Abstract
Chronic obstructive pulmonary disease (COPD) is a progressive, inflammatory lung disease that affects a large number of patients and has significant impact. One hallmark of the disease is the presence of bacteria in the lower airways. Objective: The aim of this study was to analyze the detailed structure of microbial communities found in the lungs of healthy individuals and patients with COPD. Nine COPD patients as compared and 9 healthy individuals underwent flexible bronchoscopy and BAL was performed. Bacterial nucleic acids were subjected to terminal restriction fragment (TRF) length polymorphism and clone library analysis. Overall, we identified 326 T-RFLP band, 159 in patients and 167 in healthy controls. The results of the TRF analysis correlated partly with the data obtained from clone sequencing. Although the results of the sequencing showed high diversity, the genera Prevotella, Sphingomonas, Pseudomonas, Acinetobacter, Fusobacterium, Megasphaera, Veillonella, Staphylococcus, and Streptococcus constituted the major part of the core microbiome found in both groups. A TRF band possibly representing Pseudomonas sp. monoinfection was associated with a reduction of the microbial diversity. Non-cultural methods reveal the complexity of the pulmonary microbiome in healthy individuals and in patients with COPD. Alterations of the microbiome in pulmonary diseases are correlated with disease.
Highlights
Chronic obstructive pulmonary disease (COPD) is a respiratory disease associated with chronic inflammation of the lung leading to tissue destruction and emphysema
As Terminal restriction fragment length polymorphism (T-RFLP) results based on PCR with one labeled primer cannot exactly determine the species, such correlations should be viewed with the appropriate caution
The results of the present study reveal the presence of highly diverse bacterial communities in the lungs of healthy individuals and COPD patients
Summary
Chronic obstructive pulmonary disease (COPD) is a respiratory disease associated with chronic inflammation of the lung leading to tissue destruction and emphysema. The ‘‘microbial hypothesis’’ highlights a vicious cycle, in which smoking results in impaired innate lung defense with subsequent changes in the pulmonary microbiome. This chronic colonization and infection results in further impairment of the mucociliary clearance and host defense apparatus due to aberrant mucus secretion, disrupted ciliary activity, and airway epithelial injury. Multiple pathways have been described how smoke exposure destroys lung host defense mechanisms, including the suppression of antimicrobial peptides [3], the destruction of the epithelial barrier [4], and the colonization of lower airways with tobaccoassociated microbes [5].
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