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体内全身性炎症过程中捕获到的大型细胞外囊泡 (EV) 和中性粒细胞细胞外陷阱 (NET) 相互作用。

Large extracellular vesicle (EV) and neutrophil extracellular trap (NET) interaction captured in vivo during systemic inflammation.

机构信息

Department of Experimental Hematology, Institute of Zoology and Biomedical Research, Jagiellonian University, Gronostajowa 9 Str, 30-387, Krakow, Poland.

Doctoral School of Exact and Natural Sciences, Jagiellonian University, Krakow, Poland.

出版信息

Sci Rep. 2024 Feb 26;14(1):4680. doi: 10.1038/s41598-024-55081-x.

DOI:10.1038/s41598-024-55081-x
PMID:38409254
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10897202/
Abstract

Extracellular vesicles (EVs) and neutrophil extracellular traps (NETs) are pivotal bioactive structures involved in various processes including inflammation. Herein we report the interactions between EVs and NETs during murine endotoxemia studied in situ directly in the vasculature (cremaster muscle, liver sinusoids) using intravital microscopy (IVM). We captured NETs and EV release in real time by both non- and polarized neutrophils in liver but not in cremaster vasculature. When comparing numbers of circulating EVs of various origin (nanoparticle tracking analysis-NTA, flow cytometry) with those interacting with endothelium and NETs (IVM) we observed that whereas platelet and monocyte/macrophage-derived EVs dominate in blood and peritoneal lavage, respectively, mostly neutrophil-derived EVs interact with the vascular lining, NETs and leukocytes. Despite the interaction, NETs do not affect EV formation as NET release inhibition did not alter EV release. However, EVs inhibit NETs formation and in particular, erythrocyte-derived EVs downregulate NET release and this effect is mediated via Siglec-E-dependent interactions with neutrophils. Overall, we report that EVs are present in NETs in vivo and they do modulate their release but the process in not bidirectional. Moreover, EVs isolated from body fluids might not reflect their importance in direct endothelial- and leukocyte-related interactions.

摘要

细胞外囊泡 (EVs) 和中性粒细胞细胞外陷阱 (NETs) 是参与各种过程的关键生物活性结构，包括炎症。在此，我们报告了在原位（肠系膜肌、肝窦）通过活体显微镜 (IVM) 研究鼠内毒素血症期间 EVs 和 NETs 之间的相互作用。我们通过非极化和极化中性粒细胞实时捕获了肝内但肠系膜血管中不存在的 NETs 和 EV 释放。当将各种来源的循环 EVs 的数量（纳米颗粒跟踪分析-NTA、流式细胞术）与与内皮和 NETs 相互作用的数量（IVM）进行比较时，我们观察到血小板和单核细胞/巨噬细胞衍生的 EVs 分别在血液和腹腔灌流中占优势，而主要是中性粒细胞衍生的 EVs 与血管衬里、NETs 和白细胞相互作用。尽管存在相互作用，但 NETs 不会影响 EV 的形成，因为 NET 释放抑制不会改变 EV 的释放。然而，EVs 抑制 NETs 的形成，特别是红细胞衍生的 EVs 下调 NETs 的释放，这种作用是通过 Siglec-E 与中性粒细胞的依赖相互作用介导的。总的来说，我们报告说 EVs 存在于体内的 NETs 中，它们确实调节其释放，但该过程不是双向的。此外，从体液中分离的 EVs 可能无法反映它们在与内皮和白细胞直接相关的相互作用中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/965ef33ddaa3/41598_2024_55081_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/cea40c529888/41598_2024_55081_Fig1_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/93058328813f/41598_2024_55081_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/66ea1d7b2c20/41598_2024_55081_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/7e57f0c9d95e/41598_2024_55081_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/7d22879682bf/41598_2024_55081_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/965ef33ddaa3/41598_2024_55081_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/cea40c529888/41598_2024_55081_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/2c5e0e5f669a/41598_2024_55081_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/ab79972b8d49/41598_2024_55081_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/93058328813f/41598_2024_55081_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/66ea1d7b2c20/41598_2024_55081_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/7e57f0c9d95e/41598_2024_55081_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/7d22879682bf/41598_2024_55081_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3767/10897202/965ef33ddaa3/41598_2024_55081_Fig8_HTML.jpg

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