文献综述

脂质代谢在哮喘中作用机制的研究进展

  • 陈少甜 综述 ,
  • 杨男 审校
展开
  • 中国医科大学附属盛京医院小儿呼吸内科(辽宁沈阳 110004)

收稿日期: 2023-03-14

  网络出版日期: 2024-05-10

基金资助

国家自然科学基金项目(81800027);辽宁省应用基础研究计划项目(2022JH2/101500004)

Research progress on mechanism of lipid metabolism in asthma

  • Shaotian Reviewer: CHEN ,
  • Nan Reviser: YANG
Expand
  • Department of Pediatric Pulmonology, Shengjing Hospital of China Medical University, Shenyang 110004, Liaoning, China

Received date: 2023-03-14

  Online published: 2024-05-10

摘要

哮喘是最常见的慢性呼吸系统疾病之一,累及全年龄段,其患病率与社会医疗费用逐年升高。近年来大量研究证实,脂质分子作为调节多种细胞生物过程强有力的信号分子,通过对哮喘患者气道不同细胞的调节,影响疾病的发生发展。因此,本文从近年来不断发展的脂质组学与哮喘的研究出发,总结哮喘中潜在的代谢生物标志物,探讨脂质代谢在哮喘发病过程对不同细胞发挥的作用机制,为哮喘的个性化治疗提供思路。

本文引用格式

陈少甜 综述 , 杨男 审校 . 脂质代谢在哮喘中作用机制的研究进展[J]. 临床儿科杂志, 2024 , 42(5) : 461 -466 . DOI: 10.12372/jcp.2024.23e0201

Abstract

Asthma is one of the most common chronic respiratory diseases, affecting all age group. Its prevalence and social healthcare costs are increasing every year. The results of numerous studies in recent years have conclusively demonstrated the role of lipid molecules as powerful signaling molecules that regulate a variety of cellular biological processes. By regulating different cells in the airways of asthma patients, they influence the occurrence and development of the disease. Therefore, this article summarizes the potential metabolic biomarkers in asthma, and explores the mechanisms of lipid metabolism in asthma pathogenesis on different cells to provide ideas for personalized asthma treatment from the lipidomics and asthma studies that have been developed in recent years.

