Association Between Increased Oxidative Stress, Anti-Inflammatory Fatty Acid Formation, and Airway Infection in People With Asthma and Chronic Obstructive Pulmonary Disease

• Mono-oxygenation events for C20:4, C20:5, and C22:6 as biochemical markers for enzymatic and nonenzymatic activities in asthma and COPD [ Time Frame: Measured at completion of sample analysis ] [ Designated as safety issue: No ]
  

• Impact of 5-lipoxygenase inhibition on the in vivo formation of counter-regulatory lipid mediators [ Time Frame: Measured at completion of sample analysis ] [ Designated as safety issue: No ]
  
• Kinetics for the formation of C20:4, C20:5, and C22:6 based counter-regulatory lipid mediators in COPD exacerbation and resolution [ Time Frame: Measured at completion of sample analysis ] [ Designated as safety issue: No ]
  
• Relationship between the formation of C20:4, C20:5, and C22:6 based counter-regulatory lipid mediators and airway infection in asthma [ Time Frame: Measured at completion of sample analysis ] [ Designated as safety issue: No ]
  

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) and the Antileukotriene Therapy for COPD Exacerbations (LEUKO) trials. Biological samples will undergo fatty acid mediator analysis and RNA isolation. There will be no study visits for this study.