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Fecal microbiome signatures are different in food‐allergic children compared to siblings and healthy children
Author(s) -
Kourosh Atoosa,
Luna Ruth A.,
Balderas Miriam,
Nance Christina,
Anagnostou Aikaterini,
Devaraj Sridevi,
Davis Carla M.
Publication year - 2018
Publication title -
pediatric allergy and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.269
H-Index - 89
eISSN - 1399-3038
pISSN - 0905-6157
DOI - 10.1111/pai.12904
Subject(s) - microbiome , food allergy , clostridia , feces , allergy , firmicutes , immunology , biology , metagenomics , medicine , microbiology and biotechnology , genetics , 16s ribosomal rna , gene , bacteria
Background Intestinal microbes have been shown to influence predisposition to atopic disease, including food allergy. The intestinal microbiome of food‐allergic children may differ in significant ways from genetically similar non‐allergic children and age‐matched controls. The aim was to characterize fecal microbiomes to identify taxa that may influence the expression of food allergy. Methods Stool samples were collected from children with IgE‐mediated food allergies, siblings without food allergy, and non‐allergic controls. Stool microbiome characterization was performed via next‐generation sequencing (Illumina) of the V1V3 and V4 variable regions of the 16S rRNA gene. Bacterial diversity, evenness, richness, and relative abundance of the operational taxonomic units ( OTU s) were evaluated using QIIME . ANOVA and Welch's t test were utilized to compare groups. Results Sixty‐eight children were included: food‐allergic (n = 22), non‐food‐allergic siblings (n = 25), and controls (n = 21). When comparing fecal microbial communities across groups, differences were noted in Rikenellaceae ( P  = .035), Actinomycetaceae ( P  = .043), and Pasteurellaceae ( P  = .018), and nine other distinct OTU s. Food‐allergic subjects had enrichment for specific microbes within the Clostridia class and Firmicutes phylum ( Oscillobacter valericigenes , Lachnoclostridium bolteae , Faecalibacterium sp.) compared to siblings and controls. Identification of Clostridium sp. OTU s revealed differences in specific Clostridia drive the separation of the allergic from the siblings and controls. Alistipes sp. were enriched in non‐allergic siblings. Conclusions Comparisons in the fecal microbiome of food‐allergic children, siblings, and healthy children point to key differences in microbiome signatures, suggesting the role of both genetic and environmental contributors in the manifestation of food‐allergic disease.

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