• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

COVID-19 患者的炎症反应是由炎症小体与 SARS-CoV-2 的相互作用引起的。

Inflammatory Response in COVID-19 Patients Resulting from the Interaction of the Inflammasome and SARS-CoV-2.

机构信息

Department of Biotechnology, College of Biomedical & Health Science, Konkuk University, Chungju 27478, Korea.

Department of Anesthesiology and Pain Medicine, Yonsei University College of Medicine, Seoul 03722, Korea.

出版信息

Int J Mol Sci. 2021 Jul 24;22(15):7914. doi: 10.3390/ijms22157914.

DOI:10.3390/ijms22157914
PMID:34360684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8348456/
Abstract

The outbreak of the coronavirus disease 2019 (COVID-19) began at the end of 2019. COVID-19 is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and patients with COVID-19 may exhibit poor clinical outcomes. Some patients with severe COVID-19 experience cytokine release syndrome (CRS) or a cytokine storm-elevated levels of hyperactivated immune cells-and circulating pro-inflammatory cytokines, including interleukin (IL)-1β and IL-18. This severe inflammatory response can lead to organ damage/failure and even death. The inflammasome is an intracellular immune complex that is responsible for the secretion of IL-1β and IL-18 in various human diseases. Recently, there has been a growing number of studies revealing a link between the inflammasome and COVID-19. Therefore, this article summarizes the current literature regarding the inflammasome complex and COVID-19.

摘要

2019 年底爆发了 2019 冠状病毒病(COVID-19)。COVID-19 是由严重急性呼吸系统综合征冠状病毒 2(SARS-CoV-2)感染引起的,COVID-19 患者可能出现不良临床结局。一些严重 COVID-19 患者会经历细胞因子释放综合征(CRS)或细胞因子风暴-过度激活的免疫细胞和循环促炎细胞因子水平升高,包括白细胞介素(IL)-1β和 IL-18。这种严重的炎症反应可导致器官损伤/衰竭,甚至死亡。炎性小体是一种细胞内免疫复合物,负责在各种人类疾病中分泌 IL-1β和 IL-18。最近,越来越多的研究揭示了炎性小体与 COVID-19 之间的联系。因此,本文总结了目前关于炎性小体复合物与 COVID-19 的文献。

相似文献

1
Inflammatory Response in COVID-19 Patients Resulting from the Interaction of the Inflammasome and SARS-CoV-2.COVID-19 患者的炎症反应是由炎症小体与 SARS-CoV-2 的相互作用引起的。
Int J Mol Sci. 2021 Jul 24;22(15):7914. doi: 10.3390/ijms22157914.
2
in COVID-19 Infection: Immunopathogenesis and Possible Therapeutic Perspective.在 COVID-19 感染:免疫发病机制和可能的治疗视角中。
Viral Immunol. 2021 Dec;34(10):679-688. doi: 10.1089/vim.2021.0071. Epub 2021 Dec 8.
3
Inflammasomes and SARS-CoV-2 Infection.炎症小体与 SARS-CoV-2 感染
Viruses. 2021 Dec 14;13(12):2513. doi: 10.3390/v13122513.
4
SARS-CoV-2 may trigger inflammasome and pyroptosis in the central nervous system: a mechanistic view of neurotropism.SARS-CoV-2 可能在中枢神经系统中触发炎症小体和细胞焦亡:神经嗜性的机制观点。
Inflammopharmacology. 2021 Aug;29(4):1049-1059. doi: 10.1007/s10787-021-00845-4. Epub 2021 Jul 9.
5
Hyperinflammatory Immune Response and COVID-19: A Double Edged Sword.细胞因子风暴与 COVID-19:一把双刃剑。
Front Immunol. 2021 Sep 30;12:742941. doi: 10.3389/fimmu.2021.742941. eCollection 2021.
6
Spontaneous NLRP3 inflammasome-driven IL-1-β secretion is induced in severe COVID-19 patients and responds to anakinra treatment.在重症 COVID-19 患者中可诱导自发 NLRP3 炎性小体驱动的 IL-1-β 分泌,并对阿那白滞素治疗有反应。
J Allergy Clin Immunol. 2022 Oct;150(4):796-805. doi: 10.1016/j.jaci.2022.05.029. Epub 2022 Jul 11.
7
NLRP3 Inflammasome: The Stormy Link Between Obesity and COVID-19.NLRP3 炎性小体:肥胖与 COVID-19 之间的暴风雨联系。
Front Immunol. 2020 Oct 30;11:570251. doi: 10.3389/fimmu.2020.570251. eCollection 2020.
8
Diagnosis of SARS-CoV-2 infection in the setting of the cytokine release syndrome.在细胞因子释放综合征背景下 SARS-CoV-2 感染的诊断。
Expert Rev Mol Diagn. 2020 Nov;20(11):1087-1097. doi: 10.1080/14737159.2020.1830760. Epub 2020 Oct 12.
9
SARS-CoV-2 Causes a Different Cytokine Response Compared to Other Cytokine Storm-Causing Respiratory Viruses in Severely Ill Patients.SARS-CoV-2 引起的细胞因子反应与其他严重感染患者中导致细胞因子风暴的呼吸道病毒不同。
Front Immunol. 2021 Mar 1;12:629193. doi: 10.3389/fimmu.2021.629193. eCollection 2021.
10
Therapeutic Role of Tocilizumab in SARS-CoV-2-Induced Cytokine Storm: Rationale and Current Evidence.托珠单抗在 SARS-CoV-2 诱导的细胞因子风暴中的治疗作用:原理和现有证据。
Int J Mol Sci. 2021 Mar 17;22(6):3059. doi: 10.3390/ijms22063059.

