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Cytokines in rat lung in response to antigen challenge

In humans, it has been demonstrated that Th-2 type cytokines (interleukin (IL)-4 and IL-5) are highly expressed in bronchial biopsies from asthmatics. Our hypothesis is that a distinct cytokine response comprising Th-2 cytokines occurs during the late airway response (LR) after antigen challenge and that a different Th-1 response (interferon (IFN)-$ gamma$) is related to the absence of a physiological response after antigen challenge. We have tested this hypothesis in different strains of rats, Brown Norway (BN) rats are high IgE producers that develop LR and increased airway responsiveness after antigen challenge, whilst Sprague Dawley (SD) rats are low IgE producers that do not develop physiological changes following antigen challenge. We assessed the expression of cytokines in these two strains of rats using semi-quantitative polymerase chain reaction (SQPCR). Fourteen days after sensitisation to ovalbumin (OA), the rats underwent general anaesthesia and were killed either immediately or eight hours after OA challenge. The lungs were frozen in liquid nitrogen for total RNA preparation. cDNA was prepared from total RNA, and mRNA expression for IL-4, IL-5 and IFN-$ gamma$ was assessed before and after challenge in BN and SD rats using Cyclophilin as a housekeeping gene. (Abstract shortened by UMI.)

Identiferoai:union.ndltd.org:LACETR/oai:collectionscanada.gc.ca:QMM.27267
Date January 1997
CreatorsAl-Assaad, Ali-Samer.
ContributorsHamid, Qutayba A. (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: 001565198, proquestno: MQ29641, Theses scanned by UMI/ProQuest.

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