参考文献

[1] Porsbjerg C, Melén E, Lehtim?ki L, et al. Asthma[J]. Lancet, 2023, 401(10379): 858-873.
[2] García-Marcos L, Asher MI, Pearce N, et al. The burden of asthma, hay fever and eczema in children in 25 countries: GAN Phase I study[J]. Eur Respir J, 2022, 60(3): 2102866.
[3] Mortimer K, Lesosky M, García-Marcos L, et al. The burden of asthma, hay fever and eczema in adults in 17 countries: GAN Phase I study[J]. Eur Respir J, 2022, 60(3): 2102865.
[4] Stern J, Pier J, Litonjua AA. Asthma epidemiology and risk factors[J]. Semin Immunopathol, 2020, 42(1): 5-15.
[5] K?berlin MS, Snijder B, Heinz LX, et al. A conserved circular network of coregulated lipids modulates innate immune responses[J]. Cell, 2015, 162(1): 170-183.
[6] Sakae H, Ogiso Y, Matsuda M, et al. Ceramide nanoliposomes as potential therapeutic reagents for asthma[J]. Cells, 2023, 12(4): 591.
[7] Wang R, Li B, Lam SM, et al. Integration of lipidomics and metabolomics for in-depth understanding of cellular mechanism and disease progression[J]. J Genet Genomics, 2020, 47(2): 69-83.
[8] Jiang T, Dai L, Li P, et al. Lipid metabolism and identification of biomarkers in asthma by lipidomic analysis[J]. Biochim Biophys Acta Mol Cell Biol Lipids, 2021, 1866(2): 158853.
[9] Wang S, Tang K, Lu Y, et al. Revealing the role of glycerophospholipid metabolism in asthma through plasma lipidomics[J]. Clin Chim Acta, 2021, 513: 34-42.
[10] Delgado-Dolset MI, Obeso D, Rodríguez-Coira J, et al. Understanding uncontrolled severe allergic asthma by integration of omic and clinical data[J]. Allergy, 2022, 77(6): 1772-1785.
[11] Daley-Yates P, Keppler B, Brealey N, et al. Inhaled glucocorticoid-induced metabolome changes in asthma[J]. Eur J Endocrinol, 2022, 187(3): 413-427.
[12] Daley-Yates P, Keppler B, Baines A, et al. Metabolomic changes related to airway inflammation, asthma pathogenesis and systemic activity following inhaled fluticasone furoate/vilanterol: a randomized controlled trial[J]. Respir Res, 2022, 23(1): 258.
[13] Papamichael MM, Katsardis C, Tsoukalas D, et al. Plasma lipid biomarkers in relation to BMI, lung function, and airway inflammation in pediatric asthma[J]. Metabolomics, 2021, 17(7): 63.
[14] Rago D, Pedersen CT, Huang M, et al. Characteristics and mechanisms of a sphingolipid-associated childhood asthma endotype[J]. Am J Respir Crit Care Med, 2021, 203(7): 853-863.
[15] Zheng P, Bian X, Zhai Y, et al. Metabolomics reveals a correlation between hydroxyeicosatetraenoic acids and allergic asthma: Evidence from three years' immunotherapy[J]. Pediatr Allergy Immunol, 2021, 32(8): 1654-1662.
[16] Chang-Chien J, Huang HY, Tsai HJ, et al. Metabolomic differences of exhaled breath condensate among children with and without asthma[J]. Pediatr Allergy Immunol, 2021, 32(2): 264-272.
[17] Kelly RS, Mendez KM, Huang M, et al. Metabo-endotypes of asthma reveal differences in lung function: discovery and validation in two TOPMed cohorts[J]. Am J Respir Crit Care Med, 2022, 205(3): 288-299.
[18] Ualiyeva S, Lemire E, Aviles EC, et al. Tuft cell-produced cysteinyl leukotrienes and IL-25 synergistically initiate lung type 2 inflammation[J]. Sci Immunol, 2021, 6(66): eabj0474.
[19] Esteves P, Blanc L, Celle A, et al. Crucial role of fatty acid oxidation in asthmatic bronchial smooth muscle remodelling[J]. Eur Respir J, 2021, 58(5): 2004252.
[20] Tibbitt CA, Stark JM, Martens L, et al. Single-cell RNA sequencing of the T helper cell response to house dust mites defines a distinct gene expression signature in airway Th2 cells[J]. Immunity, 2019, 51(1): 169-184.
[21] Chen W, Luo J, Ye Y, et al. The roles of type 2 cytotoxic T cells in inflammation, tissue remodeling, and prostaglandin (PG) D2 production are attenuated by PGD2 receptor 2 antagonism[J]. J Immunol, 2021, 206(11): 2714-2724.
[22] Norlander AE, Bloodworth MH, Toki S, et al. Prostaglandin I2 signaling licenses Treg suppressive function and prevents pathogenic reprogramming[J]. J Clin Invest, 2021, 131(7): e140690.
[23] Draijer C, Florez-Sampedro L, Reker-Smit C, et al. Explaining the polarized macrophage pool during murine allergic lung inflammation[J]. Front Immunol, 2022, 13: 1056477.
[24] Batista-Gonzalez A, Vidal R, Criollo A, et al. New insights on the role of lipid metabolism in the metabolic reprogramming of macrophages[J]. Front Immunol, 2020, 10: 2993.
[25] Hou Y, Wei D, Zhang Z, et al. FABP5 controls macrophage alternative activation and allergic asthma by selectively programming long-chain unsaturated fatty acid metabolism[J]. Cell Rep, 2022, 41(7): 111668.
[26] Abreu SC, Lopes-Pacheco M, da Silva AL, et al. Eicosapentaenoic acid enhances the effects of mesenchymal stromal cell therapy in experimental allergic asthma[J]. Front Immunol, 2018, 9: 1147.
