与病毒感染有关的炎症和过敏中的氧自由基。

M Kato, Y Hayashi, H Kimura
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引用次数: 17

摘要

包括超氧阴离子(O(2)(-))和一氧化氮(NO)在内的氧自由基参与了多种由病毒感染引起的炎症性疾病。在这篇综述中,我们关注氧自由基在变应性炎症中的作用,如由病毒感染引起的支气管哮喘,特别是呼吸道合胞病毒(RSV)。幼儿期的这种感染是发展为喘息、肺功能显著下降和气道反应性增加的危险因素。呼吸道合胞病毒感染还会加重已确诊哮喘患者的反复喘息发作。最近,我们已经证明RSV通过脂质介质(如血小板活化因子)刺激嗜酸性粒细胞增加超氧化物的产生。这种反应依赖于β β 2整合素,α β 2,这是嗜酸性粒细胞效应功能的关键。我们的研究结果表明嗜酸性粒细胞及其产物促进rsv诱导的哮喘气道炎症。密切描述RSV增强哮喘嗜酸性粒细胞炎症的机制应该为更有效的治疗提供线索。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxygen radicals in inflammation and allergy related to viral infections.

Oxygen radicals including superoxide anion (O(2)(-)) and nitric oxide (NO) are involved in a variety of inflammatory diseases induced by viral infection. In this review, we focus on the role of oxygen radicals in allergic inflammation such as bronchial asthma induced by viral infection--specifically, with respiratory syncytial virus (RSV). This infection in early childhood is a risk factor for development of wheezing, significant decreases in pulmonary function, and increases in airway reactivity. RSV infection also exacerbates recurrent wheezing attacks in patients with established asthma. Recently, we have demonstrated that RSV enhanced superoxide production by human eosinophils stimulated with a lipid mediator such as platelet-activating factor. This response depends on a beta2 integrin, alphaMbeta2, which is critical for eosinophil effector functions. Our results suggest that eosinophils and their products promote RSV-induced airway inflammation in asthma. Close delineation of the mechanism by which RSV enhances eosinophilic inflammation in asthma should yield clues to more effective therapy.

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