A COMMON COLD VIRUS, RHINOVIRUS-16, POTENTIATES AIRWAY INFLAMMATION AFTER SEGMENTAL ANTIGEN BRONCHOPROVOCATION IN ALLERGIC SUBJECTS
A COMMON COLD VIRUS, RHINOVIRUS-16, POTENTIATES AIRWAY INFLAMMATION AFTER SEGMENTAL ANTIGEN BRONCHOPROVOCATION IN ALLERGIC SUBJECTS
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DOI：
10.1172/jci117581
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发表时间：
1994-12-01
影响因子：
15.9
通讯作者：
BUSSE, WW
中科院分区：
文献类型：
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作者：
CALHOUN, WJ;DICK, EC;BUSSE, WW
许多哮喘患者因感冒而喘息加剧。我们假设，鼻病毒感冒可能会在抗原攻击后通过增强气道过敏反应（组胺释放和嗜酸性粒细胞流入）来增加哮喘。 7 名过敏性鼻炎患者和 5 名正常志愿者感染 16 型鼻病毒（RV16），并通过节段支气管激发和支气管肺泡灌洗进行评估。感染前1个月、急性感染期间和感染后1个月用盐水和抗原进行分段攻击。抗原攻击后立即和48小时进行灌洗。数据采用双向方差分析，P值小于或等于0.05被认为是显着的。所有接种 RV16 的志愿者都出现了急性呼吸道感染。在急性病毒感染期间和感染后 1 个月，从过敏性鼻炎受试者获得的 BAL 液在抗原攻击后显示出以下与 RV16 相关的显着变化：(a) 局部抗原攻击后立即释放组胺； (b) 48小时后持续组胺泄漏； (c) 攻击后 48 小时，气道中更多的嗜酸性粒细胞募集。这些变化在感染 RV16 并用抗原攻击的非过敏志愿者中没有观察到，在反复用抗原攻击但未感染 RV16 的过敏志愿者中也没有观察到，在用盐水假攻击的 RV16 感染过敏志愿者中也没有观察到这些变化。我们得出的结论是，鼻病毒上呼吸道感染在局部抗原攻击后显着增强过敏个体气道中的即时和晚期过敏反应。这些数据表明，感冒期间哮喘增加的机制之一是气道过敏反应加剧，从而可能导致支气管炎症。
Many patients with asthma have increased wheezing with colds. We hypothesized that rhinovirus colds might increase asthma by augmenting airway allergic responses (histamine release and eosinophil influx) after antigen challenge. Seven allergic rhinitis patients and five normal volunteers were infected with rhinovirus type 16 (RV16) and evaluated by segmental bronchoprovocation and bronchoalveolar lavage. Segmental challenge with saline and antigen was performed 1 mo before infection, during the acute infection, and 1 mo after infection. Lavage was performed immediately and 48 h after antigen challenge. Data were analyzed by two-way analysis of variance, and a P value of less than or equal to 0.05 was considered to be significant. All volunteers inoculated with RV16 developed an acute respiratory infection. BAL fluid obtained from allergic rhinitis subjects during the acute viral infection, and 1 mo after infection, showed the following significant RV16-associated changes after antigen challenge: (a) an enhanced release of histamine immediately after local antigen challenge; (b) persistent histamine leak 48 h afterwards; and (c) a greater recruitment of eosinophils to the airway 48 h after challenge. These changes were not seen in non-allergic volunteers infected with RV16 and challenged with antigen, nor in allergic volunteers repetitively challenged with antigen but not infected with RV16, nor in RV16 infected allergic volunteers sham challenged with saline. We conclude that rhinovirus upper respiratory infection significantly augments immediate and late allergic responses in the airways of allergic individuals after local antigen challenge. These data suggest that one mechanism of increased asthma during a cold is an accentuation of allergic responses in the airway which may then contribute to bronchial inflammation.