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Intravascular Danger Signals Guide Neutrophils to Sites of Sterile Inflammation Braedon McDonald et al. Science 330, 362 (2010); DOI: 10.1126/science.1195491

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ute to the clearance of debris (1). Neutrophils, however, possess a vast arsenal of hydrolytic, oxidative, and pore-forming molecules capable of causing profound collateral tissue destruction (2). As such, overexuberant neutrophil recruitment inresponse to sterile inflammatory stimuli contributes to the immunopathology observed in many diseases, including ischemic injuries/infarction, trauma, autoimmunity, drug-induced liver injury, and others (1, 3–7). Therefore, understanding the mechanisms that allow neutrophils to respond to sterile tissue injury and cell death is fundamental to our understanding of both homeostatic innate immunefunctions and pathogenic immune responses in disease.
1 Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada. 2Gastrointestinal Research Group, Snyder Institute of Infection, Immunity and Inflammation, University of Calgary, Alberta T2N 4N1, Canada. 3Department of Pediatrics, Division of Pediatric Gastroenterology, University of Calgary, Alberta T2N 4N1, Canada. 4Department ofMedicine, University of Calgary, Alberta T2N 4N1, Canada.

Intravascular Danger Signals Guide Neutrophils to Sites of Sterile Inflammation
Braedon McDonald,1 Keir Pittman,1 Gustavo B. Menezes,1* Simon A. Hirota,2 Ingrid Slaba,1 Christopher C. M. Waterhouse,1,3 Paul L. Beck,2,4 Daniel A. Muruve,1,4 Paul Kubes1† Neutrophils are recruited from the blood to sites of sterile inflammation, where theycontribute to wound healing but may also cause tissue damage. By using spinning disk confocal intravital microscopy, we examined the kinetics and molecular mechanisms of neutrophil recruitment to sites of focal hepatic necrosis in vivo. Adenosine triphosphate released from necrotic cells activated the Nlrp3 inflammasome to generate an inflammatory microenvironment that alerted circulating...
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