[27] Fussbroich D, Colas RA, Eickmeier O, et al. A combination of LCPUFA ameliorates airway inflammation in asthmatic mice by promoting pro-resolving effects and reducing adverse effects of EPA[J]. Mucosal Immunol, 2020, 13(3): 481-492.
[28] Huang C, Du W, Ni Y, et al. The effect of short-chain fatty acids on M2 macrophages polarization in vitro and in vivo[J]. Clin Exp Immunol, 2022, 207(1): 53-64.
[29] Bottemanne P, Paquot A, Ameraoui H, et al. 25-Hydroxycholesterol metabolism is altered by lung inflammation, and its local administration modulates lung inflammation in mice[J]. FASEB J, 2021, 35(4): e21514.
[30] Miyata J, Fukunaga K, Iwamoto R, et al. Dysregulated synthesis of protectin D1 in eosinophils from patients with severe asthma[J]. J Allergy Clin Immunol, 2013, 131(2): 353-360.
[31] Carstensen S, Gress C, Erpenbeck VJ, et al. Prostaglandin D2 metabolites activate asthmatic patient-derived type 2 innate lymphoid cells and eosinophils via the DP2 receptor[J]. Respir Res, 2021, 22(1): 262.
[32] James BN, Oyeniran C, Sturgill JL, et al. Ceramide in apoptosis and oxidative stress in allergic inflammation and asthma[J]. J Allergy Clin Immunol, 2021, 147(5): 1936-1948.
[33] James BN, Weigel C, Green CD, et al. Neutrophilia in severe asthma is reduced in Ormdl3 overexpressing mice[J]. FASEB J, 2023, 37(3): e22799.
[34] Bankova LG, Boyce JA. A new spin on mast cells and cysteinyl leukotrienes: Leukotriene E4 activates mast cells in vivo[J]. J Allergy Clin Immunol, 2018, 142(4): 1056-1057.
[35] Son SE, Koh JM, Im DS. Activation of free fatty acid receptor 4 (FFA4) ameliorates ovalbumin-induced allergic asthma by suppressing activation of dendritic and mast cells in mice[J]. Int Journal Mol Sci, 2022, 23(9): 5270.
[36] Karagiannis F, Masouleh SK, Wunderling K, et al. Lipid-droplet formation drives pathogenic group 2 innate lymphoid cells in airway inflammation[J]. Immunity, 2020, 52(4): 620-634.
[37] Oyesola OO, Duque C, Huang LC, et al. The prostaglandin D2 receptor CRTH2 promotes IL-33-induced ILC2 accumulation in the lung[J]. J Immunol, 2020, 204(4): 1001-1011.
[38] Miyata J, Yokokura Y, Moro K, et al. 12/15-lipoxygenase regulates IL-33-induced eosinophilic airway inflammation in mice[J]. Front Immunol, 2021, 12: 687192.
[39] Levan SR, Stamnes KA, Lin DL, et al. Elevated faecal 12,13-diHOME concentration in neonates at high risk for asthma is produced by gut bacteria and impedes immune tolerance[J]. Nat Microbiol, 2019, 4(11): 1851-1861.
[40] Gao Y, Zhao C, Wang W, et al. Prostaglandins E2 signal mediated by receptor subtype EP2 promotes IgE production in vivo and contributes to asthma development[J]. Sci Rep, 2016, 6: 20505.
[41] Kim N, Thatcher TH, Sime PJ, et al. Corticosteroids inhibit anti-IgE activities of specialized proresolving mediators on B cells from asthma patients[J]. JCI Insight, 2017, 2(3): e88588.
[42] Ravi A, Goorsenberg AWM, Dijkhuis A, et al. Metabolic differences between bronchial epithelium from healthy individuals and patients with asthma and the effect of bronchial thermoplasty[J]. J Allergy Clin Immunol, 2021, 148(5): 1236-1248.
[43] Pascoe CD, Roy N, Turner-Brannen E, et al. Oxidized phosphatidylcholines induce multiple functional defects in airway epithelial cells[J]. Am J Physiol Lung Cell Mol Physiol, 2021, 321(4): L703-L717.
[44] Pascoe CD, Jha A, Ryu MH, et al. Allergen inhalation generates pro-inflammatory oxidised phosphatidylcholine associated with airway dysfunction[J]. Eur Respir J, 2021, 57(2): 2000839.
[45] Mochimaru T, Fukunaga K, Miyata J, et al. 12-OH-17, 18- Epoxyeicosatetraenoic acid alleviates eosinophilic airway inflammation in murine lungs[J]. Allergy, 2018, 73(2): 369-378.
[46] Kanti MM, Striessnig-Bina I, Wieser BI, et al. Adipose triglyceride lipase-mediated lipid catabolism is essential for bronchiolar regeneration[J]. JCI Insight, 2022, 7(9): e149438.
[47] Matoba A, Matsuyama N, Shibata S, et al. The free fatty acid receptor 1 promotes airway smooth muscle cell proliferation through MEK/ERK and PI3K/Akt signaling pathways[J]. Am J Physiol Lung Cell Mol Physiol, 2018, 314(3): L333-L348.
[48] Saunders R, Kaul H, Berair R, et al. DP2 antagonism reduces airway smooth muscle mass in asthma by decreasing eosinophilia and myofibroblast recruitment[J]. Sci Transl Med, 2019, 11(479): eaao6451.
[49] Blais-Lecours P, Laouafa S, Arias-Reyes C, et al. Metabolic adaptation of airway smooth muscle cells to an SPHK2 substrate precedes cytostasis[J]. Am J Respir Cell Mol Biol, 2020, 62(1): 35-42.
[50] Liu Y, Wei L, He C, et al. Lipoxin A4 inhibits ovalbumin-induced airway inflammation and airway remodeling in a mouse model of asthma[J]. Chem Biol Interact, 2021, 349: 109660.
文章导航

/