Katherine B Frayman1, Kristine M Wylie2, David S Armstrong3, Rosemary Carzino4, Stephanie D Davis5, Thomas W Ferkol6, Keith Grimwood7, Gregory A Storch8, Sarath C Ranganathan9. 1. Department of Respiratory and Sleep Medicine, Royal Children's Hospital, Victoria, Australia; Respiratory Diseases Group, Murdoch Childrens Research Institute, Victoria, Australia; Department of Paediatrics, University of Melbourne, Victoria, Australia; Allergy, Immunology and Cystic Fibrosis, Alfred Health, Victoria, Australia; Department of Respiratory Medicine, Monash Children's Hospital, Victoria, Australia. Electronic address: katherine.frayman@rch.org.au. 2. Department of Pediatrics, Washington University, St Louis, MO, United States; McDonnell Genome Institute, Washington University, St. Louis, MO, United States. 3. Department of Respiratory Medicine, Monash Children's Hospital, Victoria, Australia; Department of Paediatrics, Monash University, Victoria, Australia. 4. Department of Respiratory and Sleep Medicine, Royal Children's Hospital, Victoria, Australia; Respiratory Diseases Group, Murdoch Childrens Research Institute, Victoria, Australia. 5. Department of Pediatrics, The University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, NC, United States. 6. Department of Pediatrics, Washington University, St Louis, MO, United States; Department of Cell Biology and Physiology, Washington University, St Louis, MO, United States. 7. Menzies Health Institute Queensland, Griffith University and Gold Coast Health, Gold Coast, Queensland, Australia. 8. Department of Pediatrics, Washington University, St Louis, MO, United States. 9. Department of Respiratory and Sleep Medicine, Royal Children's Hospital, Victoria, Australia; Respiratory Diseases Group, Murdoch Childrens Research Institute, Victoria, Australia; Department of Paediatrics, University of Melbourne, Victoria, Australia.
Abstract
BACKGROUND: Cystic fibrosis (CF) lung disease commences in infancy, and understanding the role of the microbiota in disease pathogenesis is critical. This study examined and compared the lower airway microbiota of infants with and without CF and its relationship to airway inflammation in the first months of life. METHODS: Infants newly-diagnosed with CF were recruited into a single-centre study in Melbourne, Australia from 1992 to 2001. Bronchoalveolar lavage was performed at study entry. Healthy infants undergoing bronchoscopy to investigate chronic stridor acted as controls. Quantitative microbiological culture was performed and inflammatory markers were measured contemporaneously. 16S ribosomal RNA gene analysis was performed on stored samples. RESULTS: Thirteen bronchoalveolar samples from infants with CF and nine from control infants, collected at median ages of 1.8-months (25th-75th percentile 1.5 to 3.1-months) and 5-months (25th-75th percentile 2.9 to 8.2-months) respectively, provided 16S rRNA gene data. Bacterial biomass was positively associated with inflammation. Alpha diversity was reduced in infants with CF and between-group compositional differences were apparent. These differences were driven by increased Staphylococcus and decreased Fusobacterium and were most apparent in symptomatic infants with CF. CONCLUSION: In CF lung disease, differences in lower airway microbial community composition and structure are established by age 6-months.
BACKGROUND:Cystic fibrosis (CF) lung disease commences in infancy, and understanding the role of the microbiota in disease pathogenesis is critical. This study examined and compared the lower airway microbiota of infants with and without CF and its relationship to airway inflammation in the first months of life. METHODS:Infants newly-diagnosed with CF were recruited into a single-centre study in Melbourne, Australia from 1992 to 2001. Bronchoalveolar lavage was performed at study entry. Healthy infants undergoing bronchoscopy to investigate chronic stridor acted as controls. Quantitative microbiological culture was performed and inflammatory markers were measured contemporaneously. 16S ribosomal RNA gene analysis was performed on stored samples. RESULTS: Thirteen bronchoalveolar samples from infants with CF and nine from control infants, collected at median ages of 1.8-months (25th-75th percentile 1.5 to 3.1-months) and 5-months (25th-75th percentile 2.9 to 8.2-months) respectively, provided 16S rRNA gene data. Bacterial biomass was positively associated with inflammation. Alpha diversity was reduced in infants with CF and between-group compositional differences were apparent. These differences were driven by increased Staphylococcus and decreased Fusobacterium and were most apparent in symptomatic infants with CF. CONCLUSION: In CF lung disease, differences in lower airway microbial community composition and structure are established by age 6-months.
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