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Blood, 15 October 2004, Vol. 104, No. 8, pp. 2543-2548. Prepublished online as a Blood First Edition Paper on June 22, 2004; DOI 10.1182/blood-2004-01-0361. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-01-0361v1 104/8/2543    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 Gasser, O. Articles by Schifferli, J. A. Search for Related Content PubMed PubMed Citation Articles by Gasser, O. Articles by Schifferli, J. A. Related Collections Phagocytes Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PHAGOCYTES Activated polymorphonuclear neutrophils disseminate anti-inflammatory microparticles by ectocytosis Olivier Gasser, and Jürg A. Schifferli From the Department of Research and the Department of Medicine, University Hospital Basel, Basel, Switzerland. On activation, human neutrophils release microparticles, called ectosomes, directly from the cell surface membrane. Microparticles from platelets, endothelial cells, and monocytes were reported to support coagulation or to modulate vascular homeostasis by activating monocytes as well as endothelial cells. We find that neutrophil ectosomes have no proinflammatory activity on human macrophages as assessed by the release of interleukin 8 (IL-8) and tumor necrosis factor (TNF). On the contrary, ectosomes increase the release of transforming growth factor 1 (TGF1), suggesting that ectosomes down-modulate cellular activation in macrophages. Polymorphonuclear neutrophil (PMN) ectosomes are able to block inflammatory response of macrophages to zymosan and lipopolysaccharide (LPS). We show that an early-phase TGF1 secretion and the exposure of phosphatidylserine on the surface of ectosomes independently contribute to this effect. Ectosome-cell contact was sufficient for their immunomodulatory function as shown by blocking phagocytosis with cytochalasin D. Thus, neutrophils release potent anti-inflammatory effectors, in the form of ectosomes, at the earliest stage of inflammation, already providing a drive to its resolution. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: O. Morel, F. Toti, N. Morel, and J.-M. 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