• 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

通过使用疫苗持续抑制白细胞介素-18可改善三硝基苯磺酸诱导的小鼠结肠炎中的肠道炎症。

Sustained suppression of IL-18 by employing a vaccine ameliorates intestinal inflammation in TNBS-induced murine colitis.

作者信息

Guan Qingdong, Warrington Richard, Moreno Sem, Qing Gefei, Weiss Carolyn, Peng Zhikang

机构信息

Department of Immunology, University of Manitoba, Winnipeg R3E 3P4, Canada.

Department of Pediatrics & Child Health, University of Manitoba, Winnipeg, R3E 3P4, Canada.

出版信息

Future Sci OA. 2019 Jul 30;5(7):FSO405. doi: 10.2144/fsoa-2018-0125.

DOI:10.2144/fsoa-2018-0125
PMID:31428451
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6695525/
Abstract

AIM

To develop IL-18 peptide-based virus-like particle vaccines that elicit autoantibodies against IL-18 and to evaluate the effects of the vaccines in murine colitis.

METHODS

Recombinant IL-18 vaccines were constructed, and the effects of the vaccines were evaluated in trinitrobenzene sulfonic acid-induced acute and chronic colitis in mice.

RESULTS

Two murine IL-18 peptide-based vaccines (A and D) were developed, which induced relative long-lasting specific antibodies against IL-18. Vaccine-immunized mouse antisera could partially block IL-18-induced IFN-γ production . Mice receiving vaccine D, not vaccine A, had a significant decrease in intestinal inflammation, collagen deposition and pro-inflammatory cytokine levels in colon tissue.

CONCLUSION

IL-18 vaccine may provide a potential therapeutic approach in the treatment of Crohn's disease.

摘要

目的

研发基于白细胞介素-18(IL-18)肽的病毒样颗粒疫苗,以诱导产生抗IL-18的自身抗体,并评估该疫苗对小鼠结肠炎的影响。

方法

构建重组IL-18疫苗,并在三硝基苯磺酸诱导的小鼠急性和慢性结肠炎中评估疫苗的效果。

结果

研发出两种基于小鼠IL-18肽的疫苗(A和D),它们能诱导产生相对持久的抗IL-18特异性抗体。疫苗免疫小鼠的抗血清可部分阻断IL-18诱导的γ干扰素产生。接受疫苗D而非疫苗A的小鼠,其结肠组织中的肠道炎症、胶原沉积和促炎细胞因子水平显著降低。

结论

IL-18疫苗可能为克罗恩病的治疗提供一种潜在的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a16/6695525/7ac403cccaeb/fsoa-05-405-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a16/6695525/d23e3d01f656/fsoa-05-405-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a16/6695525/7ac403cccaeb/fsoa-05-405-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a16/6695525/d23e3d01f656/fsoa-05-405-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6a16/6695525/7ac403cccaeb/fsoa-05-405-g2.jpg

