Abstract
During vasculitis, activation of the kinin system induces inflammation, whereby the kinin B1-receptor is expressed andactivated after ligand binding. Additionally, activated blood cells release microvesicles into the circulation. Here wedetermined whether leukocyte-derived microvesicles bear B1-kinin receptors during vasculitis, and if microvesicles transfer functional B1-receptors to recipient cells, thus promoting inflammation. By flow cytometry, plasma from patients with vasculitis were found to contain high levels ofleukocyte-derived microvesicles bearing B1-receptors. Importantly, renal biopsies from two patients with vasculitisshowed leukocyte-derived microvesicles bearingB1-receptors docking on glomerular endothelial cellsproviding invivo relevance. Microvesicles derived fromB1-receptor-transfected human embryonic kidney cellstransferred B1-receptors to wild-type human embryonic kidney cells, lacking the receptor,and to glomerular endothelial cells. The transferred B1-receptors induced calcium influx after B1-receptor agonist stimulation: a response abrogated by a specific B1-receptor antagonist. Microvesicles derived from neutrophils also transferred B1-receptors to wild-type human embryonic kidney cells andinduced calcium influx after stimulation. Thus, we found anovel mechanism by which microvesicles transfer functional receptors and promote kinin-associated inflammation.
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