调节免疫应答在新型冠状病毒所致心肌损伤中的作用

基础医学与临床 ›› 2020, Vol. 40 ›› Issue (11): 1556-1560.

调节免疫应答在新型冠状病毒所致心肌损伤中的作用

胡恒境^1,2, 刘垚¹, 姜志胜^2*

1.南华大学附属第一医院心内科, 湖南衡阳 421000;
2.南华大学心血管疾病研究所,动脉硬化学湖南省重点实验室, 湖南衡阳 421000

收稿日期:2020-05-23 修回日期:2020-07-14 出版日期:2020-11-05 发布日期:2020-10-30
通讯作者: ^* zsjiang2015@163.com
基金资助:
国家自然科学基金(81700306);湖南省自然科学基金(2018JJ3469);中国博士后科学基金(2017M622588);湖南省卫生健康委项目(C2019115)

Role of regulatory immune response to myocardial injury caused by SARS-CoV-2

HU Heng-jing^1,2, LIU Yao¹, JIANG Zhi-sheng^2*

1. Department of Cardiology, the First Affiliated Hospital of University of South China, Hengyang 421000;
2. Institute of Cardiovascular Disease and Key Lab for Arteriosclerology of Hunan Province, University of South China, Hengyang 421000, China

Received:2020-05-23 Revised:2020-07-14 Online:2020-11-05 Published:2020-10-30
Contact: ^* zsjiang2015@163.com

摘要/Abstract

摘要： 新型冠状病毒(SARS-CoV-2)是2019年末在湖北武汉发现的第7种可以感染人类的冠状病毒,归为β属。临床统计发现该病毒常导致心肌损伤,且具有心血管基础疾病患者的感染风险更高,预后更差。目前新型冠状病毒对心肌损伤机制仍不明了。本文从新型冠状病毒与机体免疫系统相互关系阐述其对心肌损伤机制,并介绍相关的免疫治疗进展。

关键词: 新型冠状病毒, 免疫应答, 心肌损伤

Abstract: The 2019 novel coronavirus(SARS-CoV-2) belongs to β coronavirus and is the seventh one to be found as pathogen of humans in Wuhan by the end of 2019. Clinical statistics shows that the virus often leads to myocardial injury, and patients with underlying cardiovascular diseases have a higher risk of infection and worse prognosis. The mechanism of the virus on myocardial injury is still unknown. This paper discusses the role of SARS-CoV-2 in myocardial damage with regard to immune system.

Key words: SARS-CoV-2, immune response, myocardial injury

中图分类号:

胡恒境, 刘垚, 姜志胜. 调节免疫应答在新型冠状病毒所致心肌损伤中的作用[J]. 基础医学与临床, 2020, 40(11): 1556-1560.

HU Heng-jing, LIU Yao, JIANG Zhi-sheng. Role of regulatory immune response to myocardial injury caused by SARS-CoV-2[J]. Basic & Clinical Medicine, 2020, 40(11): 1556-1560.

