Food Sensitization Is Associated With Atopic Dermatitis Severity, Gut-Derived Metabolites and Leaky Gut in Adults

Gut microbiome dysbiosis may cause metabolic dysregulation and intestinal barrier impairment. The latter are hypothesized to provoke food allergy and aggravate cutaneous inflammation. Our objective was to determine the prevalence of food sensitization in adult patients with atopic dermatitis and relate it to the disease severity and the biomarkers of the gut-skin axis.

50 adult patients with atopic dermatitis and 25 controls were enrolled in this cross-sectional study. Disease severity was determined by using SCORAD and EASI scores. Liquid chromatography-mass spectrometry, Luminex, and Polycheck immunoassays were performed to detect serum concentrations of total IgE, food-specific IgEs, gut-derived metabolites, and leaky gut-related biomarkers.

Food sensitization was significantly more prevalent in patients with atopic dermatitis than in the controls. The severity of atopic dermatitis (EASI, SCORAD) was higher in patients with food sensitization and correlated with the number of positive food-specific IgEs. Higher concentrations of total IgE and higher numbers of positive food-specific IgEs were associated with lower concentrations of short-chain fatty acids and higher concentrations of indoxyl and leaky gut-related biomarkers (LBP, syndecan-4, IL-10, IL-22).

The results suggest a relationship between food sensitization and the severity of atopic dermatitis. This could be partly associated with gut-derived metabolites and intestinal barrier impairment. Fiber-rich diet and restriction of protein could hold potential for upregulating short-chain fatty acids and downregulating indoxyl, which may translate to decreasing the likelihood of food sensitization in atopic dermatitis. Notably, the cross-sectional nature of this exploratory study limits the ability to draw causal inferences, which should be further examined in future prospective research.