Fecal Microbiome and Food Allergy in Pediatric Atopic Dermatitis: A Cross-Sectional Pilot Study

Abstract

Background: Exposure to microbes may be important in the development of atopic disease. Atopic diseases have been associated with specific characteristics of the intestinal microbiome. The link between intestinal microbiota and food allergy has rarely been studied, and the gold standard for diagnosing food allergy (double-blind placebo-controlled food challenge [DBPCFC]) has seldom been used. We aimed to distinguish fecal microbial signatures for food allergy in children with atopic dermatitis (AD). Methods: Pediatric patients with AD, with and without food allergy, were included in this cross-sectional observational pilot study. AD was diagnosed according to the UK Working Party criteria. Food allergy was defined as a positive DBPCFC or a convincing clinical history, in combination with sensitization to the relevant food allergen. Fecal samples were analyzed using 16S rRNA microbial analysis. Microbial signature species, discriminating between the presence and absence food allergy, were selected by elastic net regression. Results: Eighty-two children with AD (39 girls) with a median age of 2.5 years, and 20 of whom were diagnosed with food allergy, provided fecal samples. Food allergy to peanut and cow's milk was the most common. Six bacterial species from the fecal microbiome were identified, that, when combined, distinguished between children with and without food allergy: Bifidobacterium breve, Bifidobacterium pseudocatenulatum, Bifidobacterium adolescentis, Escherichia coli, Faecalibacterium prausnitzii, and Akkermansia muciniphila (AUC 0.83, sensitivity 0.77, specificity 0.80). Conclusions: In this pilot study, we identified a microbial signature in children with AD that discriminates between the absence and presence of food allergy. Future studies are needed to confirm our findings.

The Relationship between the Infant Gut Microbiota and Allergy. The Role of Bifidobacterium breve and Prebiotic Oligosaccharides in the Activation of Anti-Allergic Mechanisms in Early Life

“…The microbiota has a crucial role in generating a balanced immune phenotype that involves maturation of the Th1 cells response and the development of T regulatory (Treg) cells, which suppress the Th2 phenotype [63]. Comparisons of the intestinal microbiota of children with allergies with that of healthy children show that children with allergic diseases primarily have a reduced diversity of their gut microbiota and low abundance of Bifidobacterium, Lactobacillus, and Bacteroides [64][65][66][67][68][69][70][71][72][73][74]. Prospective studies suggest that intestinal dysbiosis in early life precedes the development of allergy in older children.…”

“…The recently published study by Fieten et al (2018) aimed to identify the fecal microbial signatures of FA in children with AD [70]. The authors identified six bacterial species which may determine the presence or absence of FA.…”

Immunologically Active Components in Human Milk and Development of Atopic Disease, With Emphasis on Food Allergy, in the Pediatric Population

“…Kourosh et al sought to better understand fecal microbiome in children with IgE mediated food allergy and were able to show that there were significant differences in microbial composition amongst food-allergic children, especially in the Clostridia class, compared with healthy siblings and healthy children ( 32 ). Fieten et al looked for differences in fecal microbiome in children with or without food allergy in the setting of atopic dermatitis ( 33 ). Their pilot study showed significant differences in the microbiome profile between these two groups, specifically with Bifidobacterium breve, Bifidobacterium pseudocatenulatum, Bifidobacterium adolescentis, Escherichia coli, Faecalibacterium prausnitzii , and Akkermansia muciniphila .…”

Maternal Perinatal Dietary Patterns Affect Food Allergy Development in Susceptible Infants

“…67 Verrucomicrobia is one of the the dominant phyla and was reported to be decreased in infants with food allergy which was not consistent with our results. 69 This discrepancy should be addressed through further studies well designed with a large number of subjects and randomized controlled models or with mouse models about pathomechanism.…”