An overview on treatment strategies targeting on cutaneous dysbiosis in patients with Atopic Dermatitis

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by immune dysregulation, skin barrier dysfunction, microbial imbalance, and environmental triggers. Increasing evidence highlights the central role of the skin microbiome, and particularly the overgrowth of Staphylococcus aureus, in disease onset and exacerbation. The holobiont theory supports the concept that interactions between host genetics and microbial communities contribute to AD pathogenesis. Conventional therapies can positively influence cutaneous dysbiosis and promote microbial balance. “Emollients plus,” containing prebiotics and bacterial lysates such as Vitreoscilla filiformis and Aquaphilus dolomiae, may increase microbial diversity and reduce AD flares. Topical corticosteroids, calcineurin inhibitors, biologics such as dupilumab and tralokinumab, AHR agonists, and phototherapy have also demonstrated beneficial effects on microbiota composition, particularly through reduction of S. aureus colonization. Innovative microbiome-targeted therapies are emerging, including probiotics, bacteriotherapy, phage therapy, antimicrobial peptides, quorum-sensing inhibitors, and topical ozone therapy. Preliminary studies suggest these approaches may restore microbial diversity and reduce inflammation, although evidence remains limited. Overall, modulation of the skin microbiome represents a promising complementary strategy for improving AD management and preventing disease exacerbation.