• 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

Trim72是一种预防致死性白色念珠菌感染的主要宿主因子。

Trim72 is a major host factor protecting against lethal Candida albicans infection.

作者信息

Tan Wang, Liu Jiayu, Yu Renlin, Zhao Ping, Liu Yuhan, Lu Qian, Wang Ke, Ding Hao, Liu Yi, Lai Xiaofei, Cao Ju

机构信息

Department of Laboratory Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Department of Laboratory Medicine, The Seventh People's Hospital of Chongqing, Central Hospital Affiliated to Chongqing University of Technology, Chongqing, China.

出版信息

PLoS Pathog. 2024 Nov 25;20(11):e1012747. doi: 10.1371/journal.ppat.1012747. eCollection 2024 Nov.

DOI:10.1371/journal.ppat.1012747
PMID:39585917
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11627414/
Abstract

Candida albicans is the most common aetiologic pathogen of fungal infections associated with high mortality in immunocompromised patients. There is an urgent need to develop new antifungal therapies owing to the poor efficacy and resistance of current antifungals. Here, we report that Trim72 positively regulates antifungal immunity during lethal fungal infection. Trim72 levels are significantly increased after Candida albicans infection. In vivo, Trim72 knockout significantly increases mortality, organ fungal burden and kidney damage in mice after lethal Candida albicans infection. Whereas recombinant Trim72 protein treatment protects mice against invasive candidiasis. Mechanistically, Trim72 facilitates macrophage infiltration and CCL2 production, which mediates Trim72-elicited protection against lethal Candida albicans infection. Furthermore, Trim72 may enhance macrophage migration and CCL2 production via NF-κB and ERK1/2 signaling. Inhibition of NF-κB and ERK1/2 signaling abrogates Trim72-mediated protection against lethal Candida albicans infection. Therefore, these data imply that Trim72 may be developed as a host-directed therapy for treating severe systemic candidiasis.

摘要

白色念珠菌是免疫功能低下患者中与高死亡率相关的真菌感染最常见的病原体。由于目前抗真菌药物疗效不佳且存在耐药性，迫切需要开发新的抗真菌疗法。在此，我们报告Trim72在致死性真菌感染期间正向调节抗真菌免疫。白色念珠菌感染后，Trim72水平显著升高。在体内，Trim72基因敲除显著增加了致死性白色念珠菌感染后小鼠的死亡率、器官真菌负荷和肾脏损伤。而重组Trim72蛋白治疗可保护小鼠免受侵袭性念珠菌病的侵害。从机制上讲，Trim72促进巨噬细胞浸润和CCL2产生，这介导了Trim72对致死性白色念珠菌感染的保护作用。此外，Trim72可能通过NF-κB和ERK1/2信号增强巨噬细胞迁移和CCL2产生。抑制NF-κB和ERK1/2信号可消除Trim72介导的对致死性白色念珠菌感染的保护作用。因此，这些数据表明Trim72可能被开发为一种治疗严重全身性念珠菌病的宿主导向疗法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/dc68993f75d2/ppat.1012747.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/9f83b14cbce6/ppat.1012747.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/8d0eb6da400e/ppat.1012747.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/8b400b6c7eea/ppat.1012747.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/9ca6e46e610f/ppat.1012747.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/408a9f1cf4e3/ppat.1012747.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/11ce3833eaf4/ppat.1012747.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/98197bc8fc2b/ppat.1012747.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/d348f1456352/ppat.1012747.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/a3c11945370d/ppat.1012747.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/dc68993f75d2/ppat.1012747.g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/9f83b14cbce6/ppat.1012747.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/8d0eb6da400e/ppat.1012747.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/8b400b6c7eea/ppat.1012747.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/9ca6e46e610f/ppat.1012747.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/408a9f1cf4e3/ppat.1012747.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/11ce3833eaf4/ppat.1012747.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/98197bc8fc2b/ppat.1012747.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/d348f1456352/ppat.1012747.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/a3c11945370d/ppat.1012747.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e20c/11627414/dc68993f75d2/ppat.1012747.g010.jpg

