One of my New Year resolutions this year was to try to lay off the “omics” papers here on MicrobiologyBytes. Most of them are not very good and even those that are get indigestible fairly quickly. I’m making an exception for this one as it’s reasonably easy to read and highly relevant to chronic obstructive pulmonary disease (COPD), a progressive and eventually fatal lung disease that is projected to be responsible for the fifth largest burden of disease worldwide by 2020.
The results show that the lungs of “healthy” smokers contain a bacterial microbiome that is quantitatively significant, diverse (but of limited membership), and quite distinct from that reported for the oral cavity or nasopharynx. The diversity of the lung bacterial microbiome is lower in subjects with decreased lung function, most commonly associated with dominance by Pseudomonas spp. This is the first study to describe that the numerous microanatomic sites within the lung can give rise to significant differences in bacterial community structure. By demonstrating that one person’s lungs can harbor both generalized areas of “healthy” microbiome and a single site containing a “pathogenic” community, the results suggest a mechanism by which the interaction of lung pathogens and host immunity might contribute to localized disease progression, even in the absence of overt symptoms.
Even if you feel OK, stop smoking, stupid!
Analysis of the Lung Microbiome in the “Healthy” Smoker and in COPD. (2011) PLoS ONE 6(2): e16384. doi:10.1371/journal.pone.0016384
Although culture-independent techniques have shown that the lungs are not sterile, little is known about the lung microbiome in chronic obstructive pulmonary disease (COPD). We used pyrosequencing of 16S amplicons to analyze the lung microbiome in two ways: first, using bronchoalveolar lavage (BAL) to sample the distal bronchi and air-spaces; and second, by examining multiple discrete tissue sites in the lungs of six subjects removed at the time of transplantation. We performed BAL on three never-smokers (NS) with normal spirometry, seven smokers with normal spirometry (“heathy smokers”, HS), and four subjects with COPD (CS). Bacterial 16 s sequences were found in all subjects, without significant quantitative differences between groups. Both taxonomy-based and taxonomy-independent approaches disclosed heterogeneity in the bacterial communities between HS subjects that was similar to that seen in healthy NS and two mild COPD patients. The moderate and severe COPD patients had very limited community diversity, which was also noted in 28% of the healthy subjects. Both approaches revealed extensive membership overlap between the bacterial communities of the three study groups. No genera were common within a group but unique across groups. Our data suggests the existence of a core pulmonary bacterial microbiome that includes Pseudomonas, Streptococcus, Prevotella, Fusobacterium, Haemophilus, Veillonella, and Porphyromonas. Most strikingly, there were significant micro-anatomic differences in bacterial communities within the same lung of subjects with advanced COPD. These studies are further demonstration of the pulmonary microbiome and highlight global and micro-anatomic changes in these bacterial communities in severe COPD patients.