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16 S rRNA survey revealed complex bacterial communities and evidence of bacterial interference on human adenoids
Author(s) -
Ren Tiantian,
Glatt Dominique Ulrike,
Nguyen Tam Nhu,
Allen Emma Kaitlynn,
Early Stephen V.,
Sale Michele,
Winther Birgit,
Wu Martin
Publication year - 2013
Publication title -
environmental microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.954
H-Index - 188
eISSN - 1462-2920
pISSN - 1462-2912
DOI - 10.1111/1462-2920.12000
Subject(s) - biology , adenoid hypertrophy , adenoid , otitis , microbiome , pathogen , microbiological culture , microbiology and biotechnology , ecology , bacteria , immunology , genetics , medicine , tonsillectomy , adenoidectomy , surgery
Summary Adenoid microbiota plays an important role in the development of various infectious and non‐infectious diseases of the upper airways, such as otitis media, adenotonsillitis, rhinosinusitis and adenoid hypertrophy. Studies have suggested that adenoids could act as a potential reservoir of opportunistic pathogens. However, previous bacterial surveys of adenoids were mainly culture based and therefore might only provide an incomplete and potentially biased assessment of the microbial diversity. To develop an in‐depth and comprehensive understanding of the adenoid microbial communities and test the ‘pathogen reservoir hypothesis’, we carried out a 16 S rRNA based, culture‐independent survey of bacterial communities on 67 human adenoids removed by surgery. Our survey revealed highly diverse adenoid bacterial communities distinct from those of other body habitats. Despite large interpersonal variations, adenoid microbiota shared a core set of taxa and can be classified into at least five major types based on its bacterial species composition. Our results support the ‘pathogen reservoir hypothesis’ as we found common pathogens of otitis media to be both prevalent and abundant. Co‐occurrence analyses revealed evidence consistent with the bacterial interference theory in that multiple common pathogens showed ‘non‐coexistence’ relationships with non‐pathogenic members of the commensal microflora.