• 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

含PMA1的细胞外囊泡引发免疫反应和结肠炎进展。

PMA1-containing extracellular vesicles of triggers immune responses and colitis progression.

作者信息

Xu Zhen, Qiao Shuping, Wang Zelin, Peng Chen, Hou Yayi, Liu Baorui, Cao Guochun, Wang Tingting

机构信息

Department of Oncology, Nanjing Drum Tower Hospital, State Key Laboratory of Pharmaceutical Biotechnology, Affiliated Hospital of Medical School, Nanjing University, Nanjing, China.

The Comprehensive Cancer Centre of Drum Tower Hospital, Medical School of Nanjing University & Clinical Cancer Institute of Nanjing University, Nanjing, China.

出版信息

Gut Microbes. 2025 Dec;17(1):2455508. doi: 10.1080/19490976.2025.2455508. Epub 2025 Jan 31.

DOI:10.1080/19490976.2025.2455508
PMID:39886799
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11792855/
Abstract

() exhibits aberrant changes in patients with colitis, and it has been reported to dominate the colonic mucosal immune response. Here, we found that PMA1 expression was significantly increased in from patients with IBD compared to that in healthy controls. A Crispr-Cas9-based fungal strain editing system was then used to knock out PMA1 expression in . Compared to , could not aggravate colitis. Proteomic analysis showed that PMA1 was transported by extracellular vesicles (EVs) of . PMA1-containing EVs aggravated colitis, modulated the migration of cDC2 from the lamina propria to mesenteric lymph nodes, and induced TH17 cell differentiation. Moreover, the adaptor protein CARD9 was critical in PMA1-containing EV-induced colitis, and CARD9-deficient DCs did not induce TH17 cell differentiation or IL-17A production. Mechanically, CARD9 combines with the glycolytic protein GAPDH (aa2-146 domain) through its CARD region. CARD9 deficiency led to decreased enzyme activity of GAPDH and decreased glycolysis of DCs. These findings indicate that PMA1 is a potential virulence factor responsible for the pathogenesis of colitis.

摘要

（）在结肠炎患者中表现出异常变化，并且据报道它在结肠黏膜免疫反应中起主导作用。在此，我们发现与健康对照相比，IBD患者的[具体内容未给出]中PMA1表达显著增加。然后使用基于Crispr-Cas9的真菌菌株编辑系统敲除[具体内容未给出]中的PMA1表达。与[具体内容未给出]相比，[具体内容未给出]不会加重结肠炎。蛋白质组学分析表明，PMA1由[具体内容未给出]的细胞外囊泡（EVs）转运。含PMA1的EVs加重结肠炎，调节cDC2从固有层向肠系膜淋巴结的迁移，并诱导TH17细胞分化。此外，衔接蛋白CARD9在含PMA1的EV诱导的结肠炎中起关键作用，CARD9缺陷的DCs不会诱导TH17细胞分化或IL-17A产生。从机制上讲，CARD9通过其CARD区域与糖酵解蛋白GAPDH（aa2 - 146结构域）结合。CARD9缺陷导致GAPDH酶活性降低和DCs糖酵解减少。这些发现表明PMA1是导致[具体内容未给出]结肠炎发病机制的潜在毒力因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/e448e98ae87a/KGMI_A_2455508_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/260a234e0a70/KGMI_A_2455508_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/b1c04394cd9d/KGMI_A_2455508_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/704f85100bcb/KGMI_A_2455508_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/8acc38634339/KGMI_A_2455508_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/1e6b27585d11/KGMI_A_2455508_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/46cde48acf8f/KGMI_A_2455508_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/a83264ceb675/KGMI_A_2455508_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/1223d320d23e/KGMI_A_2455508_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/e448e98ae87a/KGMI_A_2455508_F0009_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/260a234e0a70/KGMI_A_2455508_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/b1c04394cd9d/KGMI_A_2455508_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/704f85100bcb/KGMI_A_2455508_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/8acc38634339/KGMI_A_2455508_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/1e6b27585d11/KGMI_A_2455508_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/46cde48acf8f/KGMI_A_2455508_F0006_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/a83264ceb675/KGMI_A_2455508_F0007_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/1223d320d23e/KGMI_A_2455508_F0008_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/212b/11792855/e448e98ae87a/KGMI_A_2455508_F0009_OC.jpg

