Editors' ChoiceMicrobiome

Distressing microbial consequences of smoking

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Science Translational Medicine  14 Mar 2018:
Vol. 10, Issue 432, eaat1639
DOI: 10.1126/scitranslmed.aat1639


Changes in lung microbiota associated with smoking might contribute to the development of acute respiratory distress syndrome in subjects with blunt trauma.

Smoking is harmful to the lungs in many different ways. Despite considerable knowledge about the effects of smoking, there are multiple associations between smoking and pulmonary injury with unknown mechanisms. An example of this is the increased susceptibility of smokers to develop acute respiratory distress syndrome (ARDS) in subjects with trauma. We know that smoking affects lung epithelial permeability, endothelial injury, and lung inflammation, all of which may be contributing factors for ARDS. For the most part, the bacteria present in the lungs have been neglected as a contributor to the pathogenesis in this condition. In a recent study by Panzer et al., the lung microbiome was longitudinally characterized using culture-independent techniques in 74 subjects with severe blunt trauma. Subjects were categorized based on their smoking status, and endotracheal aspirates were obtained at baseline and after 48 hours of being intubated in the intensive care unit. In these subjects, enrichment with Haemophilus, Streptococcus, Prevotella, Porphyromonas, and Campylobacter was associated with smoking. Further, expansion of some of these taxa, as well as some gut-associated taxa (such as Enterobacteriaceae), was associated with development of ARDS. These data broaden the current model of trauma-associated ARDS by suggesting that microbes present in the lower airways might influence the susceptibility to ARDS. The lung microbiota signatures associated with ARDS coincided with several inflammatory markers such VEGF, RAGE, ANG-2, PENT3, and interleukin-8, suggesting potential pathways by which microbes trigger lower airway inflammation. We are still at the infancy of uncovering microbial host interactions in the lungs. The use of culture-independent approaches is changing our view of what was previously thought as a sterile lower airway mucosa. The model for inflammatory processes affecting the lower airways, such as ARDS, is now shifting to a multidimensional system where microbes and microbial products interact with the host through different, and probably noncanonical pathways. Dissecting these mechanisms is not going to be easy. More and larger longitudinal studies are needed, as well as preclinical animal models to conduct the necessary mechanistic investigations that hopefully will yield novel therapeutic targets.

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