Imperial College London
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DrKieranO'Dea

Faculty of Medicine, Department of Surgery & Cancer

Senior Lecturer in Translational Critical Care
 
 
 
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Contact

 

k.odea

 
 
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Location

 

G3.43Chelsea and Westminster HospitalChelsea and Westminster Campus

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Summary

 

Publications

Citation

BibTex format

@article{Tan:2023:10.1165/rcmb.2022-0207OC,
author = {Tan, YY and O'Dea, KP and Tsiridou, DM and Soo, AP and Koh, MW and Beckett, F and Takata, M},
doi = {10.1165/rcmb.2022-0207OC},
journal = {American Journal of Respiratory Cell and Molecular Biology},
pages = {140--149},
title = {Circulating myeloid cell-derived extracellular vesicles as mediators of indirect acute lung injury},
url = {http://dx.doi.org/10.1165/rcmb.2022-0207OC},
volume = {68},
year = {2023}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Blood-borne myeloid cells, neutrophils and monocytes, play a central role in the development of indirect acute lung injury (ALI) during sepsis and noninfectious systemic inflammatory response syndrome. By contrast, the contribution of circulating myeloid cell–derived extracellular vesicles (EVs) to ALI is unknown, despite acute increases in their numbers during sepsis and systemic inflammatory response syndrome. Here, we investigated the direct role of circulating myeloid-EVs in ALI using a mouse isolated perfused lung system and a human cell coculture model of pulmonary vascular inflammation consisting of lung microvascular endothelial cells and peripheral blood mononuclear cells. Total and immunoaffinity-isolated myeloid (CD11b+) and platelet (CD41+) EVs were prepared from the plasma of intravenous LPS-injected endotoxemic donor mice and transferred directly into recipient lungs. Two-hour perfusion of lungs with unfractionated EVs from a single donor induced pulmonary edema formation and increased perfusate concentrations of RAGE (receptor for advanced glycation end products), consistent with lung injury. These responses were abolished in the lungs of monocyte-depleted mice. The isolated myeloid- but not platelet-EVs produced a similar injury response and the acute intravascular release of proinflammatory cytokines and endothelial injury markers. In the in vitro human coculture model, human myeloid- (CD11b+) but not platelet- (CD61+) EVs isolated from LPS-stimulated whole blood induced acute proinflammatory cytokine production and endothelial activation. These findings implicate circulating myeloid-EVs as acute mediators of pulmonary vascular inflammation and edema, suggesting an alternative therapeutic target for attenuation of indirect ALI.
AU  - Tan,YY
AU  - O'Dea,KP
AU  - Tsiridou,DM
AU  - Soo,AP
AU  - Koh,MW
AU  - Beckett,F
AU  - Takata,M
DO  - 10.1165/rcmb.2022-0207OC
EP  - 149
PY  - 2023///
SN  - 1044-1549
SP  - 140
TI  - Circulating myeloid cell-derived extracellular vesicles as mediators of indirect acute lung injury
T2  - American Journal of Respiratory Cell and Molecular Biology
UR  - http://dx.doi.org/10.1165/rcmb.2022-0207OC
UR  - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000926612500006&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=1ba7043ffcc86c417c072aa74d649202
UR  - https://www.atsjournals.org/doi/10.1165/rcmb.2022-0207OC
VL  - 68
ER  -
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