Source: International Congress 2014 – New mechanisms in the pathogenesis of asthma and other lung diseases
Disease area: Airway diseases

Abstract

RationaleIn rodents commensal bacteria in gut are critical for normal maturation of the immune system and microbiota alterations have been linked to development of eosinophilic airway inflammation. However, no study has yet related airway microbiota composition and airway inflammation in humans with asthma.AimTo relate airway eosinophilia to the composition of the airway microbiota in subjects with asthma.MethodsIn 20 steroid-free, non-smoking subjects with asthma bacterial DNA was extracted from broncho-alveolar lavage (BAL) and subjected to Illumina MiSeq sequencing of the 16S rDNA V4 region. Eosinophils in submucosa were quantified by immunohistochemichal identification and computerized image analysis. Asthmatics were divided into eosinophil low and eosinophil high using the median as cut-off.ResultsMicrobiota diversity was lower and microbiota composition was significantly different in BAL from eosinophil high asthma compared to eosinophil low asthma. Bacteroidetes, Firmicutes, Proteobacteria, Fusobacteria and Actinobacteria were identified in all samples and accounted for more than 97% of the microbial load. The proportion of Bacteroidetes was reduced in eosinophil high asthma compared to eosinophil low (median [IQR]: 0.17 [0.11] vs. 0.29 [0.16], p=0.009), whereas the proportion of Proteobacteria was increased (median [IQR]: 0.33 [0.11] vs. 0.25 [0.09], p=0.035). The degree of eosinophilia was negatively correlated with the proportion of Bacteroidetes, rho(s): -0.69, p=0.001.ConclusionThe airway microbiota is significantly altered in eosinophil high asthma, suggesting dysbiosis of the airway microbiome corresponding to the degree of eosinophilia.

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A. Sverrild, P. Kiilerich, C. Porsbjerg, A. Bergqvist, J. Erjefält, K. Kristiansen, V. Backer (Copenhagen, Denmark; Lund, Sweden). The airway microbiota is significantly altered in subjects with eosinophilic asthma. Eur Respir J 2014; 44: Suppl. 58, 3874

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