SEARCH:   Advanced

Blood, 15 August 2008, Vol. 112, No. 4, pp. 1461-1471. Prepublished online as a Blood First Edition Paper on May 19, 2008; DOI 10.1182/blood-2008-02-139634. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-02-139634v1 112/4/1461    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 Soehnlein, O. Articles by Lindbom, L. Search for Related Content PubMed PubMed Citation Articles by Soehnlein, O. Articles by Lindbom, L. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 19, 2008 Accepted April 28, 2008 Neutrophil secretion products pave the way for inflammatory monocytes Oliver Soehnlein*, Alma Zernecke, Einar E Eriksson, Antonio Gigliotti Rothfuchs, Christine T Pham, Heiko Herwald, Kiril Bidzhekov, Martin E Rottenberg, Christian Weber, and Lennart Lindbom Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Aachen, Germany Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD, United States Department of Medicine, Washington University, St. Louis, MO, United States Department of Clinical Sciences, Lund University, Lund, Sweden Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden * Corresponding author; email: oliver.sohnlein{at}ki.se. The leukocyte response in inflammation is characterized by an initial recruitment of polymorphonuclear leukocytes (PMN) preceding a second wave of monocytes to the site of injury or infection. In the mouse, two populations of monocytes have been identified, Gr1-CCR2-CX3CR1hi resident monocytes and Gr1+CCR2+CX3CR1lo inflammatory monocytes. Here, intravital microscopy of the M. cremaster and a subcutaneous air pouch model were used to investigate a possible link between PMN extravasation and the subsequent emigration of inflammatory monocytes in response to local stimulation with PAF. In mice that were made neutropenic by injection of a PMN-depleting antibody, the extravasation of inflammatory monocytes, but not resident monocytes, was markedly reduced compared to mice with intact white blood cell count but was restored by local treatment with secretion of activated PMN. Components of the PMN secretion were found to directly activate inflammatory monocytes and further examination revealed PMN-derived LL-37 and heparin-binding protein (HBP/CAP37/azurocidin) as primary mediators of the recruitment of inflammatory monocytes via activation of formyl-peptide receptors. These data show that LL-37 and HBP specifically stimulate mobilization of inflammatory monocytes. This cellular cross-talk functionally results in enhanced cytokine levels and increased bacterial clearance, thus boosting the early immune response. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: O. Soehnlein, L. Lindbom, and C. Weber Mechanisms underlying neutrophil-mediated monocyte recruitment Blood, November 19, 2009; 114(21): 4613 - 4623. [Abstract] [Full Text] [PDF] M.-B. Voisin, A. Woodfin, and S. Nourshargh Monocytes and Neutrophils Exhibit Both Distinct and Common Mechanisms in Penetrating the Vascular Basement Membrane In Vivo Arterioscler Thromb Vasc Biol, August 1, 2009; 29(8): 1193 - 1199. [Abstract] [Full Text] [PDF] G. Bergsson, E. P. Reeves, P. McNally, S. H. Chotirmall, C. M. Greene, P. Greally, P. Murphy, S. J. O'Neill, and N. G. McElvaney LL-37 Complexation with Glycosaminoglycans in Cystic Fibrosis Lungs Inhibits Antimicrobial Activity, Which Can Be Restored by Hypertonic Saline J. Immunol., July 1, 2009; 183(1): 543 - 551. [Abstract] [Full Text] [PDF] A. Di Gennaro, E. Kenne, M. Wan, O. Soehnlein, L. Lindbom, and J. Z. Haeggstrom Leukotriene B4-induced changes in vascular permeability are mediated by neutrophil release of heparin-binding protein (HBP/CAP37/azurocidin) FASEB J, June 1, 2009; 23(6): 1750 - 1757. [Abstract] [Full Text] [PDF] Y. Li, Y. Jia, M. Pichavant, F. Loison, B. Sarraj, A. Kasorn, J. You, B. E. Robson, D. T. Umetsu, J. P. Mizgerd, et al. Targeted deletion of tumor suppressor PTEN augments neutrophil function and enhances host defense in neutropenia-associated pneumonia Blood, May 14, 2009; 113(20): 4930 - 4941. [Abstract] [Full Text] [PDF] R. R. Koenen, J. Pruessmeyer, O. Soehnlein, L. Fraemohs, A. Zernecke, N. Schwarz, K. Reiss, A. Sarabi, L. Lindbom, T. M. Hackeng, et al. Regulated release and functional modulation of junctional adhesion molecule A by disintegrin metalloproteinases Blood, May 7, 2009; 113(19): 4799 - 4809. [Abstract] [Full Text] [PDF] O. Soehnlein and L. Lindbom Neutrophil-derived azurocidin alarms the immune system J. Leukoc. Biol., March 1, 2009; 85(3): 344 - 351. [Abstract] [Full Text] [PDF]

	Copyright © 2008 by American Society of Hematology         Online ISSN: 1528-0020