Skin microbiota in atopic dermatitis: victim or executioner?

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder, affecting 10%–20% of the population, characterized by dryness, intense itching, and recurrent rashes. The pathophysiology of AD is multifactorial, involving skin barrier dysfunction, immune dysregulation, genetic factors (such as filaggrin mutations), and environmental factors. The skin microbiota also plays a pivotal role in AD, serving both as a target and a driver of the disease. In AD, the delicate balance of the skin microbiota is disrupted, leading to a decrease in beneficial bacteria such as Streptococcus, Cutibacterium, and Corynebacterium. Concurrently, bacterial pathobionts, notably Staphylococcus aureus, proliferate and express their virulence factors excessively. This imbalance exacerbates symptoms by damaging the skin barrier, releasing toxins, and triggering a Th2-driven immune response, thus weakening the skin defenses and making individuals with AD more susceptible to bacterial, fungal, and viral infections, thereby complicating treatment and worsening disease outcomes. Effective AD management requires a thorough understanding of the interplay among the skin microbiota, the immune system, and microbial pathobionts. Strategies that restore the microbial balance, preserve the skin barrier, and modulate the immune response show significant potential for reducing infections and improving AD symptoms, highlighting the microbiota’s dual role in AD pathology. This review examines the complex role of the skin microbiota in AD, emphasizing how dysbiosis both drives disease progression and influences immune responses, and vice versa. It also explores emerging microbiota-targeted therapies aimed at improving disease outcomes.