Thesis Defense Announcement
To:  The George Mason University Community

Candidate: Heather Branscome

Program: M.S. in Biology
Date:   Thursday November 30, 2017
Time:   2:00 PM
Place:  Bull Run Hall, Room 249
             George Mason University
Science & Tech Campus

Title: “Inflammatory Profiles of Asthma and COPD Primary Human Bronchial Epithelial Cells in Response to LPS and an Inflammatory Inhibitor”
Thesis Director: Dr. Steven Arold
Committee Chair:
Dr. Ancha Baranova
Committee Members:
 Dr. Fatah Kashanchi, Dr. Aarthi Narayanan

This is a public defense and all are invited to attend.
Chronic obstructive pulmonary disease (COPD) and asthma are two of the most common inflammatory diseases of the respiratory system. Collectively, they affect hundreds of millions of individuals worldwide and are associated with high levels of mortality.  Treatment options are currently limited to the use of long-acting bronchodilators and glucocorticoid steroids, which act only to reduce symptoms rather than to reverse disease progression. While airway inflammation is a hallmark feature of asthma and COPD, there are inherent differences in the types of cells and molecular mechanisms involved.  Previous research has highlighted the importance of the innate immune system in orchestrating the inflammatory response and unique inflammatory patterns have been identified for each of these diseases.  The current thesis examines the inflammatory profiles of ATCC human primary bronchial epithelial cells (HBECs) obtained from a variety of normal and diseased donors.  We have demonstrated by ELISA that these cell types can be activated by an exogenous stimulus (LPS) to produce increased levels of IL-8 cytokine when grown in two-dimensional culture.  The relative gene expression of other critical pro-inflammatory cytokines such as IL-6 and TNF-α was also examined and found to be dysregulated after exposure to LPS.   Taken together, these factors may contribute to disease pathogenesis. Lastly, the anti-inflammatory actions of a glucocorticoid steroid, budesonide, was evaluated in LPS-challenged HBECs.  Budesonide was effective in reducing IL-8 cytokine levels in five out of the six cell types tested.  Ongoing research will focus on expanding these studies in three-dimensional cultures to better recreate the conditions in vivo.