DYSBIOSIS AND INFLAMMATORY DERMATOSES: ATOPIC DERMATITIS, ACNE, AND PSORIASIS

The skin microbiota is a dynamic ecosystem that plays a critical role in maintaining epidermal barrier integrity, preserving immune homeostasis, and providing defense against pathogens. Disruption of this ecosystemal balance as a result of genetic predisposition, environmental stressors, hormonal changes, and immune regulatory disturbances is defined as dysbiosis and constitutes a fundamental biological component of inflammatory dermatoses such as atopic dermatitis, acne vulgaris, and psoriasis. In atopic dermatitis, filaggrin mutations, epigenetic alterations, and environmental triggers weaken the epidermal barrier, while reduced microbial diversity and increased colonization by Staphylococcus aureus markedly influence the clinical course of the disease. This process, in conjunction with excessive activation of the type 2 cytokine axis (IL-4, IL-13, IL-31, and TSLP), deepens inflammation and perpetuates the itch–scratch cycle. Acne vulgaris, in contrast, is associated not only with an increased burden of Cutibacterium acnes but also with the predominance of specific acne-associated strains, disruption of commensal microbial balance, and the amplification of TLR/NLRP3-mediated inflammatory responses. In this context, the qualitative characteristics of the microbial composition, rather than its quantitative abundance, are decisive in disease pathogenesis. In psoriasis, a distinct dysbiosis pattern has been described, characterized by an increase in Staphylococcus and Streptococcus species and a reduction in commensal bacteria, particularly Cutibacterium. These alterations contribute to the maintenance of chronic inflammatory processes through enhanced dendritic cell activation and amplification of the Th1/Th17/Th22 axis. In conclusion, the common pathophysiological basis shared by these three inflammatory dermatoses is a self-perpetuating cyclical process driven by the interplay between epidermal barrier dysfunction, loss of microbial diversity, and maladaptive immune responses. Therefore, strategies aimed at restoring microbial balance including commensal-based approaches, probiotic interventions, and targeted microbiota modulation hold significant translational potential for the future management of inflammatory dermatoses.