相似文献

1
PMA1-containing extracellular vesicles of triggers immune responses and colitis progression.含PMA1的细胞外囊泡引发免疫反应和结肠炎进展。
Gut Microbes. 2025 Dec;17(1):2455508. doi: 10.1080/19490976.2025.2455508. Epub 2025 Jan 31.
2
Card9 mediates intestinal epithelial cell restitution, T-helper 17 responses, and control of bacterial infection in mice.Card9 介导了肠道上皮细胞修复、辅助性 T 细胞 17 反应以及对小鼠细菌感染的控制。
Gastroenterology. 2013 Sep;145(3):591-601.e3. doi: 10.1053/j.gastro.2013.05.047. Epub 2013 May 31.
3
The adaptor CARD9 is required for adaptive but not innate immunity to oral mucosal Candida albicans infections.衔接蛋白 CARD9 对于口腔黏膜白念珠菌感染的适应性免疫而非固有免疫是必需的。
Infect Immun. 2014 Mar;82(3):1173-80. doi: 10.1128/IAI.01335-13. Epub 2013 Dec 30.
4
Inherited CARD9 deficiency in otherwise healthy children and adults with Candida species-induced meningoencephalitis, colitis, or both.在其他方面健康的儿童和成人中，因念珠菌属诱发的脑膜脑炎、结肠炎或两者兼具而出现遗传性CARD9缺陷。
J Allergy Clin Immunol. 2015 Jun;135(6):1558-68.e2. doi: 10.1016/j.jaci.2014.12.1930. Epub 2015 Feb 19.
5
Proteomics unravels extracellular vesicles as carriers of classical cytoplasmic proteins in Candida albicans.蛋白质组学揭示白色念珠菌中细胞外囊泡作为经典细胞质蛋白的载体。
J Proteome Res. 2015 Jan 2;14(1):142-53. doi: 10.1021/pr5007944. Epub 2014 Nov 12.
6
Card9 deficiency exacerbates vulvovaginal candidiasis by impairing the IL-17 production and vaginal epithelial barrier.Card9缺陷通过损害IL-17的产生和阴道上皮屏障而加重外阴阴道念珠菌病。
Med Mycol. 2025 Apr 2;63(4). doi: 10.1093/mmy/myaf026.
7
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.
8
Lipid Biosynthetic Genes Affect Candida albicans Extracellular Vesicle Morphology, Cargo, and Immunostimulatory Properties.脂质生物合成基因影响白色念珠菌细胞外囊泡的形态、货物及免疫刺激特性。
Eukaryot Cell. 2015 Aug;14(8):745-54. doi: 10.1128/EC.00054-15. Epub 2015 May 29.
9
Toll-like receptor 4 (TLR4) is the major pattern recognition receptor triggering the protective effect of a extracellular vesicle-based vaccine prototype in murine systemic candidiasis.Toll 样受体 4（TLR4）是触发基于细胞外囊泡的疫苗原型在小鼠系统性念珠菌病中发挥保护作用的主要模式识别受体。
mSphere. 2024 Aug 28;9(8):e0046724. doi: 10.1128/msphere.00467-24. Epub 2024 Jul 22.
10
Oral epithelial cells orchestrate innate type 17 responses to through the virulence factor candidalysin.口腔上皮细胞通过真菌毒素白念珠菌素调控对 1 型固有免疫反应。
Sci Immunol. 2017 Nov 3;2(17). doi: 10.1126/sciimmunol.aam8834.

引用本文的文献

1
Things you wanted to know about fungal extracellular vesicles (but were afraid to ask).关于真菌细胞外囊泡你想知道的事（但却不敢问）。
PLoS Negl Trop Dis. 2025 May 22;19(5):e0013038. doi: 10.1371/journal.pntd.0013038. eCollection 2025 May.

本文引用的文献

1
The hyphal-specific toxin candidalysin promotes fungal gut commensalism.菌丝体特异性毒素念珠菌溶血素促进真菌肠道共生。
Nature. 2024 Mar;627(8004):620-627. doi: 10.1038/s41586-024-07142-4. Epub 2024 Mar 6.
2
Candida albicans extracellular vesicles trigger type I IFN signalling via cGAS and STING.白色念珠菌细胞外囊泡通过 cGAS 和 STING 触发 I 型干扰素信号通路。
Nat Microbiol. 2024 Jan;9(1):95-107. doi: 10.1038/s41564-023-01546-0. Epub 2024 Jan 2.
3
Candida albicans induces neutrophil extracellular traps and leucotoxic hypercitrullination via candidalysin.
白色念珠菌通过念珠菌溶素诱导中性粒细胞胞外陷阱形成和白细胞毒性高瓜氨酸化。
EMBO Rep. 2023 Nov 6;24(11):e57571. doi: 10.15252/embr.202357571. Epub 2023 Oct 5.
4
CD4 T-Cell Subsets and the Pathophysiology of Inflammatory Bowel Disease.CD4 T 细胞亚群与炎症性肠病的病理生理学。
Int J Mol Sci. 2023 Jan 31;24(3):2696. doi: 10.3390/ijms24032696.
5
Card9 protects fungal peritonitis through regulating Malt1-mediated activation of autophagy in macrophage.Card9 通过调节巨噬细胞中 Malt1 介导的自噬来保护真菌性腹膜炎。
Int Immunopharmacol. 2022 Sep;110:108941. doi: 10.1016/j.intimp.2022.108941. Epub 2022 Jul 16.
6
Candida albicans Hyphal Extracellular Vesicles Are Different from Yeast Ones, Carrying an Active Proteasome Complex and Showing a Different Role in Host Immune Response.白色念珠菌菌丝细胞外囊泡不同于酵母细胞外囊泡，携带活性蛋白酶体复合物，并在宿主免疫反应中发挥不同的作用。
Microbiol Spectr. 2022 Jun 29;10(3):e0069822. doi: 10.1128/spectrum.00698-22. Epub 2022 May 23.
7
Immune regulation by fungal strain diversity in inflammatory bowel disease.真菌菌株多样性对炎症性肠病的免疫调节。
Nature. 2022 Mar;603(7902):672-678. doi: 10.1038/s41586-022-04502-w. Epub 2022 Mar 16.
8
Carcinogenic microbiota and its role in colorectal cancer development.致癌微生物群及其在结直肠癌发展中的作用。
Semin Cancer Biol. 2022 Nov;86(Pt 3):420-430. doi: 10.1016/j.semcancer.2022.01.004. Epub 2022 Jan 25.
9
Human gut bacterial metabolism drives Th17 activation and colitis.人体肠道细菌代谢物驱动 Th17 细胞激活并引发结肠炎。
Cell Host Microbe. 2022 Jan 12;30(1):17-30.e9. doi: 10.1016/j.chom.2021.11.001. Epub 2021 Nov 24.
10
The Gut Microbiome and Inflammatory Bowel Diseases.肠道微生物组与炎症性肠病。
Annu Rev Med. 2022 Jan 27;73:455-468. doi: 10.1146/annurev-med-042320-021020. Epub 2021 Sep 23.