Intravascular Danger Signals Guide Neutrophils to Sites of Sterile Inflammation Braedon McDonald et al. Science 330, 362 (2010); DOI: 10.1126/science.1195491
This copy is for your personal, non-commercial use only.
If you wish to distribute this article to others, you can order high-quality copies for your colleagues, clients, or customers by clicking here. Permission to republish orrepurpose articles or portions of articles can be obtained by following the guidelines here. The following resources related to this article are available online at www.sciencemag.org (this information is current as of May 16, 2012 ): A correction has been published for this article at: http://www.sciencemag.org/content/331/6024/1517.full.html Updated information and services, including high-resolutionfigures, can be found in the online version of this article at: http://www.sciencemag.org/content/330/6002/362.full.html Supporting Online Material can be found at: http://www.sciencemag.org/content/suppl/2010/10/13/330.6002.362.DC1.html http://www.sciencemag.org/content/suppl/2010/10/14/330.6002.362.DC2.html A list of selected additional articles on the Science Web sites related to this articlecan be found at: http://www.sciencemag.org/content/330/6002/362.full.html#related This article cites 23 articles, 4 of which can be accessed free: http://www.sciencemag.org/content/330/6002/362.full.html#ref-list-1 This article has been cited by 22 articles hosted by HighWire Press; see: http://www.sciencemag.org/content/330/6002/362.full.html#related-urls This article appears in the followingsubject collections: Immunology http://www.sciencemag.org/cgi/collection/immunology Downloaded from www.sciencemag.org on May 16, 2012
Science (print ISSN 0036-8075; online ISSN 1095-9203) is published weekly, except the last week in December, by the American Association for the Advancement of Science, 1200 New York Avenue NW, Washington, DC 20005. Copyright 2010 by the American Association for theAdvancement of Science; all rights reserved. The title Science is a registered trademark of AAAS.
CORRECTED 25 MARCH 2011; SEE LAST PAGE
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...
Ler documento completo
Por favor, assinar para o acesso.