Background/Objectives: The role of maternal diet in atopic dermatitis (AD) requires better understanding, as AD often manifests early in life and precedes other allergic diseases. We evaluated the association between maternal diet and AD up to 2 years of age. Methods: A total of 116 mother–child dyads from the CARE birth cohort study were included. Maternal diet during pregnancy was assessed with a validated self-administered 97-item food frequency questionnaire, and dietary scores were calculated. AD was evaluated at ages 4 months, 1 year, and 2 years. The associations between maternal dietary patterns and AD were examined by logistic regression analysis adjusting for total energy intake, gender of the child, maternal antibiotic therapy during pregnancy, and history of atopic disease among both parents. Results: Of the 116 children, 27 (23.3%) developed AD by 2 years, 11 of whom (40.7%) had persistent AD within the first 2 years. AD risk was reduced with a higher Mediterranean diet score during pregnancy (upper median > 3 points versus lower median: adjusted OR 0.24, 95% CI 0.08–0.69, p = 0.009) and with greater dietary diversity, as measured by the number of items consumed (upper median > 53 items versus lower median: OR 0.19, 95% CI 0.06–0.58, p = 0.005). No association was found with macronutrients and micronutrients. Red meat consumption showed a positive association with the persistent AD phenotype (adjusted OR 5.04, 95% CI 1.47 to 31.36, p = 0.034). Conclusions: Adherence to a Mediterranean diet and a diverse diet during pregnancy may decrease the risk of developing early childhood AD. This highlights the synergistic role of nutrients in dietary patterns as they modulate immune development and disease susceptibility.

Allergic diseases are among the most prevalent chronic disorders worldwide, and their rising incidence represents an expanding challenge for public health and clinical care

Early childhood represents a critical window for asthma susceptibility, marked by developmental and molecular changes, yet their longitudinal pattern remains unclear. To identify differences in longitudinal whole-blood gene expression during early childhood in future asthmatics compared to healthy children. We conducted a longitudinal whole-blood transcriptomic analysis at four timepoints (1, 4.5, 6, 10.5 years) in a sample of the birth cohort PASTURE (n = 378), comparing children who developed asthma between 6 and 10.5 years with non-asthmatic controls (83/295). Analyses included longitudinal differential gene expression, weighted gene co-expression network analysis, and cis-eQTL analysis. At age 1, 42 genes, mostly upregulated in future asthmatics, were associated with neutrophilic inflammation and NLRP3 inflammasome-markers. By 4.5 years, this shifted to a novel eosinophil-related signature (40 genes), remaining increased in asthmatics until 10.5 years. Co-expression analysis confirmed a neutrophilic module at 1 year and eosinophilic modules at 4.5, 6 and 10.5 years, all associated with asthma. Fractional exhaled nitric oxide was associated with the eosinophilic module at age 6 (P = .003). 86 SNPs were identified modulating the expression of 10 eosinophil-associated genes and GSDMB from this eosinophilic signature. A variant-based genetic risk score was associated with asthma diagnosis (aOR[95% CI]= 1.47[1.13-1.93]). We identified a shift from a neutrophil-driven gene signature at age 1 to a persistent eosinophilic signature at 4.5 to 10.5 years in asthmatic children, highlighting the 1 to 4.5-year period as most vulnerable period. Genetic variants strongly influenced the persistent eosinophilic gene signature, comprising potential novel therapeutic targets.

During the first year of life, infant diet changes from liquid to solid food. Resistant starch is one of the first complex carbohydrates available to gut microbiota. With the overall goal to gain mechanistic understanding on the development of microbial starch utilization capacity and its impact on fermentation activity, we investigated the interplay of diet, starch utilizers Ruminococcus bromii and Bifidobacterium adolescentis and the butyrate producer Anaerobutyricum hallii using samples from the longitudinal CARE cohort, and in vitro. Infants started to consume resistant starch at 4 months. While less than one quarter of the infants harboured starch utilizers at 5 months, occurrence increased until the end of year one. In vitro, R. bromii and B. adolescentis degraded resistant starch but only R. bromii released reducing sugars. B. adolescentis formed acetate and lactate. In co‐cultures, R. bromii with A. hallii produced more butyrate via reducing sugars than with lactate and acetate from B. adolescentis . At one year of age, infants that harboured both starch utilizer and A. hallii had higher faecal butyrate levels than those without these species. Our results suggest that differences in the mode of resistant starch degradation and cross‐feeding contributed to functional redundancy and affected butyrate formation.