参考文献

[1] Xu XW, Wu XX, Jiang XG, et al. Clinical findings in a group of patients infected with the 2019 novel coronavirus (SARS-CoV-2) outside of Wuhan, China: retrospective case series[J]. Br Med J, 2020,19:368:m606. doi: 10.1136/bmj.m606.
[2] Lippi G, Lavie CJ, Sanchis-Gomar F. Cardiac troponin I in patients with coronavirus disease 2019 (COVID-19): evidence from a meta-analysis[J]. Prog Cardiovasc Dis, 2020.10. doi: 10.1016/j.pcad.2020.03.001.
[3] Channappanavar R, Fett C, Mack M, et al. Sex-based differences in susceptibility to severe acute respiratory syndrome coronavirus infection[J]. J Immunol, 2017, 198:4046-4053.
[4] Wu Z, McGoogan JM. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: summary of a report of 72 314 cases from the Chinese Center for Disease Control and Preven-tion[J]. JAMA, 2020,24. doi: 10.1001/jama.2020.2648.
[5] Fan Q, Tao R1, Zhang H, et al. Dectin-1 contributes to myocardial ischemia/reperfusion injury by regulating macrophage polarization and neutrophil infiltration[J]. Circulation, 2019, 139:663-678.
[6] Xu Z, Shi L, Wang Y, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome[J]. Lancet Respir Med, 2020, 8:420-422.
[7] Bin Jardan YA, Ansari MA, Raish M, et al. Sinapic acid ameliorates oxidative stress, inflammation, and apoptosis in acute doxorubicin-induced cardiotoxicity via the NF-κB-mediated pathway[J]. Biomed Res Int, 2020:3921796. doi: 10.1155/2020/3921796.
[8] Folz RJ, Elkordy MA. Coronavirus pneumonia following autologous bone marrow transplantation for breast cancer[J]. Chest, 1999, 115:901-905.
[9] Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study[J]. Lancet, 2020, 395:1054-1062.
[10] Mahmud-Al-Rafat A, Majumder A, Taufiqur Rahman KM, et al. Decoding the enigma of antiviral crisis: does one target molecule regulate all?[J]. Cytokine, 2019, 115:13-23.
[11] Basu R, Poglitsch M, Yogasundaram H, et al. Roles of angiotensin peptides and recombinant human ACE2 in heart failure[J]. J Am Coll Cardiol, 2017, 69:805-819.
[12] Rosenthal DG, Parwani P, Murray TO, et al. Long-term corticosteroid-sparing immunosuppression for cardiac sarcoidosis[J]. J Am Heart Assoc, 2019, 8:e010952. doi: 10.1161/JAHA.118.010952.
[13] Jensen AV, Egelund GB, Andersen SB, et al. The impact of blood glucose on community-acquired pneumonia: a retrospective cohort study[J]. ERJ Open Res, 2017, 3:00114-2016. doi: 10.1183/23120541.00114-2016.
[14] Hunter CA, Jones SA. IL-6 as a keystone cytokine in health and disease[J]. Nat Immunol, 2015, 16:448-457.
[15] Perez-Moreiras JV, Gomez-Reino JJ, Maneiro JR, et al. Efficacy of tocilizumab in patients with moderate-to-severe corticosteroid-resistant graves orbitopathy: a randomized clinical trial[J]. Am J Ophthalmol, 2018, 195:181-190.
[16] Knudsen JG, Gudiksen A, Bertholdt L, et al. Skeletal muscle IL-6 regulates muscle substrate utilization and adipose tissue metabolism during recovery from an acute bout of exercise[J]. PLoS One, 2017, 12:e0189301. doi:10.1371/journal.pone.0189301.
[17] Jing H, Gao X, Xu L, et al. H2S promotes a glycometabolism disorder by disturbing the Th1/Th2 balance during LPS-induced inflammation in the skeletal muscles of chickens[J]. Chemosphere, 2019, 222:124-131.
[18] Rahman MA, Cumming BM, Addicott KW, et al. Hydrogen sulfide dysregulates the immune response by suppressing central carbon metabolism to promote tuberculosis[J]. Proc Natl Acad Sci U S A, 2020, 117:6663-6674.
[19] Hu D, Linders A, Yamak A, et al. Metabolic maturation of human pluripotent stem cell-derived cardiomyocytes by inhibition of HIF1α and LDHA[J]. Circ Res, 2018, 123:1066-1079.
[20] Maddaloni E, Buzzetti R. COVID-19 and diabetes melli-tus: unveiling the interaction of two pandemics[J]. Diabetes Metab Res Rev, 2020,31:e33213321. doi: 10.1002/dmrr.3321.
[21] Conti P, Ronconi G, Caraffa A, et al. Induction of pro-inflammatory cytokines (IL-1 and IL-6) and lung inflammation by Coronavirus-19 (COVID-19 or SARS-CoV-2): anti-inflammatory strategies[J]. J Biol Regul Homeost Agents, 2020,34. doi: 10.23812/CONTI-E.
[22] Toldo S, Mezzaroma E, Van Tassell BW, et al. Interleukin-1β blockade improves cardiac remodelling after myocardial infarction without interrupting the inflammasome in the mouse[J]. Exp Physiol, 2013, 98:734-745.
[23] Zhao J, Zhao J, Mangalam AK, et al. Airway memory CD4(+) T cells mediate protective immunity against emerging respiratory coronaviruses[J]. Immunity, 2016, 44:1379-1391.
[24] Kritas SK, Ronconi G, Caraffa A, et al. Mast cells contribute to coronavirus-induced inflammation: new anti-inflammatory strategy[J]. J Biol Regul Homeost Agents, 2020,34. doi: 10.23812/20-Editorial-Kritas.
[25] Lu R, Zhao X, Li J, et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: implications for virus origins and receptor binding[J]. Lancet, 2020, 395:565-574.
[26] Yang CW, Lee YZ, Hsu HY, et al. Targeting coronaviral replication and cellular JAK2 mediated dominant NF-κB activation for comprehensive and ultimate inhibition of coronaviral activity[J]. Sci Rep, 2017, 7:4105. doi: 10.1038/s41598-017-04203-9.
[27] Wang W, Ye S, Zhang L, et al. Granulocyte colony-stimulating factor attenuates myocardial remodeling and ventricular arrhythmia susceptibility via the JAK2-STAT3 pathway in a rabbit model of coronary microembolization[J]. BMC Cardiovasc Disord, 2020, 20:85. doi: 10.1186/s12872-020-01385-5.