• 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

在新冠时代,感染、微生态失调和炎症相互作用于儿童。

Infection, Dysbiosis and Inflammation Interplay in the COVID Era in Children.

机构信息

Department of Medical Physics, Alexandru Ioan Cuza University, 11 Carol I Boulevard, 700506 Iasi, Romania.

President of the International Society for Medical Laser Applications (ISLA Transcontinental), German Vice President of the German-Chinese Research Foundation (DCFG) for TCM, Honorary President of the European Federation of Acupuncture and Moxibustion Societies, 8053 Graz, Austria.

出版信息

Int J Mol Sci. 2023 Jun 29;24(13):10874. doi: 10.3390/ijms241310874.

DOI:10.3390/ijms241310874
PMID:37446047
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10342011/
Abstract

For over three years, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in children and adolescents has generated repercussions, especially a few weeks after infection, for symptomatic patients who tested positive, for asymptomatic ones, or even just the contacts of an infected person, and evolved from severe forms such as multisystem inflammatory syndrome in children (MIS-C) to multifarious clinical manifestations in long COVID (LC). Referred to under the umbrella term LC, the onset of persistent and highly heterogeneous symptoms such as fatigue, post-exertion malaise, cognitive dysfunction, and others have a major impact on the child's daily quality of life for months. The first aim of this review was to highlight the circumstances of the pathophysiological changes produced by COVID-19 in children and to better understand the hyperinflammation in COVID-19 and how MIS-C, as a life-threatening condition, could have been avoided in some patients. Another goal was to better identify the interplay between infection, dysbiosis, and inflammation at a molecular and cellular level, to better guide scientists, physicians, and pediatricians to advance new lines of medical action to avoid the post-acute sequelae of SARS-CoV-2 infection. The third objective was to identify symptoms and their connection to molecular pathways to recognize LC more easily. The fourth purpose was to connect the triggering factors of LC with related sequelae following acute SARS-CoV-2 injuries to systems and organs, the persistence of the virus, and some of its components in hidden reservoirs, including the gut and the central nervous system. The reactivation of other latent infectious agents in the host's immune environments, the interaction of this virus with the microbiome, immune hyperactivation, and autoimmunity generated by molecular mimicry between viral agents and host proteins, could initiate a targeted and individualized management. New high-tech solutions, molecules, probiotics, and others should be discovered to innovatively solve the interplay between RNA persistent viruses, microbiota, and our immune system.

摘要

三年多来,儿童和青少年严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)引起了反响,尤其是在感染后几周,对症状阳性的患者、无症状患者,甚至只是感染者的接触者,从儿童多系统炎症综合征(MIS-C)等严重形式演变而来,出现了长期 COVID(LC)等多种临床表现。在 LC 的总称下,持续性和高度异质性症状的出现,如疲劳、运动后不适、认知功能障碍等,对儿童的日常生活质量产生了重大影响,持续数月之久。本综述的首要目的是强调 COVID-19 引起的儿童病理生理变化的情况,更好地理解 COVID-19 中的过度炎症,以及如何避免某些患者发生危及生命的 MIS-C。另一个目标是更好地识别感染、菌群失调和炎症在分子和细胞水平上的相互作用,以便更好地指导科学家、医生和儿科医生提出新的医疗行动方案,以避免 SARS-CoV-2 感染后的急性后遗症。第三个目标是识别症状及其与分子途径的联系,以便更轻松地识别 LC。第四个目的是将 LC 的触发因素与急性 SARS-CoV-2 损伤后与系统和器官相关的后遗症、病毒的持续存在及其在隐藏储库中的一些成分(包括肠道和中枢神经系统)联系起来。宿主免疫环境中潜伏性传染因子的重新激活、该病毒与微生物组的相互作用、病毒因子与宿主蛋白之间的分子模拟引起的免疫过度激活和自身免疫,都可能引发有针对性和个体化的管理。应发现新的高科技解决方案、分子、益生菌等,以创新的方式解决 RNA 持续性病毒、微生物组和我们免疫系统之间的相互作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/dfb239e13ffb/ijms-24-10874-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/9e3c1ba9e01e/ijms-24-10874-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/b8526f734d51/ijms-24-10874-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/610c4e45667d/ijms-24-10874-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/dfb239e13ffb/ijms-24-10874-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/9e3c1ba9e01e/ijms-24-10874-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/b8526f734d51/ijms-24-10874-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/610c4e45667d/ijms-24-10874-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ddef/10342011/dfb239e13ffb/ijms-24-10874-g004.jpg

