In particular, IgE and specific IgE to food allergen play a critical role in the pathogenesis of AD and food allergy.37–39 A reduced abundance of B. fragilis in the AD group, which prevents inflammation through its polysaccharide A by restoring Th1/Th2 balance,40 was also found in previous studies.16,27 These results suggest that the redox-dysregulated gut environment of children with AD during early development could cause gut microbiome perturbation and SCFA dysbiosis in later life by limiting the colonization of B. fragilis. This evidence concerns the gene IGHE and Alzheimer disease.