Effect of influenza virus infection on ovalbumin-specific IgE responses to inhaled antigen in the rat.
Effect of influenza virus infection on ovalbumin-specific IgE responses to inhaled antigen in the rat.
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流感病毒感染对大鼠吸入抗原的卵清蛋白特异性 IgE 反应的影响。
DOI：
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发表时间：
1996
期刊：
影响因子：
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通讯作者：
G. Burleson
中科院分区：
文献类型：
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作者：
H. Lebrec;K. Sarlo;G. Burleson
在临床研究中报告了上呼吸道病毒感染作为过敏致敏的风险因素。为了研究流感病毒疾病与变态反应发展之间的关系，先前采用了过敏原致敏的鼠模型。这些模型表明，致命的流感病毒能够触发过敏原特异性免疫球蛋白E（IgE）的生产，并抑制小鼠对反复暴露于雾化过敏原的耐受性。这些鼠模型的缺点在于利用流感病毒的致敏和致死株。本实验室建立了一种非致死性大鼠适应性流感病毒（RAIV）宿主耐药模型。它被用来评估流感病毒感染对IgE反应吸入卵清蛋白（OA）在大鼠中的影响。在比较Fischer 344（F344）和BN大鼠对OA的IgE应答后，选择高IgE应答的布朗-挪威（BN）大鼠进行进一步研究。在第1天，BN大鼠通过单独皮下注射1 mg OA或与氢氧化铝（200 mg）和百日咳杆菌（每只大鼠1 ml中15 × 10（9）灭活杆菌）一起皮下注射致敏，或仅接受生理盐水。在第0天（致敏前24小时）或第15天、第17天或第57天用RAIV感染大鼠或假感染大鼠。从第18天开始，每周将大鼠暴露于雾化OA（磷酸盐缓冲盐水中的OA 3%）3分钟。在每次OA激发后3 d，通过反向酶联免疫吸附试验（ELISA）评价血清OA特异性IgE。BN大鼠引起可检测的OA特异性IgE反应，反复暴露于气溶胶后下降。流感病毒感染短暂增加OA特异性IgE反应时，大鼠单独用OA免疫，并在第一次挑战前1天感染，也当大鼠只接受生理盐水的第1天，每周暴露于雾化OA，并在第七次挑战前感染。这些结果，与先前在小鼠中报告的数据，强调上呼吸道病毒感染的重要性，在增加IgE过敏原的反应，并可能在人类疾病的重要性。
Upper respiratory tract viral infections have been reported in clinical studies to serve as risk factors for allergic sensitization. In order to study the relationship linking influenza virus illnesses to development of allergy, murine models of allergen sensitization were previously employed. These models showed that lethal influenza viruses were able to trigger allergen-specific immunoglobulin E (IgE) production and to inhibit tolerance to repeated exposure to aerosolized allergen in the mouse. The disadvantage of these murine models consists in the utilization of virulant and lethal strains of influenza virus. A nonlethal rat-adapted influenza virus (RAIV) host resistance model has been developed in our laboratory. It was used to evaluate the effect of influenza virus infection on IgE responses to inhaled ovalbumin (OA) in the rat. The high IgE-responder Brown-Norway (BN) rat was chosen for further study after comparing the IgE response to OA in Fischer 344 (F344) and BN rats. On d 1, BN rats were sensitized by administration of 1 mg OA subcutaneously alone or together with aluminum hydroxide (200 mg) and Bordetella pertussis (15 x 10(9) killed bacilli per rat in 1 ml), or only received saline. Rats were either infected with RAIV or sham-infected on d 0 (24 h prior to sensitization) or on d 15, 17, or 57. Rats were exposed for 3 min to aerosolized OA (OA 3% in phosphate-buffered saline) every week, starting on d 18. Serum OA-specific IgE was evaluated by reverse enzyme-linked immunosorbent assay (ELISA) 3 d after each OA challenge. BN rats elicited a detectable OA-specific IgE response that decreased after repeated aerosol exposures. Influenza virus infection transiently increased the OA-specific IgE response when rats were immunized with OA alone and were infected 1 d prior to the first challenge and also when rats received only saline on d 1, were exposed each week to aerosolized OA, and were infected prior to the seventh challenge. These results, with data previously reported in mice, emphasize the importance of upper respiratory tract viral infection in increasing IgE responses to allergens and may be of importance in human disease.