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Once considered cellular debris or, more recently, as biomarkers of disease progression, extracellular vesicles (EVs), comprised of exosomes, microvesicles (MVs) and apoptotic bodies, released by living and dying eukaryotic cells are now recognised as important mediators of cellular communication and function.1 EVs are a heterogeneous population of anucleate vesicles with a diameter of 100–1000 nm that are released from intracellular compartments as exosomes or by budding off the plasma membrane as MVs in response to diverse physiological, pathophysiological or external stimulus. Despite its importance in various organ injuries and cancer,2 ,3 the role of EVs in the pathogenesis of acute lung injury (ALI) is still largely unexplored.4–6 In the current issue of Thorax, Soni et al7 studied the temporal pattern of EV release in early ALI and found that MVs from alveolar macrophages were the predominant source and played a significant role as potent initiators of the inflammatory response in part by the transfer of its cargo, the cytokine tumour necrosis factor (TNF), to target cells.
By inducing ALI with intratracheal instillation of lipopolysaccharide (LPS) in C57BL6 mice, the authors found that MVs released into the injured alveolus were mainly from alveolar macrophages initially by flow cytometry, peaking at 1 hour and followed soon thereafter by MVs released by alveolar epithelial cells and neutrophils by 4 hours. More importantly, the MVs in the bronchoalveolar fluid (BALF) at 1 hour contained a substantial amount of TNF but low levels …
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