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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 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 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 CrossRef Google Scholar Articles by Soehnlein, O. Articles by Lindbom, L. PubMed PubMed Citation Articles by Soehnlein, O. Articles by Lindbom, L. Related Collections Phagocytes Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PHAGOCYTES Neutrophil secretion products pave the way for inflammatory monocytes Oliver Soehnlein1, Alma Zernecke2, Einar E. Eriksson1, Antonio Gigliotti Rothfuchs3, Christine T. Pham4, Heiko Herwald5, Kiril Bidzhekov2, Martin E. Rottenberg6, Christian Weber2, and Lennart Lindbom1 1 Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden; 2 Institute for Molecular Cardiovascular Research (IMCAR), RWTH Aachen University, Aachen, Germany; 3 Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD; 4 Department of Medicine, Washington University, St Louis, MO; 5 Department of Clinical Sciences, Lund University, Lund, Sweden; and 6 Microbiology and Tumor Biology Center, Karolinska Institute, Stockholm, Sweden 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, 2 populations of monocytes have been identified, Gr1–CCR2–CX3CR1hi resident monocytes and Gr1+CCR2+CX3CR1lo inflammatory monocytes. Here, intravital microscopy of the musculus 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 with 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?

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