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Prepublished online as a Blood First Edition Paper on July 12, 2002; DOI 10.1182/blood-2002-03-0673. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-03-0673v1 100/10/3663    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 van Rijt, L. S. Articles by Lambrecht, B. N. Search for Related Content PubMed PubMed Citation Articles by van Rijt, L. S. Articles by Lambrecht, B. N. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 November 2002, Vol. 100, No. 10, pp. 3663-3671 IMMUNOBIOLOGY Allergen-induced accumulation of airway dendritic cells is supported by an increase in CD31hiLy-6Cneg bone marrow precursors in a mouse model of asthma Leonie S. van Rijt, Jan-Bas Prins, Pieter J. M. Leenen, Kris Thielemans, Victor C. de Vries, Henk C. Hoogsteden, and Bart N. Lambrecht From the Department of Pulmonary and Critical Care Medicine and the Department of Immunology, Erasmus University Medical Center, Rotterdam, The Netherlands, and the Department of Physiology, Free University Brussels, Belgium. Airway dendritic cells (DCs) are held responsible for inducing sensitization to inhaled antigen, leading to eosinophilic airway inflammation, typical of asthma. However, less information is available about the role of these cells in ongoing inflammation. In a mouse model of asthma, sensitization to ovalbumin (OVA) was induced by intratracheal injection of myeloid OVA-pulsed DCs. Upon OVA aerosol challenge and induction of eosinophilic airway inflammation in sensitized mice, there was a time-dependent and almost 100-fold increase in the number of MHCII+ CD11b+ CD11c+ endogenous airway DCs as well as CD11b+ blood DCs. The mechanism of this increase was studied. Adoptive transfer experiments demonstrated that accumulation of airway DCs was not due to reduced migration to the mediastinal lymph nodes. Rather, the massive increase in airway and lymph node DCs was supported by an almost 3-fold expansion of myeloid CD31hiLy-6Cneg hematopoietic precursor cells in the bone marrow (BM). There was no change in any of the other 5 populations revealed by CD31/Ly-6C staining. When these CD31hiLy-6Cneg BM precursors were sorted and grown in granulocyte macrophage-colony-stimulating factor, they differentiated into MHCII+ CD11c+ DCs. The same CD31hiLy-6Cneg precursors also expressed the eotaxin receptor CCR3 and differentiated into eosinophils when grown in interleukin 5. Serum levels of eotaxin were doubled in mice with inflammation. These findings in an animal model of asthma suggest that the BM increases its output of myeloid precursors to meet the enhanced demand for DCs and eosinophils in inflamed airways. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Miyahara, H. Ohnishi, H. Matsuda, S. Miyahara, K. Takeda, T. Koya, S. Matsubara, M. Okamoto, A. Dakhama, B. Haribabu, et al. Leukotriene B4 Receptor 1 Expression on Dendritic Cells Is Required for the Development of Th2 Responses and Allergen-Induced Airway Hyperresponsiveness J. Immunol., July 15, 2008; 181(2): 1170 - 1178. [Abstract] [Full Text] [PDF] C. H. GeurtsvanKessel, M. A.M. Willart, L. S. van Rijt, F. Muskens, M. 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	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020