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Blood, 15 November 2007, Vol. 110, No. 10, pp. 3773-3779. Prepublished online as a Blood First Edition Paper on August 15, 2007; DOI 10.1182/blood-2007-06-094565. This Article Full Text (PDF) All Versions of this Article: blood-2007-06-094565v1 110/10/3773    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Zarbock, A. Articles by Ley, K. Search for Related Content PubMed PubMed Citation Articles by Zarbock, A. Articles by Ley, K. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted June 8, 2007 Accepted August 6, 2007 Gi2 is required for chemokine-induced neutrophil arrest Alexander Zarbock, Tracy L Deem, Tracy L Burcin, and Klaus Ley* Dept of Anesthesiology & Intensive Care Medicine, University of Munster, Munster, Germany Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, VA, United States Department of Biomedical Engineering, Molecular Physiology & Biological Physics, University of Virginia, Charlottesville, VA, United States * Corresponding author; email: klausley{at}virginia.edu. Chemokines including CXCL1 participate in neutrophil recruitment by triggering the activation of integrins, which leads to arrest from rolling. The downstream signaling pathways which lead to integrin activation and neutophil arrest following G-protein coupled receptor engagement are incompletely understood. To test whether Gi2 is involved, mouse neutrophils in their native whole blood were investigated in mouse cremaster postcapillary venules and in flow chambers coated with P-selectin, ICAM-1 and CXCL1. Gnai2-/- neutrophils showed significantly reduced CXCL1-induced arrest in vitro and in vivo. Similar results were obtained with LTB4. Lethally irradiated mice reconstituted with Gnai2-/- bone marrow showed a similar defect in chemoattractant-induced arrest as Gnai2-/- mice. In thioglycollate-induced peritonitis and LPS-induced lung inflammation, chimeric mice lacking Gi2 in hematopoietic cells showed about 50% reduced neutrophil recruitment similar to that seen in Gnai2-/- mice. These data show that neutrophil Gi2 is necessary for chemokine-induced arrest, which is relevant for neutrophil recruitment to sites of acute inflammation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Zarbock and K. Ley Mechanisms and Consequences of Neutrophil Interaction with the Endothelium Am. J. Pathol., January 1, 2008; 172(1): 1 - 7. [Abstract] [Full Text] [PDF]

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