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Mediators of Inflammation
Volume 2017, Article ID 5047403, 10 pages
https://doi.org/10.1155/2017/5047403
Research Article

Comparison of Oropharyngeal Microbiota from Children with Asthma and Cystic Fibrosis

1Department of Infectious Diseases, Medical Microbiology and Hygiene, University Hospital Heidelberg, Heidelberg, Germany
2Translational Lung Research Center Heidelberg (TLRC), German Center for Lung Research (DZL), Heidelberg, Germany
3Dr. von Hauner Children’s Hospital, LMU Munich, Munich, Germany
4Division of Pediatric Pulmonology and Allergy and Cystic Fibrosis Center, Department of Pediatrics, University Hospital Heidelberg, Heidelberg, Germany
5Department of Translational Pulmonology, University of Heidelberg, Heidelberg, Germany
6Department of Pneumology and Critical Care Medicine, Thoraxklinik, University Hospital Heidelberg, Heidelberg, Germany

Correspondence should be addressed to Alexander H. Dalpke; ed.grebledieh-inu.dem@ekplad.rednaxela

Received 30 May 2017; Revised 24 August 2017; Accepted 22 October 2017; Published 27 December 2017

Academic Editor: Pierre-Régis Burgel

Copyright © 2017 Sébastien Boutin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

A genuine microbiota resides in the lungs which emanates from the colonization by the oropharyngeal microbiota. Changes in the oropharyngeal microbiota might be the source of dysbiosis observed in the lower airways in patients suffering from asthma or cystic fibrosis (CF). To examine this hypothesis, we compared the throat microbiota from healthy children () and that from children with asthma () and CF () aged 6 to 12 years using 16S rRNA amplicon sequencing. Our results show high levels of similarities between healthy controls and children with asthma and CF revealing the existence of a core microbiome represented by Prevotella, Streptococcus, Neisseria, Veillonella, and Haemophilus. However, in CF, the global diversity, the bacterial load, and abundances of 53 OTUs were significantly reduced, whereas abundances of 6 OTUs representing opportunistic pathogens such as Pseudomonas, Staphylococcus, and Streptococcus were increased compared to those in healthy controls controls and asthmatics. Our data reveal a core microbiome in the throat of healthy children that persists in asthma and CF indicating shared host regulation favoring growth of commensals. Furthermore, we provide evidence for dysbiosis with a decrease in diversity and biomass associated with the presence of known pathogens consistent with impaired host defense in children with CF.