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Thorax trauma (TxT) is strongly associated with trauma\u2010related death, an unbalanced innate immune response, sepsis, acute respiratory distress syndrome, and multiple organ dysfunction. It is shown that different in vivo traumata, such as TxT or an in vitro polytrauma cytokine cocktail trigger secretion of small extracellular nanovesicles (sEVs) from endothelial cells with pro\u2010inflammatory cargo. These sEVs transfer transcripts for ICAM\u20101, VCAM\u20101, E\u2010selectin, and cytokines to systemically activate the endothelium, facilitate neutrophil\u2010endothelium interactions, and destabilize barrier integrity. Inhibition of sEV\u2010release after TxT in mice ameliorates local as well as systemic inflammation, neutrophil infiltration, and distant organ damage in kidneys (acute kidney injury, AKI). Vice versa, injection of TxT\u2010plasma\u2010sEVs into healthy animals is sufficient to trigger pulmonary and systemic inflammation as well as AKI. 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