on oxygen radical production by bronchoalveolar cells after allergen or ozone in dogs

Wil H.M. Stevens , Ellinor Ädelroth , Mark J. Woolley , Jennifer Wattie , Magnus Dahlbäck , Paul M. O'Byrne
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引用次数: 9

Abstract

Both ozone and allergen inhalation increase the capacity to produce oxygen radicals by bronchoalveolar lavage cells in dogs. The purpose of these studies was to determine whether inhaled corticosteroids inhibits these increases in oxygen radical production from bronchoalveolar lavage cells. Six random source dogs were studied after dry air or ozone inhalation (3 ppm, 30 min). Seven random source dogs were studied after diluent or allergen inhalation. The dogs inhaled budesonide (2.74 mg/day) or lactose powder, twice daily for 7 days before ozone and allergen. 90 min after ozone or dry air, and 24 h after Ascaris suum or diluent a bronchoalveolar lavage was carried out. Spontaneous luminol-enhanced chemiluminescence was measured from bronchoalveolar lavage cells (4 × 106 cells) for 10 min, followed by a measurement of phorbol myristate acetate (PMA 2.4 μmol/I) stimulated chemiluminescence for 10 min. Both ozone and allergen inhalation caused an increase in PMA stimulated chemiluminescence (P < 0.05). Budesonide pretreatment inhibited ozone-induced (P < 0.008), but not allergen-induced PMA stimulated chemiluminescence (P > 0.90). Both ozone and allergen inhalation caused an increase in the bronchoalveolar lavage neutrophils. Budesonide pretreatment significantly inhibited the ozone-induced (P = 0.007), but not the ascaris-induced neutrophil influx (P = 0.93). These results demonstrate that ozone, but not allergen, stimulated oxygen radical release and neutrophil influx are attenuated by inhaled corticosteroids. This suggests that luminol-enhanced chemiluminescence from bronchoalveolar lavage cells measures oxygen radicals derived from neutrophils, and that ozone-and allergen-induced bronchoalveolar lavage neutrophilia are caused by different mechanisms.

吸入皮质类固醇对犬过敏原或臭氧后支气管肺泡细胞产生氧自由基的影响
吸入臭氧和过敏原均可增加狗支气管肺泡灌洗细胞产生氧自由基的能力。这些研究的目的是确定吸入皮质类固醇是否抑制支气管肺泡灌洗细胞产生氧自由基的增加。随机选取6只源犬,在吸入干燥空气或臭氧(3ppm, 30 min)后进行研究。随机选取7只源犬,在吸入稀释剂或过敏原后进行研究。狗吸入布地奈德(2.74 mg/d)或乳糖粉,每天两次,连续7天,然后再吸入臭氧和过敏原。使用臭氧或干燥空气后90 min,使用蛔虫泡或稀释剂后24 h进行支气管肺泡灌洗。在支气管肺泡灌洗细胞(4 × 106个细胞)中测量自发鲁米诺增强的化学发光10 min,然后测量肉豆酸酯磷(PMA 2.4 μmol/I)刺激的化学发光10 min。吸入臭氧和过敏原均引起PMA刺激的化学发光增加(P <0.05)。布地奈德预处理抑制臭氧诱导(P <0.008),但没有过敏原诱导的PMA刺激的化学发光(P >0.90)。臭氧和过敏原吸入均引起支气管肺泡灌洗液中性粒细胞增加。布地奈德预处理对臭氧诱导的中性粒细胞内流有显著抑制作用(P = 0.007),对蛔虫诱导的中性粒细胞内流无显著抑制作用(P = 0.93)。这些结果表明,臭氧,而不是过敏原,刺激的氧自由基释放和中性粒细胞内流被吸入皮质类固醇减弱。这表明,支气管肺泡灌洗细胞鲁米诺增强的化学发光测量了中性粒细胞产生的氧自由基,臭氧和过敏原诱导的支气管肺泡灌洗中性粒细胞是由不同的机制引起的。
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