NASAL CHALLENGE WITH COLD, DRY AIR RESULTS IN RELEASE OF INFLAMMATORY MEDIATORS - POSSIBLE MAST-CELL INVOLVEMENT
NASAL CHALLENGE WITH COLD, DRY AIR RESULTS IN RELEASE OF INFLAMMATORY MEDIATORS - POSSIBLE MAST-CELL INVOLVEMENT
复制标题
DOI：
10.1172/jci112113
复制
发表时间：
1985-01-01
影响因子：
15.9
通讯作者：
LICHTENSTEIN, LM
中科院分区：
文献类型：
--
作者：
TOGIAS, AG;NACLERIO, RM;LICHTENSTEIN, LM
我们的研究目的是评估冷干空气(CDA)对选定个体鼻黏膜与肥大细胞相关的炎性介质释放的影响。对12名有鼻漏和鼻塞症状的受试者进行了CDA鼻腔呼吸和温湿空气(WMA)的刺激。每个受试者都被测试了两次，挑战的顺序颠倒了过来。记录症状积分，测定鼻灌洗液中组胺、前列腺素(PG)D2、激动素和[~3H]-N-对甲苯磺酰-L-精氨酸甲酯(TAME)活性。与基线或WMA相比，CDA导致中介物水平和症状评分显著增加。在WMA挑战后，除了激动素的轻微增加外，症状评分或介体没有显著增加。无论挑战顺序如何，对CDA的反应都是相似的。介质的变化相互关联，症状评分与组胺、激动素和PGD2水平显著相关。5名无冷空气暴露鼻部症状的受试者在CDA或WMA挑战后的介质或症状评分没有变化。我们认为CDA可引起可能与肥大细胞相关的炎症介质的释放，推测CDA可能参与了CDA诱发哮喘患者支气管痉挛的机制。
The purpose of our study was to assess the effect of cold, dry air (CDA) on the nasal mucosa of selected individuals in relation to the release of inflammatory mediators associated with mast cells. 12 subjects with a history of nasal symptoms of rhinorrhea and congestion upon cold or dry environmental exposure were challenged by nasal breathing of CDA and warm, moist air (WMA). Each subject was tested on two occasions with the order of the challenges reversed. Symptom scores were recorded, and the levels of histamine, prostaglandin (PG) D2, kinins, and [3H]-N-.alpha.-tosyl-L-arginine methyl ester (TAME)-esterase activity in nasal lavage fluids were measured. CDA caused a significant increase in mediator levels and in symptom scores as compared to baseline or to WMA. No significant increase in symptom scores or mediators was noted after WMA challenge, with the exception of a marginal increase in kinins. The response to CDA was similar, regardless of challenge order. Changes in mediators correlated with one another, and symptom scores correlated significantly with the levels of histamine, kinins, and PGD2. Five subjects without a history of nasal symptoms on cold air exposure had no change in mediators or symptom scores after CDA or WMA challenge. We conclude that CDA causes the release of inflammatory mediators possibly associated with mast cells and speculate that such a mechanism may be involved in the bronchospasm induced by CDA in asthmatics.