Host DNases prevent vascular occlusion by neutrophil extracellular traps
| Autor: | Stefan Kluge, Tobias A. Fuchs, Rostyslav Bilyy, Hans Georg Mannherz, Christoph Renné, Veit Krenn, Chandini Rangaswamy, Rachita Panda, Yashin J. Simsek, Josephine Bitterling, Ulf Panzer, Thomas Renné, Markus Napirei, Daisuke Kitamura, Martin Herrmann, Ryushin Mizuta, Miguel Jiménez-Alcázar, Andy T. Long |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Pathology medicine.medical_specialty Neutrophils Inflammation Vascular occlusion Extracellular Traps Fibrin 03 medical and health sciences Mice Sepsis Granulocyte Colony-Stimulating Factor Medicine Animals Deoxyribonuclease I Humans Platelet Lung Hemostatic Disorders Hemostasis Multidisciplinary Endodeoxyribonucleases biology business.industry Thrombosis Neutrophil extracellular traps DNA Neutrophilia Mice Mutant Strains 030104 developmental biology Liver biology.protein medicine.symptom business Ex vivo |
| Zdroj: | Science (New York, N.Y.). 358(6367) |
| ISSN: | 1095-9203 |
| Popis: | Blood DNases hack the NET Neutrophil extracellular traps (NETs) are lattices of processed chromatin decorated with select secreted and cytoplasmic proteins that trap and neutralize microbes. However, their inappropriate release may do more harm than good by promoting inflammation and thrombosis. Jiménez-Alcázar et al. report that two deoxyribonucleases (DNases), DNASE1 and DNASE1L3, have partially redundant roles in degrading NETs in the circulation (see the Perspective by Gunzer). Knockout mice lacking these enzymes were unable to tolerate chronic neutrophilia, quickly dying after blood vessels were occluded by NET clots. Furthermore, the damage unleashed by clots during septicemia was enhanced when these DNases were absent. Science , this issue p. 1202 ; see also p. 1126 |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
| Nepřihlášeným uživatelům se plný text nezobrazuje | K zobrazení výsledku je třeba se přihlásit. |