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自噬诱导小鼠哮喘模型嗜酸性粒细胞胞外诱捕网形成及过敏性气道炎症

2020/06/11

   摘要
   研究表明自噬参与炎症性疾病的免疫病理过程。然而,自噬在哮喘和嗜酸性粒细胞胞外诱捕网(EETs)释放中的作用还不清楚。本文中,我们试图在一个实验性哮喘模型中研究自噬在EETs释放和肺部炎症中的作用。小鼠用卵清蛋白(OVA)致敏,然后进行OVA激发。在OVA激发之前,小鼠用自噬抑制剂3-甲基腺嘌呤(3-MA)治疗。我们发现,3-MA治疗可降低肺组织中嗜酸性粒细胞数量、嗜酸性粒细胞过氧化物酶(EPO)活性、杯状细胞增生、促炎细胞因子和核因子kappa B(NF-κB)p65的免疫含量。此外,3-MA能改善氧化应激、线粒体能量代谢和Na+,K+-ATP酶活性。我们证明用自噬抑制剂3-MA治疗可以减少气道中EETs的形成。根据我们的研究结果,3-MA治疗可能是减少哮喘患者肺部炎症、氧化应激、线粒体损伤和EETs形成的一种有意义的替代疗法。

 
(中日友好医院呼吸与危重症医学科 顾宪民 摘译 林江涛 审校 )
(J Cell Physiol. 2020 Jan;235(1):267-280. doi: 10.1002/jcp.28966. Epub 2019 Jun 17)

 
 
Autophagy Induces Eosinophil Extracellular Traps Formation and Allergic Airway Inflammation in a Murine Asthma Model.
 
Josiane Silva Silveira, Géssica Luana Antunes, Daniela Benvenutti Kaiber, Mariana Severo da Costa, Fernanda Silva Ferreira, Eduardo Peil Marques, Felipe Schmitz, Rodrigo Benedetti Gassen, Ricardo Vaz Breda, Angela T S Wyse, Renato Tetelbom Stein, Paulo Márcio Pitrez, Aline Andrea da Cunha.
 
Abstract
D Studies have shown autophagy participation in the immunopathology of inflammatory diseases. However, autophagy role in asthma and in eosinophil extracellular traps (EETs) release is poorly understood. Here, we attempted to investigate the autophagy involvement in EETs release and in lung inflammation in an experimental asthma model. Mice were sensitized with ovalbumin (OVA), followed by OVA challenge. Before the challenge with OVA, mice were treated with an autophagy inhibitor, 3-methyladenine (3-MA). We showed that 3-MA treatment decreases the number of eosinophils, eosinophil peroxidase (EPO) activity, goblet cells hyperplasia, proinflammatory cytokines, and nuclear factor kappa B (NFκB) p65 immunocontent in the lung. Moreover, 3-MA was able to improve oxidative stress, mitochondrial energy metabolism, and Na+, K+-ATPase activity. We demonstrated that treatment with autophagy inhibitor 3-MA reduced EETs formation in the airway. On the basis of our results, 3-MA treatment can be an interesting alternative for reducing lung inflammation, oxidative stress, mitochondrial damage, and EETs formation in asthma.
 


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