title: Alterations in airway microbiota in patients with PaO2/FiO2 ratio ≤ 300 after burn and inhalation injury.
abstract: BACKGROUND
  Injury to the airways after smoke inhalation is a major mortality risk factor in victims of burn injuries, resulting in a 15-45% increase in patient deaths. Damage to the airways by smoke may induce acute respiratory distress syndrome (ARDS), which is partly characterized by hypoxemia in the airways. While ARDS has been associated with bacterial infection, the impact of hypoxemia on airway microbiota is unknown. Our objective was to identify differences in microbiota within the airways of burn patients who develop hypoxemia early after inhalation injury and those that do not using next-generation sequencing of bacterial 16S rRNA genes.
  
  
  RESULTS
  DNA was extracted from therapeutic bronchial washings of 48 patients performed within 72 hours of hospitalization for burn and inhalation injury at the North Carolina Jaycee Burn Center. DNA was prepared for sequencing using a novel molecule tagging method and sequenced on the Illumina MiSeq platform. Bacterial species were identified using the MTToolbox pipeline. Patients with hypoxemia, as indicated by a PaO2/FiO2 ratio ≤ 300, had a 30% increase in abundance of Streptococcaceae and Enterobacteriaceae and 84% increase in Staphylococcaceae as compared to patients with a PaO2/FiO2 ratio > 300. Wilcoxon rank-sum test identified significant enrichment in abundance of OTUs identified as Prevotella melaninogenica (p = 0.042), Corynebacterium (p = 0.037) and Mogibacterium (p = 0.048). Linear discriminant effect size analysis (LefSe) confirmed significant enrichment of Prevotella melaninognica among patients with a PaO2/FiO2 ratio ≤ 300 (p<0.05). These results could not be explained by differences in antibiotic treatment.
  
  
  CONCLUSIONS
  The airway microbiota following burn and inhalation injury is altered in patients with a PaO2/FiO2 ratio ≤ 300 early after injury. Enrichment of specific taxa in patients with a PaO2/FiO2 ratio ≤ 300 may indicate airway environment and patient changes that favor these microbes. Longitudinal studies are necessary to identify stably colonizing taxa that play roles in hypoxemia and ARDS pathogenesis.
authors.affiliation: Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, United States of America.
authors.forename: Dana M
authors.identifier: http://orcid.org/0000-0002-8919-0079
authors.initials: DM
authors.lastname: Walsh
authors.affiliation: National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, North Carolina, United States of America.
authors.forename: Shaun D
authors.initials: SD
authors.lastname: McCullough
authors.affiliation: Department of Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Program in Bioinformatics and Computational Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.
authors.forename: Scott
authors.initials: S
authors.lastname: Yourstone
authors.affiliation: Department of Surgery, University of North Carolina, Chapel Hill, North Carolina, United States of America.|North Carolina Jaycee Burn Center, University of North Carolina, Chapel Hill, North Carolina, United States of America.
authors.forename: Samuel W
authors.initials: SW
authors.lastname: Jones
authors.affiliation: Department of Surgery, University of North Carolina, Chapel Hill, North Carolina, United States of America.|North Carolina Jaycee Burn Center, University of North Carolina, Chapel Hill, North Carolina, United States of America.
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Cairns
authors.affiliation: Department of Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Program in Bioinformatics and Computational Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Curriculum in Genetics and Molecular Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, North Carolina, United States of America.
authors.forename: Corbin D
authors.initials: CD
authors.lastname: Jones
authors.affiliation: Curriculum in Toxicology, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Department of Pediatrics, University of North Carolina, Chapel Hill, North Carolina, United States of America.|Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina, Chapel Hill, North Carolina, United States of America.
authors.forename: Ilona
authors.initials: I
authors.lastname: Jaspers
authors.affiliation: National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, North Carolina, United States of America.
authors.forename: David
authors.initials: D
authors.lastname: Diaz-Sanchez
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002059:Burns, Inhalation / Q000235:genetics / Q000382:microbiology; D002648:Child; D002675:Child, Preschool; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000235:genetics* / Q000382:microbiology / Q000473:pathology; D007223:Infant; D008137:Longitudinal Studies; D008297:Male; D064307:Microbiota / Q000235:genetics*; D008875:Middle Aged; D009657:North Carolina; D011446:Prospective Studies; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D012128:Respiratory Distress Syndrome / Q000209:etiology / Q000235:genetics* / Q000382:microbiology; D012137:Respiratory System / Q000382:microbiology / Q000473:pathology; D012307:Risk Factors; D015208:Smoke Inhalation Injury / Q000235:genetics* / Q000382:microbiology / Q000473:pathology
chemical_list: D012336:RNA, Ribosomal, 16S