Effects of Smoking on Bronchial Epithelium
NCT00849433 · Status: COMPLETED · Type: OBSERVATIONAL · Enrollment: 60
Last updated 2015-01-16
Summary
Asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory airway diseases affecting millions of people worldwide. Inhaled corticosteroids (ICS) are by far the most effective treatment with a broad anti-inflammatory spectrum. Nevertheless, most COPD patients and a proportion of severe asthma patients are corticosteroid-resistant (CR) and to fail to respond to ICS even when higher doses are given. These corticosteroid-resistant patients suffer from persistent symptoms and repeated asthma exacerbations. It has been suggested that smoking and oxidative stress may induce corticosteroid-resistance. The reactive oxygen species (ROS) responsible for oxidative stress can be generated exogenously (air pollutants, cigarette smoke) and endogenously by metabolic reactions. After inhaling air pollutants or cigarette smoke, the bronchial epithelium is exposed. Preliminary data from our own lab suggest that smoking and oxidative stress may decrease epithelial cell-cell contact formation. This results not only in a decreased barrier function, but also in an increased production of pro-inflammatory mediators.
Conditions
Sponsors & Collaborators
-
University Medical Center Groningen
lead OTHER
Principal Investigators
-
Maarten van den Berge, MD, PhD · University Medical Center Groningen
-
Dirkje S Postma, Professor · University Medical Center Groningen
Eligibility
- Min Age
- 18 Years
- Max Age
- 75 Years
- Sex
- ALL
- Healthy Volunteers
- No
Timeline & Regulatory
- Start
- 2009-04-30
- Primary Completion
- 2012-04-30
- Completion
- 2013-04-30
Countries
- Netherlands
Study Locations
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