Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease
Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease
Chronic obstructive pulmonary disease (COPD) and asthma are common respiratory diseases in
 which people experience long-term inflammation of the lungs. Exacerbations, or prolonged
 worsening of symptoms, of asthma and COPD are often life-threatening and can lead to frequent
 need for hospitalization. Even with the proper use of bronchodilators, corticosteroids, and
 other currently available medications, clinical responses among people with COPD and asthma
 are variable. There remains a significant unmet clinical need for new therapeutic approaches
 and insights, including the identification of biomarkers to accurately assess the presence of
 airway infection and intensity of airway inflammation. This study will investigate potential
 natural biological causes and new biomarkers for increased susceptibility to persistent
 airway infection in asthma and COPD.
COPD and asthma are chronic lung diseases that result in impaired air flow in the lungs,
 often causing coughing, wheezing, and shortness of breath. In uncontrolled COPD and asthma,
 people may experience a rapid worsening of symptoms, which may include fever, difficulty
 breathing, and chest pain. These exacerbations are the most serious expression of asthma and
 COPD and are usually caused by lung infections or air allergens. However, the biological
 basis for susceptibility to airway infection and inflammation is not well understood.
 Increased oxidative stress within the airways has been linked to several airway diseases.
 This increase in oxidative stress may reduce production of key fatty acid anti-inflammatory
 mediators. In turn, this may disrupt the airway's natural immune response mechanisms, making
 the airways more vulnerable to infection or inflammation during COPD and asthma
 exacerbations. This ancillary study will determine whether susceptibility to persistent
 airway infection in asthma and COPD stems from increased oxidative stress that impairs the
 natural formation of protective fatty acid mediators.

 This ancillary study will use data biological samples, including blood and sputum, from
 participants currently enrolled in the Macrolides in Asthma (MIA; NCT00318708) and the
 Antileukotriene Therapy for COPD Exacerbations (KIA; NCT01097694). Biological samples will
 undergo fatty acid mediator analysis and RNA isolation. There will be no study visits for
 this study.
Inclusion Criteria:

 -  No change from the MIA and LEUKO trials

 Exclusion Criteria:

 -  No change from the MIA and LEUKO trials