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dc.contributor.authorAlonso, Pedro A.en_US
dc.date.accessioned2019-09-26T14:33:25Z
dc.date.issued1994
dc.date.submitted1994
dc.identifier.otherb20377678
dc.identifier.urihttps://hdl.handle.net/2144/37997
dc.descriptionThesis (Ph.D.)--Boston Universityen_US
dc.descriptionPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.en_US
dc.description.abstractThe hamster model of experimental chronic bronchitis comprises a persistent increase in the proportion of bronchial granulated secretory cells after a single intratracheal instillation of elastase. This granulated secretory cell increase, which does not occur in the trachea, has been termed secretory cell metaplasia (SCM). Susceptibility of the bronchial epithelium may be due to a large population of elastase-responsive cells specific to this region. Three dimensional reconstruction of the major form of bronchial secretory cells revealed very little or no rough endoplasmic reticulum (RER), thus demonstrating significant regional heterogeneity since all epithelial secretory cells in the trachea have abundant RER. Animals with bronchial SCM were stimulated with pilocarpine to determine whether the cells subsequent to discharge would re-accumulate granules, thus indicating a permanent phenotypic change. However, bronchial secretory cells failed to discharge at doses equal to and greater than those claimed to be effective in rats. Elastase instilled intratracheally was immuno-localized in the hamster airways to assess the possibility of regional differences in cellular uptake of the enzyme. Elastase was not seen intracellularly in trachea or bronchus suggesting that initiation of bronchial SCM results from a cell surface effect, possibly because of elastase-specific sites on bronchial but not tracheal cells. Tracheal resistance was tested by challenging the epithelial cells in vivo and in vitro with very high doses of elastase. Light and electron microscopy revealed no evidence of a stimulation of the mucus synthetic apparatus, suggesting that tracheal epithelial cells are inherently resistant to proteolytic up-regulation.en_US
dc.language.isoen_US
dc.publisherBoston Universityen_US
dc.subjectHamsteren_US
dc.subjectGranulated secretory cellsen_US
dc.subjectIn vivoen_US
dc.subjectIn vitroen_US
dc.titleRegional differences in the response of the hamster airway epithelium to elastase: In vivo and In vitro studiesen_US
dc.typeThesis/Dissertationen_US
dc.description.embargo2031-01-01
etd.degree.nameDoctor of Philosophyen_US
etd.degree.leveldoctoralen_US
etd.degree.disciplinePathologyen_US
etd.degree.grantorBoston Universityen_US
dc.identifier.barcode11719018076283
dc.identifier.mmsid99191621710001161


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