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Glyceraldehyde-3-Phosphate Dehydrogenase Binds with Spike Protein and Inhibits the Entry of SARS-CoV-2 into Host Cells. 甘油醛-3-磷酸脱氢酶(GAPDH)与尖峰蛋白结合,抑制 SARS-CoV-2 进入宿主细胞。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-02-07 DOI: 10.1159/000535634
Rahul Dilawari, Gaurav Kumar Chaubey, Radheshyam Modanwal, Asmita Dhiman, Sharmila Talukdar, Ajay Kumar, Chaaya Iyengar Raje, Manoj Raje

Introduction: Coronavirus disease 2019 caused by coronavirus-2 (SARS-CoV-2) has emerged as an aggressive viral pandemic. Health care providers confront a challenging task for rapid development of effective strategies to combat this and its long-term after effects. Virus entry into host cells involves interaction between receptor-binding domain (RBD) of spike (S) protein S1 subunit with angiotensin converting enzyme present on host cells. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is a moonlighting enzyme involved in cellular glycolytic energy metabolism and micronutrient homeostasis. It is deployed in various cellular compartments and the extra cellular milieu. Though it is known to moonlight as a component of mammalian innate immune defense machinery, till date its role in viral restriction remains unknown.

Method: Recombinant S protein, the RBD, and human GAPDH protein were used for solid phase binding assays and biolayer interferometry. Pseudovirus particles expressing four different strain variants of S protein all harboring ZsGreen gene as marker of infection were used for flow cytometry-based infectivity assays.

Results: Pseudovirus entry into target cells in culture was significantly inhibited by addition of human GAPDH into the extracellular medium. Binding assays demonstrated that human GAPDH binds to S protein and RBD of SARS-CoV-2 with nanomolar affinity.

Conclusions: Our investigations suggest that this interaction of GAPDH interferes in the viral docking with hACE2 receptors, thereby affecting viral ingress into mammalian cells.

引言由冠状病毒 2(SARS-CoV-2)引起的 2019 年冠状病毒病(COVID-19)已成为一种咄咄逼人的病毒性流行病。医疗保健提供者面临着一项具有挑战性的任务,即迅速制定有效的策略来应对这一疾病及其长期后果。病毒进入宿主细胞涉及穗状(S)蛋白 S1 亚基的受体结合域(RBD)与宿主细胞上的血管紧张素转换酶(ACE)之间的相互作用。甘油醛-3-磷酸脱氢酶(GAPDH)是一种参与细胞糖酵解能量代谢和微量营养素平衡的兼职酶。它存在于各种细胞区和细胞外环境中。尽管人们知道它是哺乳动物先天免疫防御机制的一个组成部分,但迄今为止,它在病毒限制中的作用仍然未知:方法:使用重组 S 蛋白、受体结合域(RBD)和人 GAPDH 蛋白进行固相结合测定和生物层干涉测量(BLI)。表达 S 蛋白四种不同株系变体的伪病毒颗粒均携带 ZsGreen 基因作为感染标记,用于基于流式细胞仪的感染性检测:结果:在细胞外培养基中加入人 GAPDH 能显著抑制伪病毒进入培养的靶细胞。结合试验表明,人 GAPDH 与 SARS-CoV-2 的 S 蛋白和 RBD 结构域结合的亲和力为纳米级:我们的研究表明,GAPDH 的这种相互作用会干扰病毒与 hACE2 受体的对接,从而影响病毒进入哺乳动物细胞。
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引用次数: 0
Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy. 揭开错综复杂的网络:补体激活决定败血症诱发凝血病的发病机制
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-05-31 DOI: 10.1159/000539502
Xin Wei, Ye Tu, Shuhong Bu, Guimei Guo, Hongbin Wang, Zhibin Wang

Background: Sepsis-associated coagulopathy specifically refers to widespread systemic coagulation activation accompanied by a high risk of hemorrhage and organ damage, which in severe cases manifests as disseminated intravascular coagulation (DIC), or even develops into multiple organ dysfunction syndrome (MODS). The complement system and the coagulation system as the main columns of innate immunity and hemostasis, respectively, undergo substantial activation after sepsis.

