Fecal Microbiome Signatures are Different in Food Allergic Children Compared to Siblings and Healthy Children
Sunday, March 4, 2018: 2:00 PM
S220EF (Convention Center)
Atoosa Kourosh, MD, , , , ,
RATIONALE: 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 V1,V3 and V4 variable regions of the 16S rRNA gene. Bacterial diversity, evenness, richness, and relative abundance of the OTUs 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=0.035), Actinomycetaceae (p=0.043), and Pasteurellaceae (p=0.018), and nine other distinct OTUs. 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. OTUs 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.