Innate Immunity in Ozone-induced Airway Inflammation in COPD
Last updated on July 2021Recruitment
- Recruitment Status
- Recruiting
- Estimated Enrollment
- Same as current
Summary
- Conditions
- Airway Disease
- COPD Exacerbation
- Pollution Related Respiratory Disorder
- Pollution Exposure
- Pulmonary Disease, Chronic Obstructive
- Type
- Interventional
- Phase
- Not Applicable
- Design
- Allocation: N/AIntervention Model: Single Group AssignmentIntervention Model Description: Controlled inhalational challenge to ozoneMasking: None (Open Label)Primary Purpose: Other
Participation Requirements
- Age
- Between 45 years and 75 years
- Gender
- Both males and females
Description
A major cause of morbidity and mortality in COPD is exacerbation. The mechanisms underlying COPD exacerbation are poorly understood, but airway innate immune system has been implicated in its development. Air pollution contributes to development of COPD exacerbation, and exposure to ozone, a major c...
A major cause of morbidity and mortality in COPD is exacerbation. The mechanisms underlying COPD exacerbation are poorly understood, but airway innate immune system has been implicated in its development. Air pollution contributes to development of COPD exacerbation, and exposure to ozone, a major component of air pollution, is associated with increased healthcare utilization among patients with COPD. Inhalation of ambient levels of ozone is known to affect airway innate immune system. This proposal sets out to characterize and investigate the role of innate immune system and in particular airway macrophages in ozone-induced COPD exacerbation through establishing an experimental model that employs controlled ozone exposure and longitudinal sampling via bronchoscopy. The research plan proposes to examine human immune cells trafficking in airways during the process of ozone-induced airway injury and inflammation in patients with COPD. The investigator's overall hypothesis is that inhalational challenge to a high ambient level of ozone in patients with COPD provides a safe human model of airway injury with resulting intraluminal shifts in the population and polarization of macrophages to study innate immunity processes relevant to ozone-induced COPD exacerbation.
Tracking Information
- NCT #
- NCT04669743
- Collaborators
- Not Provided
- Investigators
- Principal Investigator: Mehrdad Arjomandi, M.D. University of California, San Francisco