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本文引用的文献

1
Bioenergetic Differences in the Airway Epithelium of Lean Obese Asthmatics Are Driven by Nitric Oxide and Reflected in Circulating Platelets.瘦胖型哮喘患者气道上皮细胞的生物能量差异由一氧化氮驱动，并反映在循环血小板中。
Antioxid Redox Signal. 2019 Oct 1;31(10):673-686. doi: 10.1089/ars.2018.7627. Epub 2019 Mar 6.
2
Arginine metabolic endotypes related to asthma severity.与哮喘严重程度相关的精氨酸代谢内型。
PLoS One. 2017 Aug 10;12(8):e0183066. doi: 10.1371/journal.pone.0183066. eCollection 2017.
3
L-Arginine Modulates T Cell Metabolism and Enhances Survival and Anti-tumor Activity.L-精氨酸调节T细胞代谢并增强其存活及抗肿瘤活性。
Cell. 2016 Oct 20;167(3):829-842.e13. doi: 10.1016/j.cell.2016.09.031. Epub 2016 Oct 13.
4
Increased mitochondrial arginine metabolism supports bioenergetics in asthma.线粒体精氨酸代谢增强有助于哮喘中的生物能量学。
J Clin Invest. 2016 Jul 1;126(7):2465-81. doi: 10.1172/JCI82925. Epub 2016 May 23.
5
Eotaxin-Rich Proangiogenic Hematopoietic Progenitor Cells and CCR3+ Endothelium in the Atopic Asthmatic Response.嗜酸性粒细胞趋化因子丰富的促血管生成造血祖细胞与CCR3+内皮细胞在特应性哮喘反应中的作用
J Immunol. 2016 Mar 1;196(5):2377-87. doi: 10.4049/jimmunol.1500770. Epub 2016 Jan 25.
6
The immunology of asthma.哮喘的免疫学
Nat Immunol. 2015 Jan;16(1):45-56. doi: 10.1038/ni.3049.
7
IL-17 in severe asthma. Where do we stand?白细胞介素-17 在重症哮喘中的作用。我们处于什么位置？
Am J Respir Crit Care Med. 2014 Nov 15;190(10):1094-101. doi: 10.1164/rccm.201405-0859PP.
8
Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity.白细胞介素-17 产生的固有淋巴细胞和 NLRP3 炎性小体促进肥胖相关的气道高反应性。
Nat Med. 2014 Jan;20(1):54-61. doi: 10.1038/nm.3423. Epub 2013 Dec 15.
9
Lung macrophages contribute to house dust mite driven airway remodeling via HIF-1α.肺巨噬细胞通过 HIF-1α 促进屋尘螨诱导的气道重塑。
PLoS One. 2013 Jul 23;8(7):e69246. doi: 10.1371/journal.pone.0069246. Print 2013.
10
T cell–derived inducible nitric oxide synthase switches off Th17 cell differentiation.T 细胞衍生的诱导型一氧化氮合酶使 Th17 细胞分化失活。
J Exp Med. 2013 Jul 1;210(7):1447-62. doi: 10.1084/jem.20122494.

精氨酸代谢对气道炎症的调控。

Arginine metabolic control of airway inflammation.

机构信息

Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic, Cleveland, Ohio, USA.

Division of Genetics, Genomics and Precision Medicine, Department of Medicine, College of Medicine, University of Arizona, Tucson, Arizona, USA.

出版信息

JCI Insight. 2020 Jan 30;5(2):127801. doi: 10.1172/jci.insight.127801.

DOI:10.1172/jci.insight.127801
PMID:31996482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7098726/
Abstract

Inducible nitric oxide synthase (iNOS) and arginase-2 (ARG2) share a common substrate, arginine. Higher expression of iNOS and exhaled NO are linked to airway inflammation in patients. iNOS deletion in animal models suggests that eosinophilic inflammation is regulated by arginine metabolism. Moreover, ARG2 is a regulator of Th2 response, as shown by the development of severe eosinophilic inflammation in ARG2-/- mice. However, potential synergistic roles of iNOS and ARG2 in asthma have not been explored. Here, we hypothesized that arginine metabolic fate via iNOS and ARG2 may govern airway inflammation. In an asthma cohort, ARG2 variant genotypes were associated with arginase activity. ARG2 variants with lower arginase activity, combined with levels of exhaled NO, identified a severe asthma phenotype. Airway inflammation was present in WT, ARG2-/-, iNOS-/-, and ARG2-/-/iNOS-/- mice but was greatest in ARG2-/-. Eosinophilic and neutrophilic infiltration in the ARG2-/- mice was abrogated in ARG2-/-/iNOS-/- animals. Similarly, angiogenic airway remodeling was greatest in ARG2-/- mice. Cytokines driving inflammation and remodeling were highest in lungs of asthmatic ARG2-/- mice and lowest in the iNOS-/-. ARG2 metabolism of arginine suppresses inflammation, while iNOS metabolism promotes airway inflammation, supporting a central role for arginine metabolic control of inflammation.

摘要

诱导型一氧化氮合酶（iNOS）和精氨酸酶-2（ARG2）共享一个共同的底物，精氨酸。iNOS 的高表达和呼出的 NO 与患者气道炎症有关。动物模型中的 iNOS 缺失表明，精氨酸代谢调节嗜酸性粒细胞炎症。此外，ARG2 是 Th2 反应的调节剂，如 ARG2-/- 小鼠中严重嗜酸性粒细胞炎症的发展所示。然而，iNOS 和 ARG2 在哮喘中的潜在协同作用尚未得到探索。在这里，我们假设通过 iNOS 和 ARG2 的精氨酸代谢命运可能控制气道炎症。在哮喘队列中，ARG2 变体基因型与精氨酸酶活性相关。ARG2 变体的精氨酸酶活性较低，与呼出的 NO 水平相结合，确定了严重哮喘表型。WT、ARG2-/-、iNOS-/-和 ARG2-/-/iNOS-/- 小鼠均存在气道炎症，但 ARG2-/-小鼠的气道炎症最严重。ARG2-/- 小鼠中的嗜酸性粒细胞和中性粒细胞浸润在 ARG2-/-/iNOS-/-动物中被消除。同样，ARG2-/- 小鼠的血管生成性气道重塑最为严重。驱动炎症和重塑的细胞因子在哮喘 ARG2-/- 小鼠的肺部最高，而在 iNOS-/- 中最低。精氨酸的 ARG2 代谢抑制炎症，而 iNOS 代谢促进气道炎症，支持精氨酸代谢控制炎症的核心作用。