Summary: Dysfunction of the complement, coagulation/fibrinolytic cascades caused by sepsis leads to "thromboinflammation," which ultimately amplifies the systemic inflammatory response and accelerates the development of MODS. Recent studies have revealed that massive activation of the complement system exacerbates sepsis-induced coagulation and even results in DIC, which suggests that inhibition of complement activation may have therapeutic potential in the treatment of septic coagulopathy.

Key messages: Sepsis-associated thrombosis involves the upregulation or activation of procoagulant factors, down-regulation or inactivation of anticoagulant factors, and impairment of the fibrinolytic mechanism. This review aims to summarize the latest literature and analyze the underlying molecular mechanisms of the activation of the complement system on the abnormal coagulation cascades in sepsis.

脓毒症相关凝血病特指广泛的全身性凝血活化,伴随着出血和器官损伤的高风险,严重者表现为弥散性血管内凝血(DIC),甚至发展为多器官功能障碍综合征(MODS)。补体系统和凝血系统分别作为先天免疫和止血的主要支柱,在败血症后会被大量激活。脓毒症引起的补体、凝血和纤维蛋白溶解级联功能失调会导致 "血栓炎",最终扩大全身炎症反应,加速 MODS 的发展。最近的研究表明,补体系统的大量激活会加剧脓毒症引起的凝血,甚至导致 DIC,这表明抑制补体激活可能具有治疗脓毒症凝血病的潜力。脓毒症相关血栓形成涉及促凝因子的上调或激活、抗凝因子的下调或失活以及纤溶机制的损害。本综述旨在总结最新文献,分析脓毒症中补体系统激活导致凝血级联异常的潜在分子机制。
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引用次数: 0
TLR2 and NLRP3 Orchestrate Regulatory Roles in Escherichia coli Infection-Induced Septicemia in Mouse Models. TLR2 和 NLRP3 在大肠埃希菌感染诱发的小鼠模型败血症中发挥调节作用。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-10-15 DOI: 10.1159/000541819
Zhiguo Gong, Wei Mao, Jiamin Zhao, Peipei Ren, Zhuoya Yu, Yunjie Bai, Chao Wang, Yuze Liu, Shuang Feng, Surong Hasi

Introduction: Escherichia coli (E. coli) is a significant commensal gram-negative bacterium that can give rise to various diseases. The roles of Toll-like receptor 2 (TLR2) and the NOD-like receptor pyrin domain-containing protein 3 (NLRP3) inflammasome in sepsis induced by E. coli infection remain unclear.

Methods: In vivo, we investigated differences in mortality, production of inflammatory mediators, organ damage, neutrophil count, and bacterial load during E. coli infection in C57BL/6J mice, as well as in mice deficient in TLR2 or NLRP3. In vitro, we investigated the impact of E. coli on the activation of TLR2 and NLRP3 in macrophages and the influence of TLR2 and NLRP3 on the activation of inflammatory signaling pathways and the secretion of inflammatory mediators in macrophages induced by E. coli infection.

Results: TLR2-deficient (TLR2-/-) and NLRP3-deficient (NLRP3-/-) mice exhibit significantly increased mortality and organ damage after E. coli infection. These mice also show elevated levels of TNF-α and IL-10 in serum and peritoneal lavage fluid. Additionally, TLR2-/- and NLRP3-/- mice display heightened neutrophil recruitment and increased bacterial load in the blood. Furthermore, macrophages from these mice demonstrate a significant reduction in the activation of the MAPK signaling pathway.

Conclusion: TLR2 and NLRP3 play crucial roles in modulating inflammatory mediator expression, immune cell recruitment, and bactericidal activity, thereby preventing excessive tissue damage and reducing mortality in E. coli-induced sepsis.

