Bascom R, Wachs M, Naclerio R M, Pipkorn U, Galli S J, Lichtenstein L M
Johns Hopkins Medical Institutions, Baltimore, Md.
J Allergy Clin Immunol. 1988 Mar;81(3):580-9.
Both the pattern of mediator release during the late-phase response (LPR) and the reduction of the LPR with corticosteroid pretreatment have suggested that basophils, not mast cells, represent the main source of histamine in the late response to nasal antigen challenge. We tested this hypothesis by examining alcian blue-stained cytospin slides of nasal washings obtained before and for 11 hours after nasal antigen challenge in 11 asymptomatic subjects with seasonal allergic rhinitis. In a double-blind manner, subjects received placebo or topical flunisolide (50 micrograms, each nostril, twice daily) for 1 week before antigen challenge. One month later, the challenge was repeated with the alternate pretreatment. On placebo-treatment days, a twelve-fold increase occurred in the number and a threefold increase in the percentage of alcian blue-stained positive cells in nasal washings in the LPR compared to baseline. At least 68% of these alcian blue-stained positive cells were basophils, as determined by light microscopic criteria. Alcian blue-stained cell influx correlated with increases in histamine levels in nasal washes (p less than 0.001). Topical steroid pretreatment blocked the influx of alcian blue-stained positive cells, as well as other inflammatory cells, including eosinophils, neutrophils, and mononuclear cells. Symptoms and mediator release were also blocked. These data demonstrate an influx of basophils and suggest that these cells are responsible for the histamine release observed in the LPR. Our findings indicate that pharmacologic control of basophil histamine release may represent a strategy for the treatment of a variety of chronic allergic diseases that are believed to resemble the LPR.
迟发相反应（LPR）期间介质释放的模式以及皮质类固醇预处理对LPR的减轻作用均提示，在对鼻内抗原激发的迟发反应中，嗜碱性粒细胞而非肥大细胞是组胺的主要来源。我们通过检查11名季节性变应性鼻炎无症状受试者在鼻内抗原激发前及激发后11小时获得的鼻洗液的阿尔辛蓝染色细胞涂片来验证这一假设。受试者在抗原激发前以双盲方式接受安慰剂或局部氟尼缩松（每侧鼻孔50微克，每日两次）治疗1周。1个月后，用交替的预处理重复激发试验。在接受安慰剂治疗的日子里，与基线相比，LPR期间鼻洗液中阿尔辛蓝染色阳性细胞的数量增加了12倍，百分比增加了3倍。根据光学显微镜标准确定，这些阿尔辛蓝染色阳性细胞中至少68%为嗜碱性粒细胞。阿尔辛蓝染色细胞流入与鼻洗液中组胺水平的升高相关（p<0.001）。局部类固醇预处理可阻止阿尔辛蓝染色阳性细胞以及其他炎症细胞（包括嗜酸性粒细胞、中性粒细胞和单核细胞）的流入。症状和介质释放也被阻断。这些数据证明了嗜碱性粒细胞的流入，并提示这些细胞是LPR中观察到的组胺释放的原因。我们的研究结果表明，对嗜碱性粒细胞组胺释放的药物控制可能是治疗多种被认为类似于LPR的慢性变应性疾病的一种策略。