相似文献

1
Infection, Dysbiosis and Inflammation Interplay in the COVID Era in Children.在新冠时代,感染、微生态失调和炎症相互作用于儿童。
Int J Mol Sci. 2023 Jun 29;24(13):10874. doi: 10.3390/ijms241310874.
2
Pathogenic mechanisms of post-acute sequelae of SARS-CoV-2 infection (PASC).SARS-CoV-2 感染后后遗症(PASC)的发病机制。
Elife. 2023 Mar 22;12:e86002. doi: 10.7554/eLife.86002.
3
Gut Microbiota and Mitochondria: Health and Pathophysiological Aspects of Long COVID.肠道微生物组与线粒体:长新冠的健康与病理生理方面。
Int J Mol Sci. 2023 Dec 6;24(24):17198. doi: 10.3390/ijms242417198.
4
Multisystem Inflammatory Syndrome in Children and Long COVID: The SARS-CoV-2 Viral Superantigen Hypothesis.儿童多系统炎症综合征与长新冠:SARS-CoV-2 病毒超抗原假说。
Front Immunol. 2022 Jul 7;13:941009. doi: 10.3389/fimmu.2022.941009. eCollection 2022.
5
The Spectrum of Postacute Sequelae of COVID-19 in Children: From MIS-C to Long COVID.儿童 COVID-19 后急性后遗症的范围:从 MIS-C 到长新冠。
Annu Rev Virol. 2024 Sep;11(1):327-341. doi: 10.1146/annurev-virology-093022-011839. Epub 2024 Aug 30.
6
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.
7
COVID-19 influenced gut dysbiosis, post-acute sequelae, immune regulation, and therapeutic regimens.COVID-19 影响肠道菌群失调、急性后期后遗症、免疫调节和治疗方案。
Front Cell Infect Microbiol. 2024 May 28;14:1384939. doi: 10.3389/fcimb.2024.1384939. eCollection 2024.
8
Laboratory Findings and Biomarkers in Long COVID: What Do We Know So Far? Insights into Epidemiology, Pathogenesis, Therapeutic Perspectives and Challenges.长新冠的实验室发现和生物标志物:目前我们了解多少?对流行病学、发病机制、治疗前景和挑战的洞察。
Int J Mol Sci. 2023 Jun 21;24(13):10458. doi: 10.3390/ijms241310458.
9
Persistent SARS-CoV-2 Infection, EBV, HHV-6 and Other Factors May Contribute to Inflammation and Autoimmunity in Long COVID.持续的 SARS-CoV-2 感染、EBV、HHV-6 及其他因素可能导致长新冠中的炎症和自身免疫。
Viruses. 2023 Jan 31;15(2):400. doi: 10.3390/v15020400.
10
Autoimmunity and COVID-19 - The microbiotal connection.自身免疫与 COVID-19:微生物组的关联。
Autoimmun Rev. 2021 Aug;20(8):102865. doi: 10.1016/j.autrev.2021.102865. Epub 2021 Jun 10.

引用本文的文献

1
Longitudinal Fecal Microbiota Profiles in A Cohort of Non-Hospitalized Adolescents and Young Adults with COVID-19: Associations with SARS-CoV-2 Status and Long-Term Fatigue.一组非住院新冠病毒感染青少年和青年的纵向粪便微生物群概况:与新冠病毒状态及长期疲劳的关联
Pathogens. 2024 Oct 31;13(11):953. doi: 10.3390/pathogens13110953.
2
Gut Microbiota and Mitochondria: Health and Pathophysiological Aspects of Long COVID.肠道微生物组与线粒体:长新冠的健康与病理生理方面。
Int J Mol Sci. 2023 Dec 6;24(24):17198. doi: 10.3390/ijms242417198.

本文引用的文献

1
The enteric nervous system relays psychological stress to intestinal inflammation.肠神经系统将心理压力传递给肠道炎症。
Cell. 2023 Jun 22;186(13):2823-2838.e20. doi: 10.1016/j.cell.2023.05.001. Epub 2023 May 25.
2
Chronic stress can inflame the gut - now scientists know why.长期压力会使肠道发炎——现在科学家们知道原因了。
Nature. 2023 Jun;618(7964):221-222. doi: 10.1038/d41586-023-01700-y.
3
PANDAS/PANS in the COVID-19 Age: Autoimmunity and Epstein-Barr Virus Reactivation as Trigger Agents?新冠疫情时代的儿童自身免疫性神经精神障碍/儿童急性发作性神经精神综合征:自身免疫和爱泼斯坦-巴尔病毒再激活是触发因素吗?
Children (Basel). 2023 Mar 30;10(4):648. doi: 10.3390/children10040648.
4
Persistent SARS-CoV-2 Nucleocapsid Protein Presence in the Intestinal Epithelium of a Pediatric Patient 3 Months After Acute Infection.一名儿科患者急性感染3个月后,肠道上皮中持续存在严重急性呼吸综合征冠状病毒2核衣壳蛋白
JPGN Rep. 2021 Dec 3;3(1):e152. doi: 10.1097/PG9.0000000000000152. eCollection 2022 Feb.
5
Viral persistence, reactivation, and mechanisms of long COVID.病毒持续存在、再激活与长新冠的机制。
Elife. 2023 May 4;12:e86015. doi: 10.7554/eLife.86015.
6
Increased interleukin-6 is associated with long COVID-19: a systematic review and meta-analysis.白细胞介素-6 水平升高与长新冠有关:系统评价和荟萃分析。
Infect Dis Poverty. 2023 Apr 24;12(1):43. doi: 10.1186/s40249-023-01086-z.
7
Elevated circulating monocytes and monocyte activation in COVID-19 convalescent individuals.新冠肺炎康复个体中循环单核细胞升高和单核细胞活化。
Front Immunol. 2023 Apr 3;14:1151780. doi: 10.3389/fimmu.2023.1151780. eCollection 2023.
8
COVID-19 in immunocompromised children and adolescents.免疫功能低下儿童和青少年的新冠病毒病
Clin Exp Pediatr. 2023 May;66(5):182-189. doi: 10.3345/cep.2022.00878. Epub 2023 Apr 18.
9
Clinical Course and Severity of COVID-19 in 940 Infants with and without Comorbidities Hospitalized in 2020 and 2021: The Results of the National Multicenter Database SARSTer-PED.2020年和2021年住院的940名有或无合并症婴儿的COVID-19临床病程及严重程度:国家多中心数据库SARSTer-PED的结果
J Clin Med. 2023 Mar 24;12(7):2479. doi: 10.3390/jcm12072479.
10
Distinct phenotypes of multisystem inflammatory syndrome in children: a cohort study.儿童多系统炎症综合征的不同表型:一项队列研究。
Pediatr Rheumatol Online J. 2023 Apr 12;21(1):33. doi: 10.1186/s12969-023-00815-w.