引用本文的文献

1
Antiviral and anti-inflammatory efficacy of nanoencapsulated brazilian green propolis against SARS-CoV-2.纳米包封的巴西绿蜂胶对严重急性呼吸综合征冠状病毒2的抗病毒和抗炎功效
Sci Rep. 2025 Jul 1;15(1):21627. doi: 10.1038/s41598-025-05683-w.
2
iPSC-derived human cortical organoids display profound alterations of cellular homeostasis following SARS-CoV-2 infection and Spike protein exposure.诱导多能干细胞衍生的人类皮质类器官在感染新冠病毒和暴露于刺突蛋白后,细胞稳态出现了显著改变。
FASEB J. 2025 Feb 28;39(4):e70396. doi: 10.1096/fj.202401604RRR.
3
An Overview of Pediatric Pulmonary Complications During COVID-19 Pandemic: A Lesson for Future.

本文引用的文献

1
An evidence that SARS-Cov-2/COVID-19 spike protein (SP) damages hematopoietic stem/progenitor cells in the mechanism of pyroptosis in Nlrp3 inflammasome-dependent manner.有证据表明,严重急性呼吸综合征冠状病毒2/冠状病毒病(SARS-CoV-2/COVID-19)刺突蛋白(SP)以Nlrp3炎性小体依赖性方式通过细胞焦亡机制损害造血干细胞/祖细胞。
Leukemia. 2021 Oct;35(10):3026-3029. doi: 10.1038/s41375-021-01332-z. Epub 2021 Jun 23.
2
The SARS-CoV-2 spike protein subunit S1 induces COVID-19-like acute lung injury in Κ18-hACE2 transgenic mice and barrier dysfunction in human endothelial cells.SARS-CoV-2 刺突蛋白亚单位 S1 在 Κ18-hACE2 转基因小鼠中诱导 COVID-19 样急性肺损伤,并在人内皮细胞中引起屏障功能障碍。
Am J Physiol Lung Cell Mol Physiol. 2021 Aug 1;321(2):L477-L484. doi: 10.1152/ajplung.00223.2021. Epub 2021 Jun 22.
3
儿童在 COVID-19 大流行期间的肺部并发症概述:未来的教训。
Immun Inflamm Dis. 2024 Nov;12(11):e70049. doi: 10.1002/iid3.70049.
4
Comparative Efficacy of Inhaled and Intravenous Corticosteroids in Managing COVID-19-Related Acute Respiratory Distress Syndrome.吸入性和静脉注射皮质类固醇治疗 COVID-19 相关急性呼吸窘迫综合征的疗效比较
Pharmaceutics. 2024 Jul 18;16(7):952. doi: 10.3390/pharmaceutics16070952.
5
Inhibition of SARS-CoV-2-Induced NLRP3 Inflammasome-Mediated Lung Cell Inflammation by Triphala-Loaded Nanoparticle Targeting Spike Glycoprotein S1.靶向刺突糖蛋白S1的三果制剂纳米颗粒对严重急性呼吸综合征冠状病毒2诱导的NLRP3炎性小体介导的肺细胞炎症的抑制作用
Pharmaceutics. 2024 Jun 2;16(6):751. doi: 10.3390/pharmaceutics16060751.
6
Investigating the Nexus of NLRP3 Inflammasomes and COVID-19 Pathogenesis: Unraveling Molecular Triggers and Therapeutic Strategies.探讨 NLRP3 炎性小体与 COVID-19 发病机制的关联:揭示分子触发因素和治疗策略。
Viruses. 2024 Jan 31;16(2):213. doi: 10.3390/v16020213.
7
Phase angle and rectus femoris cross-sectional area as predictors of severe malnutrition and their relationship with complications in outpatients with post-critical SARS-CoV2 disease.作为预测严重营养不良指标的相角和股直肌横截面积及其与重症新冠病毒感染后疾病门诊患者并发症的关系。
Front Nutr. 2023 Nov 21;10:1218266. doi: 10.3389/fnut.2023.1218266. eCollection 2023.
8