引言 大肠杆菌(E. coli)是一种重要的革兰氏阴性共生菌,可引发多种疾病。Toll 样受体 2(TLR2)和含 NLR pyrin 结构域的炎性体 3(NLRP3)在大肠杆菌感染诱导的败血症中的作用仍不清楚。方法 在体内,我们研究了 C57BL/6J 小鼠以及 TLR2 或 NLRP3 缺陷小鼠感染大肠杆菌期间死亡率、炎症介质产生、器官损伤、中性粒细胞计数和细菌负荷的差异。在体外,我们研究了大肠杆菌对巨噬细胞中 TLR2 和 NLRP3 激活的影响,以及 TLR2 和 NLRP3 对大肠杆菌感染诱导的巨噬细胞炎症信号通路激活和炎症介质分泌的影响。结果 TLR2 缺失(TLR2-/-)和 NLRP3 缺失(NLRP3-/-)的小鼠在感染大肠杆菌后死亡率和器官损伤显著增加。这些小鼠血清和腹腔灌洗液(PLF)中的 TNF-α 和 IL-10 水平也有所升高。此外,TLR2-/- 和 NLRP3-/- 小鼠表现出中性粒细胞募集增加、血液中细菌负荷增加。此外,这些小鼠的巨噬细胞显示出 MAPK 信号通路的激活显著减少。结论 TLR2 和 NLRP3 在调节炎症介质表达、免疫细胞募集和杀菌活性方面起着至关重要的作用,从而防止大肠杆菌诱导的败血症造成过度的组织损伤并降低死亡率。
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引用次数: 0
Obituary of Prof. Uli Theopold, 1957-2023. 乌利-西奥波德教授的讣告,1957-2023。
IF 5.3 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-01-08 DOI: 10.1159/000535642
Ylva Engström, Bruno Lemaitre, Dan Hultmark
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引用次数: 0
Role of Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 in Inflammation and Pathogen-Associated Interactions. 胶原蛋白样氧化低密度脂蛋白受体-1(LOX-1)在炎症和病原体相关相互作用中的作用。
IF 5.3 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-01-17 DOI: 10.1159/000535793
Sarah Truthe, Tilman E Klassert, Stefan Schmelz, Danny Jonigk, Wulf Blankenfeldt, Hortense Slevogt

Background: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is known as a major receptor for oxidized low-density lipoproteins (oxLDL) and plays a significant role in the genesis of atherosclerosis. Recent research has shown its involvement in cancer, ischemic stroke, and diabetes. LOX-1 is a C-type lectin receptor and is involved in the activation of immune cells and inflammatory processes. It may further interact with pathogens, suggesting a role in infections or the host's response.

Summary: This review compiles the current knowledge of potential implications of LOX-1 in inflammatory processes and in host-pathogen interactions with a particular emphasis on its regulatory role in immune responses. Also discussed are genomic and structural variations found in LOX-1 homologs across different species as well as potential involvements of LOX-1 in inflammatory processes from the angle of different cell types and organ-specific interactions.

Key messages: The results presented reveal both similar and different structures in human and murine LOX-1 and provide clues as to the possible origins of different modes of interaction. These descriptions raise concerns about the suitability, particularly of mouse models, that are often used in the analysis of its functionality in humans. Further research should also aim to better understand the mostly unknown binding and interaction mechanisms between LOX-1 and different pathogens. This pursuit will not only enhance our understanding of LOX-1 involvement in inflammatory processes but also identify potential targets for immunomodulatory approaches.

背景:众所周知,凝集素样氧化低密度脂蛋白受体-1(LOX-1)是氧化低密度脂蛋白(oxLDL)的主要受体,在动脉粥样硬化的形成过程中起着重要作用。最近的研究表明,它还与癌症、缺血性中风和糖尿病有关。LOX-1 是一种 C 型凝集素受体,参与激活免疫细胞和炎症过程。摘要:这篇综述汇编了目前关于 LOX-1 在炎症过程和宿主与病原体相互作用中的潜在影响的知识,特别强调了它在免疫反应中的调节作用。还讨论了不同物种 LOX-1 同源物的基因组和结构变异,以及从不同细胞类型和器官特异性相互作用的角度探讨了 LOX-1 在炎症过程中的潜在作用:本文介绍的结果揭示了人类和鼠类 LOX-1 既相似又不同的结构,并为不同相互作用模式的可能起源提供了线索。这些描述引起了人们对其适用性的关注,特别是小鼠模型的适用性。进一步的研究还应旨在更好地了解 LOX-1 与不同病原体之间大部分未知的结合和相互作用机制。这不仅能加深我们对 LOX-1 参与炎症过程的理解,还能为免疫调节方法确定潜在的靶点。
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引用次数: 0
Eosinophils Are an Endogenous Source of Interleukin-4 during Filarial Infections and Contribute to the Development of an Optimal T Helper 2 Response. 嗜酸性粒细胞是丝虫感染期间 IL-4 的内源性来源,有助于形成最佳的 T 辅助细胞 2 反应。
IF 5.3 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-02-26 DOI: 10.1159/000536357
Cécile Guth, Pia Philippa Schumacher, Archena Vijayakumar, Hannah Borgmann, Helene Balles, Marianne Koschel, Frederic Risch, Benjamin Lenz, Achim Hoerauf, Marc P Hübner, Jesuthas Ajendra

