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dc.contributor.authorLeichner, Teri Lynnen_US
dc.date.accessioned2014-03-14T20:41:35Z
dc.date.available2014-03-14T20:41:35Z
dc.date.issued2001-06-21en_US
dc.identifier.otheretd-07182001-123625en_US
dc.identifier.urihttp://hdl.handle.net/10919/34047
dc.description.abstractRecent studies suggest that lymphocyte apoptosis serves to regulate pulmonary inflammation. Equine COPD, an allergic disease of the lower airway, is likely due to dysregulation of the pulmonary immune response. In this study, the hypothesis tested was COPD affected horses would have less apoptotic airway lymphocytes than control horses during clinical disease. To achieve this, 3 methods of measuring apoptosis, Vindelov's propidium iodide with Triton-X (PI/Triton-X), 7-aminoactinomycin D (7-AAD), and Annexin V with propidium iodide (Annexin/PI) were evaluated in equine airway lymphocytes. A significant linear relationship was found for equine bronchoalveolar lavage (BAL) lymphocytes stained with 7-AAD and Annexin/PI . No relationship was identified with cells stained with PI/Triton-X and Annexin/PI, and 7-AAD and PI/Triton-X indicating that methods which preserve cell membrane characteristics are more comparable when measuring BAL lymphocytes apoptosis in a heterogeneous population of cells. Additionally, all stains appear to perform the same in COPD and normal horses in remission and disease. Comparison of predominately BAL lymphocyte apoptosis using the above methods were performed at baseline, after natural challenge, and after dexamethasone administration in nine horses, five of which were affected with COPD. No differences in bronchoalveolar lavage lymphocyte apoptosis between COPD and control horses were detected either before or after dexamethasone administration, although numerical trends in COPD horses identified less apoptosis after natural challenge indicating that defective apoptosis may play a role in equine COPD pathogenesis. Dexamethasone administration was associated with trends of improvement in the pulmonary gas exchange and increased apoptosis toward baseline in the COPD horses.en_US
dc.publisherVirginia Techen_US
dc.relation.haspartLeichnerthesis.pdfen_US
dc.rightsI hereby certify that, if appropriate, I have obtained and attached hereto a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to Virginia Tech or its agents the non-exclusive license to archive and make accessible, under the conditions specified below, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report.en_US
dc.subjectlymphocytesen_US
dc.subject7-AADen_US
dc.subjectpropidium iodideen_US
dc.subjectAnnexin-Ven_US
dc.titleAdaptation of Three Different Apoptotic Methods in Equine Bronchoalveolar Cells and Comparison of Bronchoalveolar Lavage Cell Apoptosis in Normal and COPD Affected Horses Before and After Dexamethasone Administrationen_US
dc.typeThesisen_US
dc.contributor.departmentVeterinary Medical Sciencesen_US
thesis.degree.nameMaster of Scienceen_US
thesis.degree.levelmastersen_US
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen_US
dc.contributor.committeechairBuechner-Maxwell, Virginia A.en_US
dc.contributor.committeememberAhmed, S. Ansaren_US
dc.contributor.committeememberGogal, Robert M. Jr.en_US
dc.contributor.committeememberCrisman, Mark Virgilen_US
dc.contributor.committeememberElvinger, Francois C.en_US
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-07182001-123625/en_US
dc.date.sdate2001-07-18en_US
dc.date.rdate2002-07-25
dc.date.adate2001-07-25en_US


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