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细菌成孔毒素肺炎溶血素通过感染期间释放的宿主细胞外囊泡驱动致病性。

Bacterial pore-forming toxin pneumolysin drives pathogenicity through host extracellular vesicles released during infection.

作者信息

Parveen Saba, Bhat Chinmayi V, Sagilkumar Aswathy C, Aziz Shaheena, Arya J, Dutta Asmita, Dutta Somit, Show Sautan, Sharma Kuldeep, Rakshit Sumit, Johnson John Bernet, Nongthomba Upendra, Banerjee Anirban, Subramanian Karthik

机构信息

Host-Pathogen Laboratory, Pathogen Biology Division, Rajiv Gandhi Centre for Biotechnology, Thiruvananthapuram 695014, India.

Regional Centre for Biotechnology, Faridabad 121001, India.

出版信息

iScience. 2024 Jul 25;27(8):110589. doi: 10.1016/j.isci.2024.110589. eCollection 2024 Aug 16.

DOI:10.1016/j.isci.2024.110589
PMID:39211544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11357855/
Abstract

is a global priority respiratory pathogen that kills over a million people annually. The pore-forming cytotoxin, pneumolysin (PLY) is a major virulence factor. Here, we found that recombinant PLY as well as wild-type pneumococcal strains, but not the isogenic PLY mutant, upregulated the shedding of extracellular vesicles (EVs) harboring membrane-bound toxin from human THP-1 monocytes. PLY-EVs induced cytotoxicity and hemolysis dose-dependently upon internalization by recipient monocyte-derived dendritic cells. Proteomics analysis revealed that PLY-EVs are selectively enriched in key inflammatory host proteins such as IFI16, NLRC4, PTX3, and MMP9. EVs shed from PLY-challenged or infected cells induced dendritic cell maturation and primed them to infection. , zebrafish administered with PLY-EVs showed pericardial edema and mortality. Adoptive transfer of bronchoalveolar-lavage-derived EVs from infected mice to healthy recipients induced lung damage and inflammation in a PLY-dependent manner. Our findings identify that host EVs released during infection mediate pneumococcal pathogenesis.

摘要

是一种全球重点关注的呼吸道病原体，每年导致超过一百万人死亡。成孔细胞毒素肺炎溶血素（PLY）是一种主要的毒力因子。在此，我们发现重组PLY以及野生型肺炎球菌菌株，而非同基因PLY突变体，上调了人THP-1单核细胞中携带膜结合毒素的细胞外囊泡（EVs）的释放。PLY-EVs被受体单核细胞衍生的树突状细胞内化后，剂量依赖性地诱导细胞毒性和溶血。蛋白质组学分析表明，PLY-EVs选择性地富集了关键的炎症宿主蛋白，如IFI16、NLRC4、PTX3和MMP9。从受PLY刺激或感染的细胞中释放的EVs诱导树突状细胞成熟，并使其对感染产生致敏作用。此外，给斑马鱼注射PLY-EVs会出现心包水肿和死亡。将感染小鼠支气管肺泡灌洗来源的EVs过继转移至健康受体，以PLY依赖的方式诱导肺损伤和炎症。我们的研究结果表明，感染期间释放的宿主EVs介导了肺炎球菌的发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/1adc10aadb48/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/44bb0bdfa15d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/8568fb76162c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/4d0571d113f9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/7a6da4043171/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/9b5547397615/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/10629650d8fc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/1adc10aadb48/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/44bb0bdfa15d/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/8568fb76162c/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/4d0571d113f9/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/7a6da4043171/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/9b5547397615/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/10629650d8fc/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adff/11357855/1adc10aadb48/gr6.jpg

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本文引用的文献

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Cells Responding to Closely Related Cholesterol-Dependent Cytolysins Release Extracellular Vesicles with a Common Proteomic Content Including Membrane Repair Proteins.细胞对密切相关的胆固醇依赖性细胞溶素的反应是释放具有共同蛋白质组内容的细胞外囊泡，包括膜修复蛋白。
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