EXPERIMENTAL RHINOVIRUS-16 INFECTION POTENTIATES HISTAMINE-RELEASE AFTER ANTIGEN BRONCHOPROVOCATION IN ALLERGIC SUBJECTS
EXPERIMENTAL RHINOVIRUS-16 INFECTION POTENTIATES HISTAMINE-RELEASE AFTER ANTIGEN BRONCHOPROVOCATION IN ALLERGIC SUBJECTS
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DOI：
10.1164/ajrccm/144.6.1267
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发表时间：
1991-12-01
期刊：
影响因子：
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通讯作者：
BUSSE, WW
中科院分区：
文献类型：
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作者：
CALHOUN, WJ;SWENSON, CA;BUSSE, WW
病毒性呼吸道感染会加重许多患者的哮喘。我们推测，这种效应发生的一种机制可能包括肥大细胞和/或嗜碱性粒细胞促进或改变介质的释放，从而有利于晚期哮喘反应(LAR)的发展。因此，我们研究了8名过敏性鼻炎患者，这些患者在实验诱导的16号鼻病毒(RV16)感染之前和期间都患有变应性鼻炎。我们测定了血浆组胺和类胰蛋白酶的水平，并观察了吸入抗原攻击后出现的与呼吸道阻塞相关的模式。在RV16疾病期间，支气管对组胺、乙酰甲胆碱和抗原的反应性都显著增加。此外，在感染期间LAR的发生率(八分之五)明显高于感染前(八分之一；p=0.014)。此外，在那些在抗原攻击后的反应模式从感染前的即刻反应转变为感染期间的双重反应(即刻+后期)的患者中，攻击后的血浆组胺浓度显著高于反应模式没有改变的患者。我们得出结论，RV16感染增加LAR可能性的一个机制可能包括肺肥大细胞或循环中或招募的嗜碱性粒细胞释放更多的介质。
Viral respiratory infections exacerbate asthma in many patients. We hypothesized that one mechanism by which this effect occurs may include potentiated or altered mediator release by mast cells and/or basophils to favor the development of late-phase asthmatic reactions (LAR). Therefore, we studied eight subjects with allergic rhinitis before and during an experimentally induced rhinovirus 16 (RV16) infection. We determined levels of plasma histamine and tryptase, and we observed the associated patterns of airway obstruction that developed following inhaled antigen challenge. Bronchial responsiveness to histamine, methacholine, and antigen were all significantly increased during the RV16 illness. Further, the incidence of LAR was significantly higher (five of eight) during the infection than before (one of eight; p = 0.014). In addition, in those patients whose pattern of response following antigen challenge converted from an immediate response only before infection to a dual response (immediate + late phase) during infection, plasma histamine concentrations after challenge were significantly greater than in those whose pattern of response did not change. We conclude that one mechanism by which RV16 infection increases the likelihood of LAR could include enhanced mediator release from pulmonary mast cells or from circulating or recruited basophils.