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

Mass General Brigham

Status: Completed

Conditions: Asthma; Pulmonary Disease, Chronic Obstructive

Study type: Observational

Funder types: Other; NIH

Identifiers

NCT00595114

HL090927

1421

R01HL090927 (U.S. NIH Grant/Contract)

Details and patient eligibility

About

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.

Full description

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.

Enrollment: 43 patients

Sex: All

Ages: 18+ years old

Volunteers: No Healthy Volunteers

Inclusion criteria

• No change from the MIA and LEUKO trials

Exclusion criteria

• No change from the MIA and LEUKO trials

Trial design

43 participants in 6 patient groups

MIA 1

Description:

Participants from the MIA trial who are polymerase chain reaction (PCR) negative and have received treatment with placebo

MIA 2

Description:

Participants from the MIA trial who are PCR negative and have received treatment with the antibiotic clarithromycin

MIA 3

Description:

Participants from the MIA trial who are PCR positive and have received treatment with placebo

MIA 4

Description:

Participants from the MIA trial who are PCR positive and have received treatment with the antibiotic clarithromycin

LEUKO 1

Description:

Participants from the LEUKO trial who have received treatment with placebo

LEUKO 2

Description:

Participants from the LEUKO trial who have received treatment with zileuton