Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disorder affecting both children and adults, characterized by pruritus, eczematous lesions, and compromised skin barrier function. A key feature of AD is dysbiosis of the skin microbiome, marked by reduced microbial diversity and the overgrowth of Staphylococcus aureus in lesional skin. S. aureus exacerbates skin barrier dysfunction and immune dysregulation, leading to recurrent infections and disease flares. In contrast, commensal bacteria such as Staphylococcus epidermidis and Roseomonas mucosa may exert protective effects by inhibiting S. aureus colonization and modulating immune responses. Beyond microbial composition, microbial metabolites play a crucial role in AD pathophysiology. Short-chain fatty acids, indole derivatives, and other bacterial metabolites influence cutaneous immune responses, lipid metabolism, and skin barrier integrity. Altered metabolite profiles, including reduced levels of beneficial microbial metabolites, are associated with AD severity and disease progression. Notably, S. aureus overabundance correlates with disruption in lipid metabolism, further compromising the skin barrier. This review explores recent advances in understanding the relationship between microbial metabolites and AD pathogenesis and examines the therapeutic potential of microbiome-targeted interventions. Strategies such as probiotics, prebiotics, and topical microbiome transplantation aim to restore microbial diversity and rebalance metabolite production, ultimately improving clinical outcomes in AD patients. Future therapeutic approaches focusing on commensal-derived metabolites offer promising avenues for alleviating symptoms and modulating disease severity in AD.