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Chemokine receptors on airway epithelial cells and their potential role in regulating mucin production

Chemokines, small molecular weight chemotactic cytokines, are produced mostly by airway epithelial cells and are known to play an instrumental role in the recruitment of inflammatory cells. Studies have documented a dramatic increase in the chemokine levels in the airways of asthmatics and many other studies have shown the induction of these chemokines by cytokines and growth factors in airway epithelial cells in vitro. Thus, given the high levels of chemokines in asthmatic airways and abundant evidence supporting strong interactions between cytokines and epithelial cells, we hypothesized that chemokine receptors are present on airway epithelium, and that chemokines may act through these receptors to increase mucin production. Here we demonstrate constitutive expression of chemokine receptors CCR3, CCR5 and CXCR4 in the A549 cell line by Western blot and RT-PCR. / The results of this study show that chemokine receptors are present on airway epithelial cells and that chemokines may act as a stimulus for epithelial cell mucin gene expression. Our novel finding that several CC chemokines upregulate the expression of MUC5AC mRNA might be an important mechanism regulating airway epithelial cell phenotype and function under conditions of inflammation in asthma.

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.78396
Date January 2003
CreatorsKontolemos, Mario
ContributorsHamid, Qutayba (advisor)
PublisherMcGill University
Source SetsLibrary and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada
LanguageEnglish
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation
Formatapplication/pdf
CoverageMaster of Science (Department of Pathology.)
RightsAll items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated.
Relationalephsysno: 001974793, proquestno: AAIMQ88231, Theses scanned by UMI/ProQuest.

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