4 years ago

Sputum microbiota in severe asthma patients: Relationship to eosinophilic inflammation

Sputum microbiota in severe asthma patients: Relationship to eosinophilic inflammation
Altered composition of airway microbiota has been reported in subjects suffering from asthma but its relation to eosinophilic phenotype is unclear. Objective To examine the relationship between sputum microbiota, asthma severity and inflammatory type in asthmatic subjects from Guangzhou, China. Methods Induced sputum samples were obtained from 49 non-smoking asthma patients, 25 severe and 24 non-severe, and 15 healthy subjects. Total DNA was amplified using primers specific for the V3-V5 hypervariable region of bacterial 16s rRNA and sequenced using the 454 GS FLX sequencer. Sequences were assigned to bacterial taxa by comparing them with 16s rRNA sequences in the Ribosomal Database Project. Results Sputum eosinophil counts were higher and FEV1 (% predicted) was lower in severe compared to non-severe asthmatics. There were no significant differences in operational taxonomic unit (OTU) numbers at the phylum level and in diversity scores between non-severe asthmatics and severe asthmatics, and healthy subjects. At the family level, Porphyromonadaceae was most abundant in healthy subjects whereas Pseudomonadaceae and Enterobacteriaceae were higher in severe asthmatics compared to non-severe asthmatics (p < 0.05). Actinomycetaceae was particularly abundant in eosinophilic asthma patients compared to non-eosinophilic asthma (p = 0.011). Bacteroidaceae was positively correlated with FEV1 in all subjects (r = 0.335, p < 0.01), whereas body mass index was negatively associated with the number of species observed (r = −0.3, p < 0.05). Principal component analysis confirmed the positive association of Actinomycetaceae and Enterobacteriaceae abundance with eosinophilic asthma. Conclusion Patients with asthma have an altered airway microbiota, with specific bacteria associated with severe asthma and the eosinophilic inflammatory phenotype.

Publisher URL: www.sciencedirect.com/science

DOI: S095461111730286X

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