Gut microbiota modulation: a key determinant of atopic dermatitis susceptibility in children

Abstract

Atopic dermatitis is a chronic inflammatory skin condition with a higher incidence rate among children. In recent years, the role of the gut microbiota in the pathogenesis of atopic dermatitis has garnered increasing attention. This review systematically delineates the research advancements in the structural characteristics of the gut microbiota in children with atopic dermatitis and its influencing factors. Studies have revealed significant differences in the gut microbiota structure between children with atopic dermatitis and healthy controls, characterized by a reduction in microbial diversity, a decrease in beneficial bacteria, and an increase in harmful bacteria. Dietary patterns, environmental factors, birth patterns, antibiotic use, and gestational diabetes mellitus are factors could impact the gut microbiota hence influencing the susceptibility of children to atopic dermatitis. Moreover, this review explores the interplay between the gut microbiota and the immune system in atopic dermatitis, with the potential to inform more effective probiotic treatment strategies for children with atopic dermatitis.

Keywords: atopic dermatitis; children; gut microbiome; influencing factor; structural feature.

Figure 1

Relationship between intestinal microecology and AD in children Overgrowth of microorganisms such as Escherichia coli, Klebsiella pneumoniae, and Clostridium difficile perturbs gut microbiota homeostasis. Probiotics stimulate short-chain fatty acids (SCFAs) synthesis and generate indole-3-lactic acid (ILA) and Indole-3-carbaldehyde (I3C) through the metabolism of tryptophan (Trp). ILA inhibits the production of lipopolysaccharide (LPS), reducing toll-like receptor (TLR)-mediated inflammatory responses. I3C suppresses the production of thymic stromal lymphopoietin (TSLP) via the aryl hydrocarbon receptor (AhR)-mediated immune response, which reduces Th2 immune responses, alleviating atopic dermatitis (AD). SCFAs regulate the Th2 immune response in the skin and inhibit the production of AD-related inflammatory cytokines such as IL-4, IL-13 and IL-31 to inhibit the onset of AD. Breast milk, rich in human milk oligosaccharides (HMOs), through SCFAs, IgA, and ILA help to bolster gut immunity and probiotic growth. Oral vitamin D can inhibit the colonization of Staphylococcus aureus (S. aureus) in the skin, reducing the release of virulence factors. Colonization of S. aureus in the skin leads to the release of virulence factors, which activate mast cell degranulation to release inflammatory cytokines IL-13. Factors such as vaginal delivery (VD) of infants and rural environments are AD -protective, whereas early antibiotic exposure disrupts probiotic colonization and elevates AD risk. Filaggrin (FLG) gene mutation is also an important risk factor for the development of AD. (Created with BioRender.com).