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Nat Microbiol. 2016 Apr 4;1:16031. doi: 10.1038/nmicrobiol.2016.31.

Enrichment of the lung microbiome with oral taxa is associated with lung inflammation of a Th17 phenotype.

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Division of Pulmonary, Critical Care and Sleep Medicine, New York University School of Medicine, New York, USA.
Department of Medicine, New York University School of Medicine, New York, New York, USA.
Department of Genetics and Genomic Sciences, Icahn School of Medicine at Mount Sinai, New York, USA.
Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, USA.
Department of Pathology, New York University School of Medicine, New York, New York, USA.
Division of Pulmonary and Critical Care Medicine, The Ohio State University, Columbus, Ohio, USA.
Department of Biology, Center for Genomics &Systems Biology, College of Global Public Health, New York University, New York, New York, USA.
Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh, Pennsylvania, USA.
Department of Medicine, University of California San Francisco, San Francisco, California, USA.
Department of Molecular and Cellular Biology &Genome Center, University of California, Davis, California, USA.
Center for Public Health Research, FISABIO, Valencia, Spain.
Department of Medicine and Microbiology, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA.


Microaspiration is a common phenomenon in healthy subjects, but its frequency is increased in chronic inflammatory airway diseases, and its role in inflammatory and immune phenotypes is unclear. We have previously demonstrated that acellular bronchoalveolar lavage samples from half of the healthy people examined are enriched with oral taxa (here called pneumotypeSPT) and this finding is associated with increased numbers of lymphocytes and neutrophils in bronchoalveolar lavage. Here, we have characterized the inflammatory phenotype using a multi-omic approach. By evaluating both upper airway and acellular bronchoalveolar lavage samples from 49 subjects from three cohorts without known pulmonary disease, we observed that pneumotypeSPT was associated with a distinct metabolic profile, enhanced expression of inflammatory cytokines, a pro-inflammatory phenotype characterized by elevated Th-17 lymphocytes and, conversely, a blunted alveolar macrophage TLR4 response. The cellular immune responses observed in the lower airways of humans with pneumotypeSPT indicate a role for the aspiration-derived microbiota in regulating the basal inflammatory status at the pulmonary mucosal surface.

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