The gut microbiota in patients with food allergy, and the skin microbiota in atopic dermatitis patients differ from those of healthy people. We hypothesize that relationships may exist between gut and skin microbiota in patients with allergies. The aim of this study was to determine the possible relationship between gut and skin microbiota in patients with allergies, hence simultaneous analysis of the two compartments of microbiota was performed in infants with and without allergic symptoms. Fifty-nine infants with food allergy and/or atopic dermatitis and 28 healthy children were enrolled in the study. The skin and gut microbiota were evaluated using 16S rRNA gene amplicon sequencing. No significant differences in the α-diversity of dermal or fecal microbiota were observed between allergic and non-allergic infants; however, a significant relationship was found between bacterial community structure and allergy phenotypes, especially in the fecal samples. Certain clinical conditions were associated with characteristic bacterial taxa in the skin and gut microbiota. Positive correlations were found between skin and fecal samples in the abundance of Gemella among allergic infants, and Lactobacillus and Bacteroides among healthy infants. Although infants with allergies and healthy infants demonstrate microbiota with similar α-diversity, some differences in β-diversity and bacterial species abundance can be seen, which may depend on the phenotype of the allergy. For some organisms, their abundance in skin and feces samples may be correlated, and these correlations might serve as indicators of the host’s allergic state.

Background Regulatory T cells (Tregs) have an essential role in tolerance and immune regulation. However, few and controversial data have been published to date on the role and number of these cells in food allergic children. The forkhead/winged-helix transcription factor box protein 3 (FOXP3) is considered the most reliable marker for Tregs. Objective This study aims to investigate the FOXP3, interleukin (IL)-10, and transforming growth factor (TGF-β) genes expression in children with IgE-dependent food allergy. Material and Methods The study group consisted of 54 children with IgE-dependent food allergy (FA) and a control group of 26 non-atopic healthy children. The diagnosis of FA was established using questionnaires, clinical criteria, skin prick tests, serum sIgE antibodies (UniCAP 100 Pharmacia Upjohn), and a double-blind placebo control food challenge. In order to assess gene expression, the isolation of nucleated cells was performed using Histopaque-1077 (Sigma-Aldrich, Germany). The concentration of RNA obtained was measured using a super-sensitive NanoDrop ND1000 spectrophotometer (Thermo Scientific, USA). A reverse transcription reaction was performed using a commercially available set of High Capacity cDNA Archive Kit (Applied Biosystems, USA). Analysis have been carried out in the genetic analyzer 7900HT Real-Time PCR (Applied Biosystems, USA). Results The average level of the FOXP3 gene expression in the studied group was 2.19 ± 1.16 and in the control group 2.88 ± 1.66 (p = 0.03). The average level of IL10 mRNA expression in the study group was 13.6 ± 1.07 and was significantly lower than corresponding values in the control group 14.3 ± 1.1 (p = 0.01). There were no significant differences in the average level of the TGF-β mRNA expression in the study group (3.4 ± 0.4) and controls (3.5 ± 0.3; p > 0.05). The FOXP3 gene expression was the highest in children who acquired tolerance to food (3.54 ± 0.75), lower in heated allergen-tolerant children (2.43 ± 0.81), and the lowest in heated allergen-reactive children (1.18 ± 0.5; p = 0.001 control vs heated allergen reactive; p = 0.005 heated allergen tolerant vs heated allergen reactive; p = 0.001 outgrown vs heated allergen reactive). The significant tendency toward lower total IgE levels with a higher FOXP3 mRNA expression was detected (n = 54; Pearson r = −0.4393; p = 0.001). Conclusions Children with FA showed statistically significant lower level of the FOXP3 and IL10 gene expression than healthy children. Children acquiring tolerance to the food show significantly higher levels of the FOXP3 gene expression than children with active FA. The correlation between the level of FOXP3 and total IgE was detected.

Cow’s milk is a key component of a child’s diet. While the consumption of even trace amounts can result in allergy to its proteins and/or hypolactasia, excessive cow’s milk consumption can result in numerous health complications, including iron deficiency, due to the diet being improperly balanced. Although the incidence of iron deficiency has declined, it remains the most widespread nutritional deficiency globally and the most common cause of anemia. One rare consequence of anemia caused by iron deficiency is protein-losing enteropathy; however, the mechanisms of its development are unclear. The following manuscript, based on a literature review, presents two rare cases of children, a 16-month-old boy and a 2.5-year-old girl, who developed severe microcytic anemia, enteropathy with hypoalbuminemia, and anasarca as a result of excessive cow’s milk consumption. It highlights the possible relationship between excessive consumption of cow’s milk in children and severe iron deficiency anemia with accompanying hypoalbuminemia; it may also result in serious clinical conditions, even in children that do not demonstrate food hypersensitivity.

The child microbiome, including gut and skin communities, is shaped by a multitude of factors, and breastfeeding is one of the most essential. Food allergy (FA) and atopic dermatitis (AD) are among the most common diseases in pediatrics, with the prevalence of each up to 6% and 20%, respectively. Therefore, we aimed at finding differences between the fecal and skin microbiomes of FA and AD patients in the context of breastfeeding, by means of the Illumina sequencing of 16S rRNA gene fragment libraries amplified from the total DNA isolated from samples collected from allergic and healthy infants. We also analyzed milk samples from the mothers of the examined children and searched for patterns of incidence suggesting milk influence on an infant’s allergy status. Here we show that a mother’s milk influences her child’s fecal and skin microbiomes and identify Acinetobacter as the taxon whose abundance is correlated with milk and child-derived samples. We demonstrate that breastfeeding makes allergic children's fecal and skin communities more similar to those of healthy infants than in the case of formula-feeding. We also identify signature taxa that might be important in maintaining health or allergy development.