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Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Philippe Joubert, Stéphane Lajoie-Kadoch, Mélanie Welman, Stephane Dragon, Séverine Létuvée, Barbara Tolloczko, Andrew J. Halayko, Abdelilah Soussi Gounni, Karim Maghni and Qutayba Hamid
J Immunol January 15, 2008, 180 (2) 1268-1275; DOI: https://doi.org/10.4049/jimmunol.180.2.1268
Philippe Joubert
*Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada;
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Stéphane Lajoie-Kadoch
*Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada;
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Mélanie Welman
†Hôpital du Sacré-Coeur de Montréal, Research Center, Montréal, Québec, Canada; and
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Stephane Dragon
‡University of Manitoba, Winnipeg, Manitoba, Canada
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Séverine Létuvée
*Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada;
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Barbara Tolloczko
*Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada;
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Andrew J. Halayko
‡University of Manitoba, Winnipeg, Manitoba, Canada
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Abdelilah Soussi Gounni
‡University of Manitoba, Winnipeg, Manitoba, Canada
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Karim Maghni
†Hôpital du Sacré-Coeur de Montréal, Research Center, Montréal, Québec, Canada; and
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Qutayba Hamid
*Meakins-Christie Laboratories, McGill University, Montréal, Québec, Canada;
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Abstract

C-C chemokines such as CCL11, CCL5, and CCL3 are central mediators in the pathogenesis of asthma. They are mainly associated with the recruitment and the activation of specific inflammatory cells, such as eosinophils, lymphocytes, and neutrophils. It has recently been shown that they can also activate structural cells, such as airway smooth muscle and epithelial cells. The aims of this study were to examine the expression of the CCL3 receptor, CCR1, on human airway smooth muscle cells (ASMC) and to document the regulation of this receptor by cytokines involved in asthma pathogenesis. We first demonstrated that CCR1 mRNA is increased in the airways of asthmatic vs control subjects and showed for the first time that ASMC express CCR1 mRNA and protein, both in vitro and in vivo. Calcium mobilization by CCR1 ligands confirmed its functionality on ASMC. Stimulation of ASMC with TNF-α and, to a lesser extent, IFN-γ resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin. Taken together, our data suggest that CCR1 might be involved in the pathogenesis of asthma, through the activation of ASMC by its ligands.

  • Received December 8, 2006.
  • Accepted November 14, 2007.
  • Copyright © 2008 by The American Association of Immunologists
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The Journal of Immunology: 180 (2)
The Journal of Immunology
Vol. 180, Issue 2
15 Jan 2008
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Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma
Philippe Joubert, Stéphane Lajoie-Kadoch, Mélanie Welman, Stephane Dragon, Séverine Létuvée, Barbara Tolloczko, Andrew J. Halayko, Abdelilah Soussi Gounni, Karim Maghni, Qutayba Hamid
The Journal of Immunology January 15, 2008, 180 (2) 1268-1275; DOI: 10.4049/jimmunol.180.2.1268

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Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma
Philippe Joubert, Stéphane Lajoie-Kadoch, Mélanie Welman, Stephane Dragon, Séverine Létuvée, Barbara Tolloczko, Andrew J. Halayko, Abdelilah Soussi Gounni, Karim Maghni, Qutayba Hamid
The Journal of Immunology January 15, 2008, 180 (2) 1268-1275; DOI: 10.4049/jimmunol.180.2.1268
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