Introduction: Interleukin-4 (IL-4) is a central regulator of type 2 immunity, crucial for the defense against multicellular parasites like helminths. This study focuses on its roles and cellular sources during Litomosoides sigmodontis infection, a model for human filarial infections.

Methods: Utilizing an IL-4 secretion assay, investigation into the sources of IL-4 during the progression of L. sigmodontis infection was conducted. The impact of eosinophils on the Th2 response was investigated through experiments involving dblGATA mice, which lack eosinophils and, consequently, eosinophil-derived IL-4.

Results: The absence of eosinophils notably influenced Th2 polarization, leading to impaired production of type 2 cytokines. Interestingly, despite this eosinophil deficiency, macrophage polarization, proliferation, and antibody production remained unaffected.

Conclusion: Our research uncovers eosinophils as a major source of IL-4, especially during the early phase of filarial infection. Consequently, these findings shed new light on IL-4 dynamics and eosinophil effector functions in filarial infections.

白细胞介素-4(IL-4)是第二类免疫的核心调节因子,对防御蠕虫等多细胞寄生虫至关重要。本研究的重点是它在丝虫感染(人类丝虫感染的模型)过程中的作用和细胞来源。我们的研究发现,嗜酸性粒细胞是 IL-4 的主要来源,尤其是在丝虫感染的早期阶段。我们利用缺乏嗜酸性粒细胞和随后嗜酸性粒细胞衍生的IL-4的dblGATA小鼠,揭示了它们对Th2反应的深刻影响。缺乏嗜酸性粒细胞会影响 Th2 极化,并导致 2 型细胞因子生成受损。令人惊讶的是,嗜酸性粒细胞的缺乏对巨噬细胞的极化和增殖以及抗体的产生没有影响。这些发现为丝虫感染中的IL-4动态和嗜酸性粒细胞效应功能提供了新的线索。
{"title":"Eosinophils Are an Endogenous Source of Interleukin-4 during Filarial Infections and Contribute to the Development of an Optimal T Helper 2 Response.","authors":"Cécile Guth, Pia Philippa Schumacher, Archena Vijayakumar, Hannah Borgmann, Helene Balles, Marianne Koschel, Frederic Risch, Benjamin Lenz, Achim Hoerauf, Marc P Hübner, Jesuthas Ajendra","doi":"10.1159/000536357","DOIUrl":"10.1159/000536357","url":null,"abstract":"<p><strong>Introduction: </strong>Interleukin-4 (IL-4) is a central regulator of type 2 immunity, crucial for the defense against multicellular parasites like helminths. This study focuses on its roles and cellular sources during Litomosoides sigmodontis infection, a model for human filarial infections.</p><p><strong>Methods: </strong>Utilizing an IL-4 secretion assay, investigation into the sources of IL-4 during the progression of L. sigmodontis infection was conducted. The impact of eosinophils on the Th2 response was investigated through experiments involving dblGATA mice, which lack eosinophils and, consequently, eosinophil-derived IL-4.</p><p><strong>Results: </strong>The absence of eosinophils notably influenced Th2 polarization, leading to impaired production of type 2 cytokines. Interestingly, despite this eosinophil deficiency, macrophage polarization, proliferation, and antibody production remained unaffected.</p><p><strong>Conclusion: </strong>Our research uncovers eosinophils as a major source of IL-4, especially during the early phase of filarial infection. Consequently, these findings shed new light on IL-4 dynamics and eosinophil effector functions in filarial infections.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"159-172"},"PeriodicalIF":5.3,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10932553/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139735439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
TLRs1-10 Protein Expression in Circulating Human White Blood Cells during Bacterial and COVID-19 Infections. 细菌和 COVID-19 感染期间循环人白细胞中的 TLRs1-10 蛋白表达。
IF 4.7 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2024-03-08 DOI: 10.1159/000536593
Louise Chomel, Mathieu Vogt, Julien Demiselle, Pierrick Le Borgne, Marine Tschirhart, Valentin Morandeau, Hamid Merdji, Laurent Miguet, Julie Helms, Ferhat Meziani, Laurent Mauvieux

