Abstract
BackgroundThe role of commensal viruses in humans is poorly understood, and the impact of the virome on lung health and smoking-related disease is particularly understudied.MethodsGenetic material from acellular bronchoalveolar lavage fluid was sequenced to identify and quantify viral members of the lower respiratory tract which were compared against concurrent bronchoalveolar lavage bacterial, metabolite, cytokine and cellular profiles, and clinical data. Twenty smoker and 10 nonsmoker participants with no significant comorbidities were studied.ResultsViruses that infect bacteria (phages) represented the vast majority of viruses in the lung. Though bacterial communities were statistically indistinguishable across smokers and nonsmokers as observed in previous studies, lung viromes and metabolic profiles were significantly different between groups. Statistical analyses revealed that changes in viral communities correlate most with changes in levels of arachidonic acid and IL-8, both potentially relevant for chronic obstructive pulmonary disease (COPD) pathogenesis based on prior studies.ConclusionsOur assessment of human lung DNA viral communities reveals that commensal viruses are present in the lower respiratory tract and differ between smokers and nonsmokers. The associations between viral populations and local immune and metabolic tone suggest a significant role for virome-host interaction in smoking related lung disease.
Highlights
The role of commensal viruses in humans is poorly understood, and the impact of the virome on lung health and smoking-related disease is understudied
No significant differences in Interleukin 8 (IL-8) or arachidonic acid levels were observed between current and former smokers (MannWhitney U-test, IL-8 p = 0.48, arachidonic acid p = 0.13). In this first study of the effects of smoking on the lung Deoxyribonucleic acid (DNA) virome, we found that, in contrast to the lung bacteriome, smoking was associated with significant changes in the lung virome and metabolome
In summary, our findings provide a foundational glimpse into the ecological interplay between viruses, bacteria, metabolites, and immune cells that likely impact the lung microenvironment and perhaps, progression from smoking to chronic obstructive pulmonary disease (COPD)
Summary
The role of commensal viruses in humans is poorly understood, and the impact of the virome on lung health and smoking-related disease is understudied. Smoking is the leading cause of chronic obstructive pulmonary disease (COPD) and the third highest cause of death globally [1, 2]. Despite the clear associated risk, only a fraction of smokers eventually develop COPD [2, 3]. Not others, to develop COPD remains unknown and an area of active research [2,3,4,5]. Recent work examining the lung bacteriome of individuals with moderate to severe COPD revealed decreased bacterial diversity compared to nonsmokers [6,7,8,9,10,11]. It has been proposed that changes in lung-resident bacterial communities may lead to COPD [4,5,6,7,8].
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