Pulmonary Disease, Chronic Obstructive Clinical Trial
Official title:
Bronchial Infection in Patients With COPD and Frequent Exacerbations; Role of Innate Immunity and the Use of an Electronic Nose for Diagnosis.
Hypothesis:
1. Innate immunity is altered in certain patients with COPD and frequent exacerbations, a
fact that makes them more susceptible to being infected by bacteria.
2. The electronic nose is able to detect patterns of specific VOCs for exacerbations of
infectious origin.
Bronchial infection has been described as the leading cause of COPD exacerbations. Different
studies with invasive endoscopic techniques have demonstrated the presence of bacteria in the
air in 40-70% of exacerbations of the disease. In addition, these patients have a higher
concentration of cells and proinflammatory cytokines in the airway. This increased
inflammation is associated with more frequent and more severe exacerbations, which worsen
this vicious circle.
It is not known why some patients with COPD are more susceptible than others to bronchial,
acute or chronic infection. Recent studies have suggested the importance of lung innate
immunity, both humoral (proteins with antibiotic activity, inflammatory mediators) and cell
(neutrophils, macrophages) as the key to the defense of the lung against infectious agents
external factor. There may be a bidirectional relationship between immune response and
bronchial infection in COPD exacerbations.
Te main objectives of our study are: 1. To study the expression of mucin, PAM and TLR in the
airway of patients with COPD and frequent exacerbations (FE) and its relationship with the
infection of the airway. 2. Determine the patterns of volatile organic compounds (VOCs)
detected by electronic nose associated with bronchial infection in patients with COPD and FE.
Secondary objectives: 1. To study the relationship between the expression of mucin, PAM and
TLR with pulmonary and systemic inflammation. 2. To study the relationship between the
expression of mucin, PAM and TLR with bronchial bacterial load. 3. To study the expression of
mucin, PAM and TLR at the time of COPD exacerbations and subsequent clinical phase stability.
4. Determine VOC patterns for specific pathogens (H. influenzae, S. pneumoniae, P.
aeurginosa). 5. To study the time evolution of patterns of VOCs after a COPD exacerbation.
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