Dynamics of the Microbiota and Its Relationship with Post-COVID-19 Syndrome.微生物群及其与新冠后综合征关系的动态变化。
Int J Mol Sci. 2023 Oct 1;24(19):14822. doi: 10.3390/ijms241914822.
9
Race between virus and inflammasomes: inhibition or escape, intervention and therapy.病毒与炎症小体的赛跑:抑制还是逃避,干预与治疗。
Front Cell Infect Microbiol. 2023 Jul 3;13:1173505. doi: 10.3389/fcimb.2023.1173505. eCollection 2023.
10
Utility of laboratory and immune biomarkers in predicting disease progression and mortality among patients with moderate to severe COVID-19 disease at a Philippine tertiary hospital.菲律宾一家三级医院的中度至重度 COVID-19 患者中,实验室和免疫生物标志物在预测疾病进展和死亡率方面的效用。
Front Immunol. 2023 Feb 28;14:1123497. doi: 10.3389/fimmu.2023.1123497. eCollection 2023.
A cohort autopsy study defines COVID-19 systemic pathogenesis.一项队列尸检研究定义了 COVID-19 的全身发病机制。
Cell Res. 2021 Aug;31(8):836-846. doi: 10.1038/s41422-021-00523-8. Epub 2021 Jun 16.
4
Long-lived macrophage reprogramming drives spike protein-mediated inflammasome activation in COVID-19.长寿巨噬细胞重编程导致 COVID-19 中 Spike 蛋白介导的炎症小体激活。
EMBO Mol Med. 2021 Aug 9;13(8):e14150. doi: 10.15252/emmm.202114150. Epub 2021 Jun 16.
5
Metformin inhibition of mitochondrial ATP and DNA synthesis abrogates NLRP3 inflammasome activation and pulmonary inflammation.二甲双胍抑制线粒体 ATP 和 DNA 合成可阻断 NLRP3 炎症小体激活和肺部炎症。
Immunity. 2021 Jul 13;54(7):1463-1477.e11. doi: 10.1016/j.immuni.2021.05.004. Epub 2021 Jun 10.
6
COVID-19 Severity Potentially Modulated by Cardiovascular-Disease-Associated Immune Dysregulation.COVID-19 严重程度可能受心血管疾病相关免疫失调的调节。
Viruses. 2021 May 28;13(6):1018. doi: 10.3390/v13061018.
7
Caspases and therapeutic potential of caspase inhibitors in moderate-severe SARS-CoV-2 infection and long COVID.Caspases 与 caspase 抑制剂在中重度 SARS-CoV-2 感染和长新冠中的治疗潜力。
Allergy. 2022 Jan;77(1):118-129. doi: 10.1111/all.14907. Epub 2021 Jun 2.
8
The NLRP3-Inflammasome-Caspase-1 Pathway Is Upregulated in Idiopathic Pulmonary Fibrosis and Acute Exacerbations and Is Inducible by Apoptotic A549 Cells.NLRP3 炎性小体-半胱天冬酶-1 通路在特发性肺纤维化和急性加重期上调,并可被凋亡的 A549 细胞诱导。
Front Immunol. 2021 Apr 23;12:642855. doi: 10.3389/fimmu.2021.642855. eCollection 2021.
9
An autopsy study of the spectrum of severe COVID-19 in children: From SARS to different phenotypes of MIS-C.儿童重症新冠病毒病的尸检研究:从严重急性呼吸综合征到儿童多系统炎症综合征的不同表型
EClinicalMedicine. 2021 May;35:100850. doi: 10.1016/j.eclinm.2021.100850. Epub 2021 Apr 26.
10
Epigenome-wide association study of COVID-19 severity with respiratory failure.COVID-19 严重程度与呼吸衰竭的全基因组关联研究。
EBioMedicine. 2021 Apr;66:103339. doi: 10.1016/j.ebiom.2021.103339. Epub 2021 Apr 15.