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并且相互促进它们的毒力因子分泌和促炎作用。

and reciprocally promote their virulence factor secretion and pro-inflammatory effects.

作者信息

Pasman Raymond, Krom Bastiaan P, Jonker Martijs J, de Leeuw Wim C, Kramer Gertjan, Brul Stanley, Zaat Sebastian A J, Zhang Jianbo

机构信息

Department of Molecular Biology and Microbial Food Safety, Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, Netherlands.

Department of Preventive Dentistry, Academic Centre for Dentistry Amsterdam (ACTA), University of Amsterdam and Free University Amsterdam, Amsterdam, Netherlands.

出版信息

Front Cell Infect Microbiol. 2025 Aug 22;15:1629373. doi: 10.3389/fcimb.2025.1629373. eCollection 2025.

DOI:10.3389/fcimb.2025.1629373
PMID:40918254
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12411458/
Abstract

BACKGROUND

Co-infections of and can significantly increase morbidity and mortality. However, the effect of co-existence on virulence factor secretion and pro-inflammatory effects remain elusive.

METHODS

We systematically investigated the virulence factors released by and under different culturing conditions using proteomics. We characterized their pro-inflammatory effects in macrophages with transcriptomics and gene set enrichment analysis.

RESULTS AND DISCUSSION

We showed that co-culturing of and promoted the secretion of 7 cytolytic, 11 proteolytic, and 3 lipolytic extracellular virulence factors (ECVFs) and impacted non-ECVFs, owing to Als1/Als3-mediated interactions, the presence of , or its pH maintenance. Co-culturing promotes hypha formation and β-glucan masking, suggesting that co-culturing enhances both invasion and immune evasion. Moreover, the secretome of co-culture increased pro-inflammatory pathways including promoting TNF-, NFKB-, and Toll-like receptor signaling pathways, as well as cytokine-cytokine receptor interactions in macrophages. Our findings support that and reciprocally promote their virulence potential and pro-inflammatory effects, which may provide mechanistic insights into the increased morbidity and mortality during their co-infection .

摘要

背景

[两种病原体名称]的合并感染可显著增加发病率和死亡率。然而，[两种病原体名称]共存对毒力因子分泌和促炎作用的影响仍不清楚。

方法

我们使用蛋白质组学系统地研究了[两种病原体名称]在不同培养条件下释放的毒力因子。我们通过转录组学和基因集富集分析来表征它们在巨噬细胞中的促炎作用。

结果与讨论

我们发现，[两种病原体名称]的共培养促进了7种溶细胞性、11种蛋白水解性和3种脂解性细胞外毒力因子（ECVF）的分泌，并由于Als1/Als3介导的相互作用、[某种物质或条件]的存在或其pH维持而影响了非ECVF。共培养促进了[病原体名称]的菌丝形成和β-葡聚糖掩盖，表明共培养增强了[病原体名称]的侵袭和免疫逃避。此外，[两种病原体名称]共培养的分泌组增加了促炎途径，包括促进肿瘤坏死因子、核因子κB和Toll样受体信号通路，以及巨噬细胞中的细胞因子-细胞因子受体相互作用。我们的研究结果支持[两种病原体名称]相互促进其毒力潜能和促炎作用，这可能为它们合并感染期间发病率和死亡率增加提供机制性见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/fa267f39984f/fcimb-15-1629373-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/d5d796aafe49/fcimb-15-1629373-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/e81ca4d7d3b3/fcimb-15-1629373-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/215a9022bb6a/fcimb-15-1629373-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/ef103d57a3a6/fcimb-15-1629373-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/fa267f39984f/fcimb-15-1629373-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/d5d796aafe49/fcimb-15-1629373-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/e81ca4d7d3b3/fcimb-15-1629373-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/215a9022bb6a/fcimb-15-1629373-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/ef103d57a3a6/fcimb-15-1629373-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7939/12411458/fa267f39984f/fcimb-15-1629373-g005.jpg

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