Introduction: Toll-like receptors play crucial roles in the sepsis-induced systemic inflammatory response. Septic shock mortality correlates with overexpression of neutrophilic TLR2 and TLR9, while the role of TLR4 overexpression remains a debate. In addition, TLRs are involved in the pathogenesis of viral infections such as COVID-19, where the single-stranded RNA of SARS-CoV-2 is recognized by TLR7 and TLR8, and the spike protein activates TLR4.

Methods: In this study, we conducted a comprehensive analysis of TLRs 1-10 expressions in white blood cells from 71 patients with bacterial and viral infections. Patients were divided into 4 groups based on disease type and severity (sepsis, septic shock, moderate, and severe COVID-19) and compared to 7 healthy volunteers.

Results: We observed a significant reduction in the expression of TLR4 and its co-receptor CD14 in septic shock neutrophils compared to the control group (p < 0.001). Severe COVID-19 patients exhibited a significant increase in TLR3 and TLR7 levels in neutrophils compared to controls (p < 0.05). Septic shock patients also showed a similar increase in TLR7 in neutrophils along with elevated intermediate monocytes (CD14+CD16+) compared to the control group (p < 0.005 and p < 0.001, respectively). However, TLR expression remained unchanged in lymphocytes.

Conclusion: This study provides further insights into the mechanisms of TLR activation in various infectious conditions. Additional analysis is needed to assess their correlation with patient outcome and to evaluate the impact of TLR-pathway modulation during septic shock and severe COVID-19.