相似文献

1
Sustained suppression of IL-18 by employing a vaccine ameliorates intestinal inflammation in TNBS-induced murine colitis.通过使用疫苗持续抑制白细胞介素-18可改善三硝基苯磺酸诱导的小鼠结肠炎中的肠道炎症。
Future Sci OA. 2019 Jul 30;5(7):FSO405. doi: 10.2144/fsoa-2018-0125.
2
Targeting IL-12/IL-23 by employing a p40 peptide-based vaccine ameliorates TNBS-induced acute and chronic murine colitis.采用基于 p40 肽的疫苗靶向 IL-12/IL-23 可改善 TNBS 诱导的急性和慢性小鼠结肠炎。
Mol Med. 2011;17(7-8):646-56. doi: 10.2119/molmed.2010.00252. Epub 2011 Mar 11.
3
Employing an IL-23 p19 vaccine to block IL-23 ameliorates chronic murine colitis.采用 IL-23 p19 疫苗阻断 IL-23 可改善慢性小鼠结肠炎。
Immunotherapy. 2013 Dec;5(12):1313-22. doi: 10.2217/imt.13.141.
4
Development of recombinant vaccines against IL-12/IL-23 p40 and in vivo evaluation of their effects in the downregulation of intestinal inflammation in murine colitis.针对白细胞介素 12/23 p40 的重组疫苗的研制及其在下调实验性结肠炎小鼠肠道炎症中的体内作用评价。
Vaccine. 2009 Nov 23;27(50):7096-104. doi: 10.1016/j.vaccine.2009.09.058. Epub 2009 Sep 26.
5
An IL-17 peptide-based and virus-like particle vaccine enhances the bioactivity of IL-17 in vitro and in vivo.一种基于白介素-17 的肽和病毒样颗粒疫苗增强了白介素-17 在体外和体内的生物活性。
Immunotherapy. 2012 Dec;4(12):1799-807. doi: 10.2217/imt.12.129.
6
Targeting TGF-beta1 by employing a vaccine ameliorates fibrosis in a mouse model of chronic colitis.利用疫苗靶向 TGF-β1 可改善慢性结肠炎小鼠模型的纤维化。
Inflamm Bowel Dis. 2010 Jun;16(6):1040-50. doi: 10.1002/ibd.21167.
7
Interleukin-6 genetic ablation protects from trinitrobenzene sulfonic acid-induced colitis in mice. Putative effect of antiinflammatory cytokines.白细胞介素-6基因缺失可保护小鼠免受三硝基苯磺酸诱导的结肠炎。抗炎细胞因子的假定作用。
Neuroimmunomodulation. 2006;13(2):114-21. doi: 10.1159/000096656. Epub 2006 Oct 14.
8
Antibodies to interleukin 12 abrogate established experimental colitis in mice.抗白细胞介素12抗体可消除已建立的小鼠实验性结肠炎。
J Exp Med. 1995 Nov 1;182(5):1281-90. doi: 10.1084/jem.182.5.1281.
9
Evidence for the critical role of interleukin-12 but not interferon-gamma in the pathogenesis of experimental colitis in mice.白细胞介素-12而非干扰素-γ在小鼠实验性结肠炎发病机制中起关键作用的证据。
J Gastroenterol Hepatol. 2003 May;18(5):578-87. doi: 10.1046/j.1440-1746.2003.03024.x.
10
Interleukin 16 is up-regulated in Crohn's disease and participates in TNBS colitis in mice.白细胞介素16在克罗恩病中上调,并参与小鼠的三硝基苯磺酸结肠炎。
Gastroenterology. 2000 Oct;119(4):972-82. doi: 10.1053/gast.2000.18164.

引用本文的文献

1
Studies on Treatment Within the Scope of Medical Biotechnology for Pancreatic Diseases.胰腺疾病的医学生物技术治疗范围研究
Mol Biotechnol. 2025 Apr;67(4):1321-1335. doi: 10.1007/s12033-024-01142-5. Epub 2024 Apr 16.
2
A Narrative Review of Cytokine Networks: Pathophysiological and Therapeutic Implications for Inflammatory Bowel Disease Pathogenesis.细胞因子网络的叙述性综述:对炎症性肠病发病机制的病理生理学和治疗意义
Biomedicines. 2023 Dec 6;11(12):3229. doi: 10.3390/biomedicines11123229.
3
Vaccines for immune tolerance against autoimmune disease.

