In light of the constantly increasing prevalence of allergic diseases, changes in dietary patterns have been suggested as a plausible environmental explanation for the development and progression of these diseases. Nowadays, much attention has been paid to the development of dietary interventions using natural substances with anti-allergy activities. In this respect, dietary polyphenols have been studied extensively as one of the most prominent natural bioactive compounds with well-documented anti-inflammatory, antioxidant, and immunomodulatory properties. This review aims to discuss the mechanisms underlying the potential anti-allergic actions of polyphenols related to their ability to reduce protein allergenicity, regulate immune response, and gut microbiome modification; however, these issues need to be elucidated in detail. This paper reviews the current evidence from experimental and clinical studies confirming that various polyphenols such as quercetin, curcumin, resveratrol, catechins, and many others could attenuate allergic inflammation, alleviate the symptoms of food allergy, asthma, and allergic rhinitis, and prevent the development of allergic immune response. Conclusively, dietary polyphenols are endowed with great anti-allergic potential and therefore could be used either for preventive approaches or therapeutic interventions in relation to allergic diseases. Limitations in studying and widespread use of polyphenols as well as future research directions are also discussed.

Food allergy represents a growing public health and socio-economic problem with an increasing prevalence over the last two decades. Despite its substantial impact on the quality of life, current treatment options for food allergy are limited to strict allergen avoidance and emergency management, creating an urgent need for effective preventive strategies. Advances in the understanding of the food allergy pathogenesis allow to develop more precise approaches targeting specific pathophysiological pathways. Recently, the skin has become an important target for food allergy prevention strategies, as it has been hypothesized that allergen exposure through the impaired skin barrier might induce an immune response resulting in subsequent development of food allergy. This review aims to discuss current evidence supporting this complex interplay between the skin barrier dysfunction and food allergy by highlighting the crucial role of epicutaneous sensitization in the causality pathway leading to food allergen sensitization and progression to clinical food allergy. We also summarize recently studied prophylactic and therapeutic interventions targeting the skin barrier repair as an emerging food allergy prevention strategy and discuss current evidence controversies and future challenges. Further studies are needed before these promising strategies can be routinely implemented as prevention advice for the general population.

In the last few decades, a dramatic increase in the global prevalence of allergic diseases and asthma was observed. It was hypothesized that diet may be an important immunomodulatory factor influencing susceptibility to allergic diseases. Fermented food, a natural source of living microorganisms and bioactive compounds, has been demonstrated to possess health-promoting potentials and seems to be a promising strategy to reduce the risk of various immune-related diseases, such as allergic diseases and asthma. The exact mechanisms by which allergic diseases and asthma can be alleviated or prevented by fermented food are not well understood; however, its potential to exert an effect through modulating the immune response and influencing the gut microbiota has been recently studied. In this review, we provide the current knowledge on the role of diet, including fermented foods, in preventing or treating allergic diseases and asthma.

Atopic eczema is the most common chronic inflammatory skin disease of early childhood and is often the first manifestation of atopic march. Therefore, one challenge is to identify the risk factors associated with atopic eczema that may also be predictors of atopic disease progression. The aim of this study was to investigate the association of SNPs in hornerin (HRNR) and filaggrin-2 (FLG2) genes with childhood atopic eczema, as well as other atopic phenotypes. Genotyping for HRNR and FLG2 was performed in 188 children younger than 2 years of age, previously screened for the FLG null mutations, and followed at yearly intervals until the age of 6. We demonstrated that risk variants of HRNR rs877776[C] and FLG2 rs12568784[T] were associated with atopic eczema, allergic sensitization, and susceptibility to the complex phenotype—asthma plus eczema. These effects seem to be supplementary to the well-known associations for FLG mutations and may be modulated by gene–gene interactions. Additionally, in children with eczema, these genetic variants may also be considered, along with FLG mutations, as predictive biomarkers for eczema-associated asthma. In conclusion, our results indicate that genetic variants in the epidermal differentiation complex gene could contribute to the pathogenesis of atopic eczema and progression to subsequent allergic disease.

As the burden of mild asthma is not well understood, the significance of expanding research in the group of patients with mild asthma is emphasized. Thymic stromal lymphopoietin (TSLP) and interleukin 33 (IL-33) are involved in the pathogenesis of atopy and the immune response to inhaled environmental insults, such as allergens, in asthmatic patients. Objectives: The objective of this study was to explore the correlation between specific polymorphisms within the genes encoding TSLP and IL-33, as well as the concentrations of TSLP and IL-33 in the serum, and the occurrence of pediatric mild asthma. Methods: The analysis encompassed 52 pediatric patients diagnosed with mild bronchial asthma, including both atopic and non-atopic cases, and a control group of 26 non-asthmatic children. Recruitment was conducted through a comprehensive questionnaire. Parameters such as allergic sensitization, serum levels of circulating TSLP and IL-33, and the identification of single-nucleotide polymorphisms in TSLP (rs11466750 and rs2289277) and IL-33 (rs992969 and rs1888909) were assessed for all participants. Results: Significantly lower mean serum TSLP concentrations were observed in asthmatic subjects compared to the control group, with atopic asthma patients showing even lower TSLP levels than non-atopic counterparts. No significant differences were found in mean serum IL-33 concentrations between the two groups. Considering the allele model, for both tested SNPs of IL-33, we observed that patients with asthma, atopic asthma, and atopy statistically less frequently possess the risk allele. Conclusions: Our study findings suggest that IL-33 and TSLP do not serve as ideal biomarkers for mild asthma in children. Their effectiveness as biomarkers might be more relevant for assessing disease severity rather than identifying asthma in pediatric patients. Further research focusing on the association between TSLP and IL-33 gene polymorphisms and asthma is expected to significantly advance disease management.

Allergic diseases commonly coexist, manifesting in a sequence described as the “allergic march”. Background/Objectives: This study aimed to evaluate TSLP’s and IL-1β’s potential as biomarkers in both single and multi-pediatric atopic diseases like atopic eczema, food allergy, and anaphylaxis and analyze specific SNPs in the TSLP and IL-1β genes to determine their associations with their occurrence and severity. Methods: This analysis included 109 atopic children diagnosed with atopic dermatitis, food allergy, or anaphylaxis alongside a control group of 57 non-atopic children. Recruitment was facilitated through the use of a comprehensive questionnaire. For the study population, the allergen profile was characterized at the molecular level by measuring specific IgE to purified natural or recombinant allergens, assessing serum levels of circulating TSLP and IL-1β, and identifying single-nucleotide polymorphisms in TSLP (rs2289277) and IL-1β (rs16944 C-511T). Results: The serum levels of TSLP and IL-1β were elevated in the study groups compared to the control group, highlighting their significance in the pathogenesis of the studied diseases. Carrying a higher number of the risk allele [C] in the TSLP SNP rs2289277 is associated with the greatest likelihood of having multiple concurrent allergic conditions, with the highest risk observed in individuals with all three conditions—atopic dermatitis, food allergy, and anaphylaxis, simultaneously. Moreover, children carrying the risk allele had a twofold increased risk of polysensitization, which rose to sixfold in those with two copies of the risk allele. Although no significant variations in genotype frequencies were detected for IL-1β rs16944, significant associations were observed for TSLP rs2289277, particularly with conditions such as atopic dermatitis, food allergy, anaphylaxis, and combinations of these diseases. Conclusions: Further research is required to elucidate these pathways and their role in the development of allergic diseases.