Imperial College London
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DrSanoojSoni

Faculty of Medicine, Department of Surgery & Cancer

Clinical Senior Lecturer in Critical and Perioperative Care
 
 
 
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s.soni

 
 
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Location

 

Commonwealth BuildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Soni:2016:10.1136/thoraxjnl-2015-208032,
author = {Soni, S and Wilson, MR and O'Dea, KP and Yoshida, M and Katbeh, U and Woods, S and Takata, M},
doi = {10.1136/thoraxjnl-2015-208032},
journal = {Thorax},
pages = {1020--1029},
title = {Alveolar macrophage-derived microvesicles mediate acute lung injury},
url = {http://dx.doi.org/10.1136/thoraxjnl-2015-208032},
volume = {71},
year = {2016}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Background Microvesicles (MVs) are important mediators of intercellular communication, packaging a variety of molecular cargo. They have been implicated in the pathophysiology of various inflammatory diseases; yet, their role in acute lung injury (ALI) remains unknown.Objectives We aimed to identify the biological activity and functional role of intra-alveolar MVs in ALI.Methods Lipopolysaccharide (LPS) was instilled intratracheally into C57BL/6 mice, and MV populations in bronchoalveolar lavage fluid (BALF) were evaluated. BALF MVs were isolated 1hour post LPS, assessed for cytokine content and incubated with murine lung epithelial (MLE-12) cells. In separate experiments, primary alveolar macrophage-derived MVs were incubated with MLE-12 cells or instilled intratracheally into mice.Results Alveolar macrophages and epithelial cells rapidly released MVs into the alveoli following LPS. At 1hour, the dominant population was alveolar macrophage-derived, and these MVs carried substantive amounts of tumour necrosis factor (TNF) but minimal amounts of IL-1β/IL-6. Incubation of these mixed MVs with MLE-12 cells induced epithelial intercellular adhesion molecule-1 (ICAM-1) expression and keratinocyte-derived cytokine release compared with MVs from untreated mice (p<0.001). MVs released in vitro from LPS-primed alveolar macrophages caused similar increases in MLE-12 ICAM-1 expression, which was mediated by TNF. When instilled intratracheally into mice, these MVs induced increases in BALF neutrophils, protein and epithelial cell ICAM-1 expression (p<0.05).Conclusions We demonstrate, for the first time, the sequential production of MVs from different intra-alveolar precursor cells during the early phase of ALI. Our findings suggest that alveolar macrophage-derived MVs, which carry biologically active TNF, may play an important role in initiating ALI.
AU  - Soni,S
AU  - Wilson,MR
AU  - O'Dea,KP
AU  - Yoshida,M
AU  - Katbeh,U
AU  - Woods,S
AU  - Takata,M
DO  - 10.1136/thoraxjnl-2015-208032
EP  - 1029
PY  - 2016///
SN  - 1468-3296
SP  - 1020
TI  - Alveolar macrophage-derived microvesicles mediate acute lung injury
T2  - Thorax
UR  - http://dx.doi.org/10.1136/thoraxjnl-2015-208032
UR  - http://hdl.handle.net/10044/1/32370
VL  - 71
ER  -
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