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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 (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 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 Social Bookmarking                   What's this? Submitted March 1, 2002 Accepted June 18, 2002 Allergen-induced accumulation of airway dendritic cells is supported by an increase in CD31hiLy-6Cnegbone marrow precursors in a mouse model of asthma Leonie S van Rijt*, Jan-Bas Prins, Pieter J Leenen, Kris Thielemans, Victor C de Vries, Henk C Hoogsteden, and Bart N Lambrecht Pulmonary and Critical Care Medicine, Erasmus MC, Rotterdam, The Netherlands Immunology, Erasmus MC, Rotterdam, The Netherlands Physiology, Free University Brussels, Brussels, Belgium * Corresponding author; email: rijt{at}longz.fgg.eur.nl. Airway dendritic cells (DCs) are held responsible for inducing sensitization to inhaled Ag leading to eosinophilic airway inflammation, typical of asthma. Less information is however available about the role of these cells in ongoing inflammation. In a mouse model of asthma, sensitization to 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 CD31hi Ly-6Cneg hematopoietic precursor cells in the BM. There was no change in any of the other 5 populations revealed by CD31/Ly-6C staining. When these CD31hi Ly-6Cneg BM precursors were sorted and grown in GM-CSF they differentiated into MHCII+ CD11c+ DC. The same CD31hi Ly-6Cneg precursors also expressed the eotaxin receptor CCR3 and differentiated into eosinophils when grown in IL-5. Serum levels of eotaxin were doubled in mice with inflammation. These findings in an animal model of asthma suggest that the bone marrow increases its output of myeloid precursors to meet the enhanced demand for DCs and eosinophils in inflamed airways. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. J. Osterholzer, J. E. Milam, G.-H. Chen, G. B. Toews, G. B. Huffnagle, and M. A. Olszewski Role of Dendritic Cells and Alveolar Macrophages in Regulating Early Host Defense against Pulmonary Infection with Cryptococcus neoformans Infect. Immun., September 1, 2009; 77(9): 3749 - 3758. [Abstract] [Full Text] [PDF] L. J. Robays, E. A. Lanckacker, K. B. Moerloose, T. Maes, K. R. Bracke, G. G. Brusselle, G. F. Joos, and K. Y. Vermaelen Concomitant Inhalation of Cigarette Smoke and Aerosolized Protein Activates Airway Dendritic Cells and Induces Allergic Airway Inflammation in a TLR-Independent Way J. Immunol., August 15, 2009; 183(4): 2758 - 2766. 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