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慢性过敏信号传导:一切都源于线粒体过度紧张吗?

Chronic allergy signaling: is it all stressed-out mitochondria?

作者信息

Hussain Syed-Rehan A, Grayson Mitchell H

机构信息

Division of Allergy and Immunology, Department of Pediatrics, Nationwide Children's Hospital - The Ohio State University College of Medicine, Columbus, OH, USA.

Center for Clinical and Translational Research, Abigail Wexner Research Institute at Nationwide Children's Hospital, Columbus, OH, USA.

出版信息

Fac Rev. 2022 Dec 15;11:37. doi: 10.12703/r/11-37. eCollection 2022.

DOI:10.12703/r/11-37
PMID:36644297
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9816874/
Abstract

Allergic diseases in general, and chronic allergic inflammation in particular, are on the rise in the United States and other developed countries. The idea of chronic allergic disease as a chronic type 2 immune response has been around for several decades. However, data suggest that other mechanisms may be important in chronic disease. Therefore, we believe it is time for a paradigm shift in understanding the mechanistic causes of disease symptoms in these diseases. In this review, we have avoided the classic canonical pathways and focused on the emerging idea that oxidative stress, changes in immuno-metabolism, mitochondrial dysfunction, and epigenetic changes (particularly microRNA profile) may be working concurrently or synergistically to potentiate allergic disease symptoms. Furthermore, we have addressed how the epidemic of obesity exacerbates allergic disease via the dysregulation of the aforementioned factors.

摘要

总体而言,过敏性疾病,尤其是慢性过敏性炎症,在美国和其他发达国家呈上升趋势。慢性过敏性疾病作为一种慢性2型免疫反应的观点已经存在了几十年。然而,数据表明其他机制在慢性疾病中可能也很重要。因此,我们认为现在是时候在理解这些疾病症状的机制性原因方面进行范式转变了。在这篇综述中,我们避开了经典的规范途径,重点关注了一个新出现的观点,即氧化应激、免疫代谢变化、线粒体功能障碍和表观遗传变化(特别是微小RNA谱)可能同时或协同作用,增强过敏性疾病症状。此外,我们还探讨了肥胖流行如何通过上述因素的失调加剧过敏性疾病。

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本文引用的文献

1
Immune Metabolism-An Opportunity to Better Understand Allergic Pathology and Improve Treatment of Allergic Diseases?免疫代谢——更好理解过敏性病理学及改善过敏性疾病治疗的契机?
Front Allergy. 2022 Mar 9;3:825931. doi: 10.3389/falgy.2022.825931. eCollection 2022.
2
PRMT5 in T Cells Drives Th17 Responses, Mixed Granulocytic Inflammation, and Severe Allergic Airway Inflammation.PRMT5 在 T 细胞中驱动 Th17 反应、混合粒细胞炎症和严重的过敏性气道炎症。
J Immunol. 2022 Apr 1;208(7):1525-1533. doi: 10.4049/jimmunol.2100994. Epub 2022 Mar 14.
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The Importance of Metabolism for Immune Homeostasis in Allergic Diseases.
代谢对于过敏性疾病中免疫稳态的重要性。
Front Immunol. 2021 Jul 28;12:692004. doi: 10.3389/fimmu.2021.692004. eCollection 2021.
4
Differential Regulation of ATP- and UTP-Evoked Prostaglandin E and IL-6 Production from Human Airway Epithelial Cells.人呼吸道上皮细胞中 ATP 和 UTP 诱发的前列腺素 E 和 IL-6 产生的差异调节。
J Immunol. 2021 Sep 1;207(5):1275-1287. doi: 10.4049/jimmunol.2100127. Epub 2021 Aug 13.
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Oxidative Imbalance as a Crucial Factor in Inflammatory Lung Diseases: Could Antioxidant Treatment Constitute a New Therapeutic Strategy?氧化失衡作为炎症性肺病的关键因素:抗氧化治疗是否构成新的治疗策略?
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Cutting edge: Metabolic immune reprogramming, reactive oxygen species, and cancer.前沿:代谢免疫重编程、活性氧和癌症。
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Asthma and its relationship to mitochondrial copy number: Results from the Asthma Translational Genomics Collaborative (ATGC) of the Trans-Omics for Precision Medicine (TOPMed) program.哮喘及其与线粒体拷贝数的关系:精准医学跨组学(TOPMed)计划的哮喘转化基因组学协作组(ATGC)的研究结果。
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The Role Played by Mitochondria in FcεRI-Dependent Mast Cell Activation.线粒体在 FcεRI 依赖性肥大细胞活化中的作用。
Front Immunol. 2020 Oct 16;11:584210. doi: 10.3389/fimmu.2020.584210. eCollection 2020.
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Epigenetic regulation of white adipose tissue in the onset of obesity and metabolic diseases.肥胖和代谢性疾病发病过程中白色脂肪组织的表观遗传调控。
Obes Rev. 2020 Nov;21(11):e13054. doi: 10.1111/obr.13054. Epub 2020 Jun 15.
10
Environmental Exposures and Asthma Development: Autophagy, Mitophagy, and Cellular Senescence.环境暴露与哮喘发病:自噬、线粒体自噬和细胞衰老。
Front Immunol. 2019 Nov 29;10:2787. doi: 10.3389/fimmu.2019.02787. eCollection 2019.