Airway eosinophilia is a prominent feature of asthma that may be mediated in part through the expression of eotaxin, a potent eosinophil-active chemokine that is highly expressed by epithelial cells and inflammatory cells in asthmatic airways. / The major aim of this study was to determine whether human airway smooth muscle (ASM) cells may be a source of eotaxin in asthma. The evidence presented in this thesis shows constitutive eotaxin gene expression in ASM in vitro that is markedly increased following stimulation with the proinflammatory cytokines TNF-alpha and IL-1beta. Release of eotaxin was confirmed in ASM culture supernatants which contained significant chemoattractant activity for eosinophils that was partly inhibited with antibodies directed against eotaxin or RANTES, and maximally inhibited by a combined blockade of both chemokines. Strong signals for eotaxin immunoreactivity were also observed in vivo in smooth muscle in asthmatic airways. / In conclusion, the results of this study suggest that ASM may contribute to airway inflammation in asthma through the production and release of eotaxin.
Identifer | oai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.20956 |
Date | January 1998 |
Creators | Ghaffar, Omar. |
Contributors | Hamid, Qutayba (advisor) |
Publisher | McGill University |
Source Sets | Library and Archives Canada ETDs Repository / Centre d'archives des thèses électroniques de Bibliothèque et Archives Canada |
Language | English |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
Format | application/pdf |
Coverage | Master of Science (Department of Pathology.) |
Rights | All items in eScholarship@McGill are protected by copyright with all rights reserved unless otherwise indicated. |
Relation | alephsysno: 001630779, proquestno: MQ50776, Theses scanned by UMI/ProQuest. |
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