Davis V L, Earp H S, Stempel D A
Am Rev Respir Dis. 1984 Aug;130(2):167-70. doi: 10.1164/arrd.1984.130.2.167.
Wheezing episodes often accompany viral respiratory infections. Viral pathogens are also known to induce interferon production. Cyclic AMP (cAMP) levels affect bronchial reactivity; therefore, we analyzed cAMP accumulation in human lymphocytes as a model to determine if interferon might influence the accumulation of this important intracellular mediator. After an overnight exposure to interferon in whole blood, a reduction in agonist-stimulated cAMP accumulation was demonstrated. Basal cAMP concentrations were equivalent in control and interferon-exposed lymphocytes from the same donor, but the response to isoproterenol and prostaglandin E1 was significantly reduced by 61 and 30%, respectively. The decreased responsiveness persisted in the presence of RO 20-1724, a phosphodiesterase inhibitor, indicating that the effect was in part due to a decrease in cAMP synthesis in intact cells. These results suggest that interferon may play a role in inducing or potentiating bronchospasm.
喘息发作常伴随病毒性呼吸道感染。已知病毒病原体可诱导干扰素产生。环磷酸腺苷（cAMP）水平影响支气管反应性；因此，我们分析了人淋巴细胞中cAMP的积累情况，以此作为模型来确定干扰素是否可能影响这种重要细胞内介质的积累。全血在过夜暴露于干扰素后，显示出激动剂刺激的cAMP积累减少。来自同一供体的对照淋巴细胞和暴露于干扰素的淋巴细胞的基础cAMP浓度相当，但对异丙肾上腺素和前列腺素E1的反应分别显著降低了61%和30%。在磷酸二酯酶抑制剂RO 20-1724存在的情况下，反应性降低仍然存在，这表明该效应部分是由于完整细胞中cAMP合成减少所致。这些结果表明，干扰素可能在诱导或增强支气管痉挛中起作用。