相似文献

1
Trim72 is a major host factor protecting against lethal Candida albicans infection.Trim72是一种预防致死性白色念珠菌感染的主要宿主因子。
PLoS Pathog. 2024 Nov 25;20(11):e1012747. doi: 10.1371/journal.ppat.1012747. eCollection 2024 Nov.
2
Myeloid cell deficiency of p38γ/p38δ protects against candidiasis and regulates antifungal immunity.p38γ/p38δ 髓系细胞缺陷可预防念珠菌病并调节抗真菌免疫。
EMBO Mol Med. 2018 May;10(5). doi: 10.15252/emmm.201708485.
3
AIM2 enhances Candida albicans infection through promoting macrophage apoptosis via AKT signaling.AIM2 通过 AKT 信号促进巨噬细胞凋亡增强白念珠菌感染。
Cell Mol Life Sci. 2024 Jun 25;81(1):280. doi: 10.1007/s00018-024-05326-9.
4
Inflammasome-mediated GSDMD activation facilitates escape of Candida albicans from macrophages.炎性小体介导的 GSDMD 活化促进白色念珠菌从巨噬细胞中逃逸。
Nat Commun. 2021 Nov 18;12(1):6699. doi: 10.1038/s41467-021-27034-9.
5
Phagocytes from Mice Lacking the Sts Phosphatases Have an Enhanced Antifungal Response to Candida albicans.缺乏 Sts 磷酸酶的小鼠吞噬细胞对白色念珠菌的抗真菌反应增强。
mBio. 2018 Jul 17;9(4):e00782-18. doi: 10.1128/mBio.00782-18.
6
Signaling through Syk or CARD9 Mediates Species-Specific Anti- Protection in Bone Marrow Chimeric Mice.Syk 或 CARD9 信号转导介导骨髓嵌合小鼠中的种属特异性抗感染作用。
mBio. 2021 Aug 31;12(4):e0160821. doi: 10.1128/mBio.01608-21.
7
C-Type Lectin Receptor CD23 Is Required for Host Defense against and Infection.C 型凝集素受体 CD23 对于宿主防御 和 感染是必需的。
J Immunol. 2018 Oct 15;201(8):2427-2440. doi: 10.4049/jimmunol.1800620. Epub 2018 Sep 5.
8
Dual-antigen fusion protein vaccination induces protective immunity against infection in mice.双抗原融合蛋白疫苗接种可诱导小鼠产生针对 感染的保护性免疫。
Hum Vaccin Immunother. 2024 Dec 31;20(1):2406065. doi: 10.1080/21645515.2024.2406065. Epub 2024 Sep 26.
9
IL-33 Coordinates Innate Defense to Systemic Infection by Regulating IL-23 and IL-10 in an Opposite Way.IL-33 通过以相反的方式调节 IL-23 和 IL-10 来协调先天防御以应对全身感染。
J Immunol. 2022 Feb 1;208(3):660-671. doi: 10.4049/jimmunol.2100495. Epub 2022 Jan 12.
10
Trained Innate Immunity Induced by Vaccination with Low-Virulence Species Mediates Protection against Several Forms of Fungal Sepsis via Ly6G Gr-1 Leukocytes.疫苗接种诱导的低毒力物种训练的固有免疫通过 Ly6G Gr-1 白细胞介导对几种形式的真菌性败血症的保护作用。
mBio. 2021 Oct 26;12(5):e0254821. doi: 10.1128/mBio.02548-21. Epub 2021 Oct 19.

本文引用的文献

1
AIM2 enhances Candida albicans infection through promoting macrophage apoptosis via AKT signaling.AIM2 通过 AKT 信号促进巨噬细胞凋亡增强白念珠菌感染。
Cell Mol Life Sci. 2024 Jun 25;81(1):280. doi: 10.1007/s00018-024-05326-9.
2
MG53/TRIM72: multi-organ repair protein and beyond.MG53/TRIM72：多器官修复蛋白及其他功能
Front Physiol. 2024 Apr 12;15:1377025. doi: 10.3389/fphys.2024.1377025. eCollection 2024.
3
Invasive Fungal Diseases in Adult Patients in Intensive Care Unit (FUNDICU): 2024 consensus definitions from ESGCIP, EFISG, ESICM, ECMM, MSGERC, ISAC, and ISHAM.
成人重症监护病房侵袭性真菌病（FUNDICU）：ESGCIP、EFISG、ESICM、ECMM、MSGERC、ISAC和ISHAM的2024年共识定义
Intensive Care Med. 2024 Apr;50(4):502-515. doi: 10.1007/s00134-024-07341-7. Epub 2024 Mar 21.
4
TRIM72 restricts lyssavirus infection by inducing K48-linked ubiquitination and proteasome degradation of the matrix protein.TRIM72 通过诱导基质蛋白的 K48 连接泛素化和蛋白酶体降解来限制狂犬病毒感染。
PLoS Pathog. 2024 Feb 26;20(2):e1011718. doi: 10.1371/journal.ppat.1011718. eCollection 2024 Feb.
5
Bone morphogenetic protein 9 is a candidate prognostic biomarker and host-directed therapy target for sepsis.骨形态发生蛋白 9 是脓毒症的候选预后生物标志物和宿主定向治疗靶点。
Sci Transl Med. 2024 Jan 31;16(732):eadi3275. doi: 10.1126/scitranslmed.adi3275.
6
Interleukin-34-NF-κB signaling aggravates myocardial ischemic/reperfusion injury by facilitating macrophage recruitment and polarization.白细胞介素-34-NF-κB 信号通路通过促进巨噬细胞募集和极化加重心肌缺血/再灌注损伤。
EBioMedicine. 2023 Sep;95:104744. doi: 10.1016/j.ebiom.2023.104744. Epub 2023 Aug 8.
7
Activation of MG53 Enhances Cell Survival and Engraftment of Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes in Injured Hearts.MG53 的激活增强了人诱导多能干细胞衍生心肌细胞在受损心脏中的存活和植入。
Stem Cell Rev Rep. 2023 Oct;19(7):2420-2428. doi: 10.1007/s12015-023-10596-0. Epub 2023 Jul 21.
8
MG53 ameliorates nerve injury induced neuropathic pain through the regulation of Nrf2/HO-1 signaling in rats.MG53 通过调节 Nrf2/HO-1 信号通路改善大鼠神经损伤诱导的神经性疼痛。
Behav Brain Res. 2023 Jul 9;449:114489. doi: 10.1016/j.bbr.2023.114489. Epub 2023 May 9.
9
Nesfatin-1 Stimulates CCL2-dependent Monocyte Migration And M1 Macrophage Polarization: Implications For Rheumatoid Arthritis Therapy.内脂素-1 可刺激 CCL2 依赖性单核细胞迁移和 M1 型巨噬细胞极化：对类风湿关节炎治疗的启示。
Int J Biol Sci. 2023 Jan 1;19(1):281-293. doi: 10.7150/ijbs.77987. eCollection 2023.
10
Protective role of MG53 against ischemia/reperfusion injury on multiple organs: A narrative review.MG53对多器官缺血/再灌注损伤的保护作用：一篇叙述性综述。
Front Physiol. 2022 Nov 21;13:1018971. doi: 10.3389/fphys.2022.1018971. eCollection 2022.