Inflammatory Responses Induced by Cigarette Smoke in Healthy Mice and in Mice with Chronic Bronchitis Public Deposited

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Last Modified
  • March 19, 2019
Creator
  • Monk, Justine
    • Affiliation: School of Medicine, Department of Pathology and Laboratory Medicine
Abstract
  • Mice overexpressing the beta-epithelial sodium channel (betaENaC) in pulmonary epithelial cells have hyperconcentrated airway mucus and develop chronic bronchitis. These mice may serve as a model for tobacco-related COPD pathogenesis when exposed to cigarette smoke. We postulated that exposure of betaENaC mice to 1 day and 5 days of cigarette smoke activates an inflammatory response in the lungs. Following smoke exposure, bronchoalveolar lavage fluid and lung tissue were examined for evidence of inflammation. betaENaC mice demonstrated higher numbers of airspace leukocytes than wild type mice, and smoke exposure resulted in additional significant alterations. Real-time PCR revealed altered gene expression in betaENaC mice with and without smoke exposure. For several chemokines, cytokines, and matrix metalloproteinases, female betaENaC mice displayed a more pronounced response to smoke exposure compared to males. Host defense was altered in betaENaC females following smoke exposure as demonstrated by altered immune cell recruitment in response to H. influenzae.
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  • In Copyright
Advisor
  • Kesimer, Mehmet
  • Doerschuk, Claire
  • Tilley, Stephen
  • Homeister, Jonathon
Degree
  • Master of Science
Degree granting institution
  • University of North Carolina at Chapel Hill Graduate School
Graduation year
  • 2015
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  • Chapel Hill, NC
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