本文引用的文献

1
Therapeutic potential of dinitrobenzene sulfonic acid (DNBS)-induced colitis in mice by targeting IL-1β and IL-18.二硝基苯磺酸(DNBS)诱导的小鼠结肠炎的 IL-1β 和 IL-18 靶向治疗潜力。
Biochem Pharmacol. 2018 Sep;155:150-161. doi: 10.1016/j.bcp.2018.06.029. Epub 2018 Jun 28.
2
Reversing Ongoing Chronic Intestinal Inflammation and Fibrosis by Sustained Block of IL-12 and IL-23 Using a Vaccine in Mice.通过在小鼠中使用疫苗持续阻断IL-12和IL-23来逆转进行性慢性肠道炎症和纤维化
Inflamm Bowel Dis. 2018 Aug 16;24(9):1941-1952. doi: 10.1093/ibd/izy142.
3
Immunopathogenesis of inflammatory bowel disease and mechanisms of biological therapies.
针对自身免疫性疾病的免疫耐受疫苗。
Adv Drug Deliv Rev. 2023 Dec;203:115140. doi: 10.1016/j.addr.2023.115140. Epub 2023 Nov 18.
4
Vaccination therapy for inflammatory bowel disease.炎症性肠病的疫苗治疗。
Hum Vaccin Immunother. 2023 Aug;19(2):2259418. doi: 10.1080/21645515.2023.2259418. Epub 2023 Sep 29.
5
Inflammasomes and adaptive immune responses.炎症小体与适应性免疫应答。
Nat Immunol. 2021 Apr;22(4):412-422. doi: 10.1038/s41590-021-00869-6. Epub 2021 Feb 18.
6
A Comprehensive Review and Update on the Pathogenesis of Inflammatory Bowel Disease.炎症性肠病发病机制的全面综述和更新。
J Immunol Res. 2019 Dec 1;2019:7247238. doi: 10.1155/2019/7247238. eCollection 2019.
炎症性肠病的免疫发病机制及生物治疗机制
Scand J Gastroenterol. 2018 Apr;53(4):379-389. doi: 10.1080/00365521.2018.1447597. Epub 2018 Mar 9.
4
Interleukin-18: Biological properties and role in disease pathogenesis.白细胞介素-18:生物学特性及其在疾病发病机制中的作用。
Immunol Rev. 2018 Jan;281(1):138-153. doi: 10.1111/imr.12616.
5
Recent Advances: The Imbalance of Cytokines in the Pathogenesis of Inflammatory Bowel Disease.最新进展:细胞因子失衡在炎症性肠病发病机制中的作用
Mediators Inflamm. 2017;2017:4810258. doi: 10.1155/2017/4810258. Epub 2017 Mar 21.
6
An Overview of the Innate and Adaptive Immune System in Inflammatory Bowel Disease.炎症性肠病中固有免疫和适应性免疫系统概述
Inflamm Bowel Dis. 2017 Jan;23(1):2-13. doi: 10.1097/MIB.0000000000000955.
7
Epithelial-derived IL-18 regulates Th17 cell differentiation and Foxp3⁺ Treg cell function in the intestine.上皮来源的白细胞介素-18调节肠道中Th17细胞的分化和Foxp3⁺调节性T细胞的功能。
Mucosal Immunol. 2015 Nov;8(6):1226-36. doi: 10.1038/mi.2015.13. Epub 2015 Mar 4.
8
The IL18RAP region disease polymorphism decreases IL-18RAP/IL-18R1/IL-1R1 expression and signaling through innate receptor-initiated pathways.IL18RAP 区域疾病多态性通过先天受体起始途径降低 IL-18RAP/IL-18R1/IL-1R1 的表达和信号转导。
J Immunol. 2014 Jun 15;192(12):5924-32. doi: 10.4049/jimmunol.1302727. Epub 2014 May 19.
9
Employing an IL-23 p19 vaccine to block IL-23 ameliorates chronic murine colitis.采用 IL-23 p19 疫苗阻断 IL-23 可改善慢性小鼠结肠炎。
Immunotherapy. 2013 Dec;5(12):1313-22. doi: 10.2217/imt.13.141.
10
Interleukin-18 and IL-18 binding protein.白细胞介素-18与白细胞介素-18结合蛋白。
Front Immunol. 2013 Oct 8;4:289. doi: 10.3389/fimmu.2013.00289.