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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.

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PHAGOCYTES

G{alpha}i2 is required for chemokine-induced neutrophil arrest

Alexander Zarbock1,2, Tracy L. Deem1, Tracy L. Burcin1, and Klaus Ley1,3

1 Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville; 2 Department of Anesthesiology and Intensive Care Medicine, University of Münster, Münster, Germany; and 3 Department of Biomedical Engineering, Molecular Physiology and Biological Physics, University of Virginia, Charlottesville

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 G{alpha}i2 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 leukotriene B4 (LTB4). Lethally irradiated mice reconstituted with Gnai2–/– bone marrow showed a similar defect in chemoattractant-induced arrest as that of Gnai2–/– mice. In thioglycollate-induced peritonitis and lipopolysaccaride (LPS)–induced lung inflammation, chimeric mice lacking G{alpha}i2 in hematopoietic cells showed about 50% reduced neutrophil recruitment similar to that seen in Gnai2–/– mice. These data show that neutrophil G{alpha}i2 is necessary for chemokine-induced arrest, which is relevant for neutrophil recruitment to sites of acute inflammation.


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A. Zarbock and K. Ley
Mechanisms and Consequences of Neutrophil Interaction with the Endothelium
Am. J. Pathol., January 1, 2008; 172(1): 1 - 7.
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