A20 Attenuates Allergic Airway Inflammation in Mice
A20 Attenuates Allergic Airway Inflammation in Mice
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DOI：
10.4049/jimmunol.0900163
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发表时间：
2009-07-15
影响因子：
4.4
通讯作者：
Park, Byung-Hyun
中科院分区：
文献类型：
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作者：
Kang, Nam-In;Yoon, Ha-Yong;Park, Byung-Hyun
TNF受体1可以激活导致NF-kappa b活化的信号通路。A20是NF-kappa b诱导蛋白，负向调节这些信号通路并作为抗炎介质。因此，A20被视为炎症性疾病的潜在治疗靶点。在本研究中，我们检测了A20对ova诱导的小鼠变应性气道炎症模型的影响。我们使用了一种含有A20 cDNA的腺病毒（Ad-A20），在OVA攻毒前经气管内传递。单次给药Ad-A20可减少气道炎症细胞募集和细支气管周围炎症，并抑制支气管肺泡液中各种细胞因子的产生。此外，Ad-A20抑制黏液的产生，阻止气道高反应性的发展。Ad-A20的保护作用是通过抑制nf - κ B信号通路介导的。综上所述，我们的研究结果表明，基于A20的免疫调节策略的开发可能具有治疗过敏性哮喘的治疗潜力。中华免疫学杂志，2009,33(3):488- 495。
TNF receptor 1 can activate signaling pathways leading to the activation of NF-kappa B. A20, an NF-kappa B-inducible protein, negatively regulates these signaling pathways and acts as an anti-inflammatory mediator. Therefore, A20 is viewed as a potential therapeutic target for inflammatory disease. In this study, we examined the effect of A20 on an OVA-induced allergic airway inflammation model in mice. We used an adenovirus containing A20 cDNA (Ad-A20) that was delivered intratracheally before OVA challenge. Single administration of Ad-A20 reduced airway inflammatory cell recruitment and peribronchiolar inflammation and suppressed the production of various cytokines in bronchoalveolar fluid. In addition, Ad-A20 suppressed mucus production and prevented the development of airway hyperresponsiveness. The protective effect of Ad-A20 was mediated by the inhibition of the NF-kappa B signaling pathway. Taken together, our results suggest that the development of an immunoregulatory strategy based on A20 may have therapeutic potential for the treatment of allergic asthma. The Journal of Immunology, 2009, 183: 1488-1495.