Intravascular Danger Signals Guide Neutrophils to Sites of Sterile Inflammation
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- Braedon McDonald
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
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- Keir Pittman
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
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- Gustavo B. Menezes
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
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- Simon A. Hirota
- Gastrointestinal Research Group, Snyder Institute of Infection, Immunity and Inflammation, University of Calgary, Alberta T2N 4N1, Canada.
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- Ingrid Slaba
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
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- Christopher C. M. Waterhouse
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
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- Paul L. Beck
- Gastrointestinal Research Group, Snyder Institute of Infection, Immunity and Inflammation, University of Calgary, Alberta T2N 4N1, Canada.
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- Daniel A. Muruve
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
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- Paul Kubes
- Immunology Research Group, University of Calgary, Alberta T2N 4N1, Canada.
説明
<jats:title>Inflammation Response in Living Color</jats:title> <jats:p> Besides responding to microbial infection, our immune system also plays an important role in responding to sterile injury, for example, during trauma or organ necrosis. In a mouse model of sterile liver inflammation, <jats:bold> McDonald <jats:italic>et al.</jats:italic> </jats:bold> (p. <jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" page="362" related-article-type="in-this-issue" vol="330" xlink:href="10.1126/science.1195491">362</jats:related-article> ) used dynamic in vivo imaging to visualize the innate immune response, which is dominated by neutrophils. Neutrophils were rapidly recruited to the site of inflammation through intravascular channels. Adenosine triphosphate generated from necrotic cells at the injury site and the Nlrp3 inflammasome were required for neutrophils to exit the circulation into the vascular endothelium, where they used integrins to adhere. A luminal chemokine gradient guided integrin-dependent, intravascular migration toward the site of injury. Finally, formyl peptides provided a signal to override the chemokine gradient and draw neutrophils into the site of injury. </jats:p>
収録刊行物
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- Science
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Science 330 (6002), 362-366, 2010-10-15
American Association for the Advancement of Science (AAAS)
