Science (New York, N.Y.) · 2017
Host DNases prevent vascular occlusion by neutrophil extracellular traps.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Jiménez-Alcázar Miguel, Rangaswamy Chandini, Panda Rachita, Bitterling Josephine, Simsek Yashin J, Long Andy T, Bilyy Rostyslav, Krenn Veit, Renné Christoph, Renné Thomas, Kluge Stefan, Panzer Ulf, Mizuta Ryushin, Mannherz Hans Georg, Kitamura Daisuke, Herrmann Martin, Napirei Markus, Fuchs Tobias A
Аннотация
Platelet and fibrin clots occlude blood vessels in hemostasis and thrombosis. Here we report a noncanonical mechanism for vascular occlusion based on neutrophil extracellular traps (NETs), DNA fibers released by neutrophils during inflammation. We investigated which host factors control NETs in vivo and found that two deoxyribonucleases (DNases), DNase1 and DNase1-like 3, degraded NETs in circulation during sterile neutrophilia and septicemia. In the absence of both DNases, intravascular NETs formed clots that obstructed blood vessels and caused organ damage. Vascular occlusions in patients with severe bacterial infections were associated with a defect to degrade NETs ex vivo and the formation of intravascular NET clots. DNase1 and DNase1-like 3 are independently expressed and thus provide dual host protection against deleterious effects of intravascular NETs.