导言Toll 样受体在脓毒症诱发的全身炎症反应中起着至关重要的作用。脓毒性休克的死亡率与中性粒细胞 TLR2 和 TLR9 的过度表达有关,而 TLR4 过度表达的作用仍存在争议。此外,TLRs 还参与了 COVID-19 等病毒感染的发病机制,SARS-CoV-2 的单链 RNA 可被 TLR7 和 TLR8 识别,而尖峰蛋白可激活 TLR4:在这项研究中,我们对 71 名细菌和病毒感染患者的白细胞中 TLRs 1-10 的表达进行了全面分析。根据疾病类型和严重程度(败血症、脓毒性休克、中度和重度 COVID-19)将患者分为 4 组,并与 7 名健康志愿者进行比较:结果:我们观察到,与对照组相比,脓毒性休克中性粒细胞中 TLR4 及其共受体 CD14 的表达明显减少(p 结论:该研究进一步揭示了脓毒性休克中性粒细胞中 TLR4 及其共受体 CD14 的表达:这项研究进一步揭示了各种感染性疾病中 TLR 的激活机制。还需要进行更多的分析,以评估它们与患者预后的相关性,并评估在脓毒性休克和严重 COVID-19 期间 TLR 通路调节的影响。
{"title":"TLRs1-10 Protein Expression in Circulating Human White Blood Cells during Bacterial and COVID-19 Infections.","authors":"Louise Chomel, Mathieu Vogt, Julien Demiselle, Pierrick Le Borgne, Marine Tschirhart, Valentin Morandeau, Hamid Merdji, Laurent Miguet, Julie Helms, Ferhat Meziani, Laurent Mauvieux","doi":"10.1159/000536593","DOIUrl":"10.1159/000536593","url":null,"abstract":"<p><strong>Introduction: </strong>Toll-like receptors play crucial roles in the sepsis-induced systemic inflammatory response. Septic shock mortality correlates with overexpression of neutrophilic TLR2 and TLR9, while the role of TLR4 overexpression remains a debate. In addition, TLRs are involved in the pathogenesis of viral infections such as COVID-19, where the single-stranded RNA of SARS-CoV-2 is recognized by TLR7 and TLR8, and the spike protein activates TLR4.</p><p><strong>Methods: </strong>In this study, we conducted a comprehensive analysis of TLRs 1-10 expressions in white blood cells from 71 patients with bacterial and viral infections. Patients were divided into 4 groups based on disease type and severity (sepsis, septic shock, moderate, and severe COVID-19) and compared to 7 healthy volunteers.</p><p><strong>Results: </strong>We observed a significant reduction in the expression of TLR4 and its co-receptor CD14 in septic shock neutrophils compared to the control group (p &lt; 0.001). Severe COVID-19 patients exhibited a significant increase in TLR3 and TLR7 levels in neutrophils compared to controls (p &lt; 0.05). Septic shock patients also showed a similar increase in TLR7 in neutrophils along with elevated intermediate monocytes (CD14+CD16+) compared to the control group (p &lt; 0.005 and p &lt; 0.001, respectively). However, TLR expression remained unchanged in lymphocytes.</p><p><strong>Conclusion: </strong>This study provides further insights into the mechanisms of TLR activation in various infectious conditions. Additional analysis is needed to assess their correlation with patient outcome and to evaluate the impact of TLR-pathway modulation during septic shock and severe COVID-19.</p>","PeriodicalId":16113,"journal":{"name":"Journal of Innate Immunity","volume":" ","pages":"216-225"},"PeriodicalIF":4.7,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11001289/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140094203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Association of Vitamin D with Severity and Outcome of COVID-19: Clinical and Experimental Evidence. 维生素D与COVID-19严重程度和结局的关系:临床和实验证据
IF 5.3 3区 医学 Q2 IMMUNOLOGY Pub Date : 2024-01-01 Epub Date: 2023-11-26 DOI: 10.1159/000535302
Georgios Renieris, Spyros Foutadakis, Theano Andriopoulou, Victoria-Marina Spanou, Dionyssia-Eirini Droggiti, Dionysios Kafousopoulos, Theologia Gkavogianni, Georgia Damoraki, Giannis Vatsellas, Evangelos J Giamarellos-Bourboulis

Introduction: The role of vitamin in COVID-19 remains controversial. We investigated the association between endogenous vitamin D and the severity of COVID-19 as well as the mechanisms of action of vitamin D supplementation.

Methods: 25(OH)D3 in serum was associated with disease severity and outcome in 190 COVID-19 patients. In a COVID-19 animal model using intravenous injection of plasma from patients with COVID-19 acute respiratory distress syndrome into C57/BL6 mice, mice were treated with 0.25 μg human 1,25(OH)D3 or vehicle. Mice were sacrificed on day 4. Cytokines and myeloperoxidase (MPO) in tissues were measured. Changes in gene expression after vitamin D supplementation were measured.

Results: Vitamin D deficiency and insufficiency were associated with increased severity and unfavorable outcome after 28 days. Vitamin D levels were negatively associated with biomarkers of COVID-19 severity. Vitamin D supplementation after challenge of mice with COVID-19 plasma led to reduced levels of TNFα, IL-6, IFNγ, and MPO in the lung, as well as down-regulation of pro-inflammatory pathways.

Conclusion: Normal levels of endogenous vitamin D are associated with reduced severity and risk of unfavorable outcome in COVID-19, possibly through attenuation of tissue-specific hyperinflammation.

