Date of Award
Restricted Access Thesis
Master of Science
Graduate School of Biomedical Sciences
The mechanisms by which stress can exacerbate asthma are still unknown. The purpose of this study was to examine the immunological links between stress controllability and asthma pathogenesis. Our studies reveal specificity of stress control and immune activation resulting in hyper-inflammatory reactions in response to allergic airway challenge. We anticipate that these studies can serve as a translational piece to facilitate clinical studies of stress and asthma prevalence. The purpose of this project was to establish a murine model of stress controllability and demonstrate the impact of stress on the development of immune allergic airway hypersensitivity as a major feature of asthma. I hypothesized that given the ability to control the degree of stress would translate into less severe allergic airway hypersensitivity. We also hypothesized that distinct changes in immune responses generated in response to uncontrolled stress would reflect the extent of airway hypersensitivity. Mice were exposed to daily regimen of uncontrollable stress, controllable stress or no stress concurrently with allergen exposure. Behavioral disposition to stress was monitored in conjunction with evaluation of severity of asthma and immune status. Our results demonstrate that exerting control over stress conditions leads to distinct changes in immunological status corresponding with positive behavioral responses and less disease severity. We anticipate that our studies will facilitate application of stress management in control of immune status as a biomarker for asthma progression.
"Investigating the Role of Stress in a Murine Model of Asthma" Fort Worth, Tx: University of North Texas Health Science Center;