IgE reactivity to antigens from Gram‐positive and Gram‐negative bacteria is common in patients suffering from respiratory and skin manifestations of allergy, but the routes and mechanisms of sensitization are not fully understood. The analysis of the genome, transcriptome and microbiome of house dust mites (HDM) has shown that Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) species are abundant bacteria within the HDM microbiome. Therefore, our aim was to investigate whether HDM are carriers of bacterial antigens leading to IgE sensitization in patients suffering from atopic dermatitis.

The food allergy epidemic of recent years has led to the search for safe and effective methods of immunotherapy for foods. Studies of epicutaneous immunotherapy (EPIT) in mice have shown promising safety and efficacy data. Murine models have also identified probable mechanisms for the development of tolerance to food allergens, including the induction of regulatory T cells. Clinical data is lacking, but relatively small and early studies among peanut and cow’s milk allergic subjects suggest that EPIT has an excellent safety profile,particularly compared to other methods of specific allergen immunotherapy.

Food allergy naturally resolves in a proportion of food-allergic children without intervention; however the underlying mechanisms governing the persistence or resolution of food allergy in childhood are not understood.

Food allergy is a common disease affecting approximately 8% of children and 5% of adults. The prevalence has increased over the last two decades, suggesting an important environmental contribution to susceptibility. Studies have identified mode of birth, pet exposure, and having older siblings as being significant risk modifying factors in the development of food allergy. With the discovery that these factors significantly impact the composition of the intestinal microbiome, which is known to play a critical role in shaping the immune system, recent studies have begun to address the role of the intestinal microbiota in the development of food allergy.

The application of recently developed sensitive, specific, culture-independent tools for identification of microbes is transforming concepts of microbial ecology, including concepts of the relationships between the vast complex populations of microbes associated with ourselves and with states of health and disease.

PRACTALL is a joint initiative of the American Academy of Allergy, Asthma & Immunology and the European Academy of Allergy and Clinical Immunology to provide shared evidence-based recommendations on cutting-edge topics in the field of allergy and immunology. PRACTALL 2017 is focused on what has been established regarding the role of the microbiome in patients with asthma, atopic dermatitis, and food allergy.

Ingestion of innocuous antigens, including food proteins, normally results in local and systemic immune nonresponsiveness in a process termed oral tolerance. Oral tolerance to food proteins is likely to be intimately linked to mechanisms that are responsible for gastrointestinal tolerance to large numbers of commensal microbes. Here we review our current understanding of the immune mechanisms responsible for oral tolerance and how perturbations in these mechanisms might promote the loss of oral tolerance and development of food allergies.

We studied 226 children with milk allergy who were enrolled at infancy in the Consortium of Food Allergy observational study of food allergy. Fecal samples were collected at age 3 to 16 months, and the children were followed longitudinally with clinical evaluation, milk-specific IgE levels, and milk skin prick test performed at enrollment, 6 months, 12 months, and yearly thereafter up until age 8 years.

Probiotics are live microorganisms that confer a health benefit on the host when applied in adequate amounts. The therapeutic effects of probiotics have been mostly studied in the gastrointestinal tract, but recent evidence points towards the potential of these bacteria to prevent and/or treat chronic airway diseases.