维生素在COVID-19中的作用仍存在争议。我们研究了内源性维生素D与COVID-19严重程度之间的关系,以及补充维生素D的作用机制。方法:190例COVID-19患者血清25(OH)D3水平与病情严重程度及转归相关。在C57/BL6小鼠静脉注射COVID-19 ARDS患者血浆的COVID-19动物模型中,小鼠分别接受0.25μg人1,25(OH)D3或对照物治疗。第4天处死小鼠。检测组织细胞因子和髓过氧化物酶(MPO)水平。测量补充维生素D后基因表达的变化。结果:维生素D缺乏和不足与28天后严重程度增加和不良结果相关。维生素D水平与COVID-19严重程度的生物标志物呈负相关。在感染COVID-19的小鼠血浆后补充维生素D导致肺中TNFα、IL-6、IFNγ和MPO水平降低,并下调促炎通路。结论:正常水平的内源性维生素D与降低COVID-19的严重程度和不良结局的风险有关,可能是通过减轻组织特异性高炎症来实现的。
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引用次数: 0
C-X-C motif chemokine ligand 1 promotes colitis by modulating the gut microbiota C-X-C motif趋化因子配体 1 通过调节肠道微生物群促进结肠炎的发生
IF 5.3 3区 医学 Q2 IMMUNOLOGY Pub Date : 2023-12-08 DOI: 10.1159/000535637
Hang Zhao, Wenhua Li, Xin Zhou, Liang Pan, Yun Feng, Pingyu Gao, Jie Ji, Huanyan Zhang, Kai Zhao, Chi Wang, Zhanjun Lu
Introduction: C-X-C motif chemokine ligand 1 (CXCL1) is a potent neutrophil chemoattractant that plays a pivotal role in recruiting neutrophils during inflammatory conditions. This study explored the role of CXCL1 in modulating the gut microbiota, influencing neutrophil infiltration, and contributing to the development of colitis. Methods: We employed quantitative PCR to assess CXCL1 expression in colon samples. A mouse model of DSS-induced colitis was utilized to explore the progression of colitis in wild-type (WT) and CXCL1-deficient (CXCL1-/-) mice. Results: Colitis attenuation was evident in CXCL1-/- mice. Significant alterations were observed in the gut microbiome, as revealed by 16S rRNA gene sequencing. Furthermore, CXCL1-/- mice exhibited reduced gut permeability and diminished endotoxin levels in peripheral blood following DSS treatment compared to WT mice. In response to DSS treatment, WT mice showed a clear increase in neutrophil infiltration, while CXCL1-/- mice exhibited lower levels of infiltration. FMT using stools from CXCL1-/- mice alleviated DSS-induced colitis. Interestingly, FMT from patients with colitis increased CXCL1 and Ly6G expression in colons of gut-sterilized mice. Clinical data analysis revealed elevated CXCL1 and CD15 expression in patients with colitis, with a positive correlation between the severity of colitis and the expression of CXCL1 and CD15. Conclusion: These findings shed light on the pivotal role of CXCL1 in promoting colitis by modulating the gut microbiota.
C-X-C基序趋化因子配体1 (CXCL1)是一种有效的中性粒细胞趋化剂,在炎症条件下募集中性粒细胞中起关键作用。本研究探讨了CXCL1在调节肠道微生物群、影响中性粒细胞浸润和促进结肠炎发生中的作用。方法:采用定量PCR法检测CXCL1在结肠组织中的表达。采用小鼠dss诱导结肠炎模型,探讨野生型(WT)和CXCL1缺陷型(CXCL1-/-)小鼠结肠炎的进展情况。结果:CXCL1-/-小鼠结肠炎消退明显。16S rRNA基因测序显示,肠道微生物组发生了显著变化。此外,与WT小鼠相比,在DSS治疗后,CXCL1-/-小鼠表现出肠道通透性降低和外周血内毒素水平降低。DSS处理后,WT小鼠的中性粒细胞浸润明显增加,而CXCL1-/-小鼠的浸润水平较低。使用CXCL1-/-小鼠粪便进行FMT可减轻dss诱导的结肠炎。有趣的是,结肠炎患者的FMT增加了肠消毒小鼠结肠中CXCL1和Ly6G的表达。临床资料分析显示结肠炎患者CXCL1和CD15表达升高,结肠炎严重程度与CXCL1和CD15表达呈正相关。结论:这些发现揭示了CXCL1通过调节肠道微生物群在促进结肠炎中的关键作用。
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引用次数: 0
Erratum. 勘误表。
IF 5.3 3区 医学 Q2 IMMUNOLOGY Pub Date : 2023-05-15 DOI: 10.1159/000530893
Geburtshilfe und Frauenheilkunde 48 (1988) , (Heft 6/88) P. Wieacker, P. Peters, M. Breckwoldt: Gonnadotropinresistenz beim Rothmund-Thomson-Syndrom
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引用次数: 0
期刊
Journal of Innate Immunity
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