Staphylococcus aureus Aggravates Atopic Dermatitis through Enhanced Bacterial Colonization

Atopic dermatitis (AD), the most prevalent chronic inflammatory skin disease in children worldwide, is characterized by skin barrier dysfunction and microbial dysbiosis. Staphylococcus aureus colonizes lesional skin in up to 70% of AD patients, exacerbating inflammation through virulence factors (e.g., enterotoxin B, SplD protease) and biofilm formation, which disrupt the skin barrier and trigger Th2 immune responses. However, existing studies primarily focus on individual virulence factors, leaving the core regulatory mechanisms enabling persistent S. aureus colonization in AD poorly understood.