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Blood, 1 January 2008, Vol. 111, No. 1, pp. 42-49. Prepublished online as a Blood First Edition Paper on October 10, 2007; DOI 10.1182/blood-2007-07-099648. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-07-099648v1 111/1/42    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Wengner, A. M. Articles by Rankin, S. M. Search for Related Content PubMed PubMed Citation Articles by Wengner, A. M. Articles by Rankin, S. M. Related Collections Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES, CYTOKINES, AND INTERLEUKINS The coordinated action of G-CSF and ELR + CXC chemokines in neutrophil mobilization during acute inflammation Antje M. Wengner1, Simon C. Pitchford1, Rebecca C. Furze1, and Sara M. Rankin1 1 Leukocyte Biology Section, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, London, United Kingdom In this study, we have identified a unique combinatorial effect of the chemokines KC/MIP-2 and the cytokine granulocyte colony-stimulating factor (G-CSF) with respect to the rapid mobilization of neutrophils from the bone marrow in a model of acute peritonitis. At 2 hours following an intraperitoneal injection of thioglycollate, there was a 4.5-fold increase in blood neutrophil numbers, which was inhibited 84% and 72% by prior administration of blocking mAbs against either the chemokines KC/MIP-2 or G-CSF, respectively. An intraperitoneal injection of G-CSF acted remotely to stimulate neutrophil mobilization, but did not elicit recruitment into the peritoneum. Further, in vitro G-CSF was neither chemotactic nor chemokinetic for murine neutrophils, and had no priming effect on chemotaxis stimulated by chemokines. Here, we show that, in vitro and in vivo, G-CSF induces neutrophil mobilization by disrupting their SDF-1–mediated retention in the bone marrow. Using an in situ perfusion system of the mouse femoral bone marrow to directly assess mobilization, KC and G-CSF mobilized 6.8 x 106 and 5.4 x 106 neutrophils, respectively, while the infusion of KC and G-CSF together mobilized 19.5 x 106 neutrophils, indicating that these factors act cooperatively with respect to neutrophil mobilization. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Sawanobori, S. Ueha, M. Kurachi, T. Shimaoka, J. E. Talmadge, J. Abe, Y. Shono, M. Kitabatake, K. Kakimi, N. Mukaida, et al. Chemokine-mediated rapid turnover of myeloid-derived suppressor cells in tumor-bearing mice Blood, June 15, 2008; 111(12): 5457 - 5466. [Abstract] [Full Text] [PDF]

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