The neutrophil in vascular inflammation

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Here we focus on how neutrophils have a key regulatory role in vascular inflammation. Recent studies using advanced imaging techniques have yielded new insights into the mechanisms by which neutrophils contribute to defense against bacterial infections and also against sterile injury. In these settings, neutrophils are recruited by various mechanisms depending on the situation. We also describe how these processes may be disrupted in systemic infections, with a particular emphasis on mouse models of sepsis. Neutrophils are often immobilized in the lungs and liver during systemic infections, and this immobilization may be a mechanism through which bacteria can evade the innate immune response or allow neutrophils to form neutrophil extracellular traps that trap and kill bacteria in blood. The platelet is also an important player in sepsis, and we describe how it collaborates with neutrophils in the formation of neutrophil extracellular traps.

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Figure 1: The neutrophil recruitment cascade.
Figure 2: Proposed model of PTEN, PI3K and p38 MAPK function during neutrophil chemotaxis.
Figure 3: Neutrophils move to sites of sterile injury by intravascular crawling.
Figure 4: Formation of neutrophil extracellular traps.
Figure 5: Platelet-neutrophil interactions within the liver vasculature during endotoxemia.


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We wish to express their thanks to the Canadian Foundation for Innovation for the funding of the University of Calgary Live Cell Imaging Facility that enabled this work and to C. Jenne, S. Massena and B. McDonald for helping with the figures. M.P. is supported by the Swedish Medical Research Council (57X-20675) and the Swedish Diabetes Foundation (DIA2010-063), and P.K., an Alberta Heritage Foundation for Medical Research Scientist, Canada Research Chair and the Snyder Chair in Critical Care Medicine, is supported by the Canadian Institutes of Health Research, the Alberta Heritage Foundation for Medical Research and the Heart and Stroke Foundation.

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Correspondence to Paul Kubes.

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