Thioredoxin suppresses airway hyperresponsiveness and airway inflammation in asthma
Thioredoxin suppresses airway hyperresponsiveness and airway inflammation in asthma
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DOI：
10.1016/j.bbrc.2005.07.007
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发表时间：
2005-09-09
影响因子：
3.1
通讯作者：
Aizawa, H
中科院分区：
文献类型：
--
作者：
Ichiki, H;Hoshino, T;Aizawa, H
硫氧还蛋白（TRX）是一种分子量为12 kDa的氧化还原（还原/氧化）活性蛋白，具有高度保守的位点（-Cys-Gly-Pro-Cys-）并清除活性氧。在此，我们研究了外源性TRX是否调节小鼠哮喘模型的气道高反应性（AHR）和气道炎症。在OVA致敏小鼠中观察到吸入乙酰胆碱的AHR增加和伴有嗜酸性粒细胞增多的气道炎症。施用野生型而不是32 S/35 S突变体TRX强烈抑制AHR和气道炎症，并上调几种细胞因子（例如，IL-1 α、IL-1 β、IL-1受体拮抗剂和IL-18）。相反，在OVA致敏小鼠中，在OVA致敏时TRX治疗没有改善AHR或气道炎症。因此，TRX抑制致敏后的哮喘反应，但不能防止致敏本身。TRX和氧化还原活性蛋白可能对哮喘患者有临床益处。(c)2005年爱思唯尔公司All rights reserved.
Thioredoxin (TRX) is a 12-kDa redox (reduction/oxidation)-active protein that has a highly conserved site (-Cys-Gly-Pro-Cys-) and scavenges reactive oxygen species. Here we examined whether exogenously administered TRX modulated airway hyperresponsiveness (AHR) and airway inflammation in a mouse asthma model. Increased AHR to inhaled acetylcholine and airway inflammation accompanied by eosinophilia were observed in OVA-sensitized mice. Administration of wild-type but not 32S/35S mutant TRX strongly suppressed AHR and airway inflammation, and upregulated expression of mRNA of several cytokines (e.g., IL-1 alpha, IL-1 beta, IL-1 receptor antagonist, and IL-18) in the lungs of OVA-sensitized mice. In contrast, TRX treatment at the time of OVA sensitization did not improve AHR or airway inflammation in OVA-sensitized mice. Thus, TRX inhibited the asthmatic response after sensitization, but did not prevent sensitization itself. TRX and redox-active protein may have clinical benefits in,patients with asthma. (c) 2005 Elsevier Inc. All rights reserved.