Microbial Dysbiosis May Shape Psoriasis Pathogenesis Through the Gut-Skin Axis

A review examining the role of microbial dysbiosis in psoriasis proposes that the microbiome may serve as a central regulatory link between genetic susceptibility, immune dysregulation, and environmental triggers, with implications for understanding disease mechanisms and developing personalized treatment strategies.

Rather than viewing microbial changes as secondary associations, the authors describe a mechanistic framework connecting gut and skin dysbiosis with psoriasis-related inflammation. “This review provides a novel, in-depth synthesis arguing that microbial dysbiosis is not merely an associative phenomenon but a central regulatory node within this triad, actively shaping immune responses and clinical phenotypes,” the authors wrote.

According to the review, gut dysbiosis in psoriasis is characterized by reduced microbial diversity, a lower Bacteroidetes/Firmicutes ratio, and depletion of short-chain fatty acid (SCFA)-producing microbes. These changes may impair intestinal barrier integrity, reduce immunoregulatory signaling associated with SCFAs, and promote Th17 polarization, contributing to systemic inflammation that can affect the skin.

Cutaneous dysbiosis may further reinforce this inflammatory process. The authors highlighted Staphylococcus aureus dominance and fungal alterations as factors that can disrupt the skin barrier, provide persistent antigenic stimulation, and amplify IL-17-driven inflammation. Specific infections, including hepatitis C virus, Helicobacter pylori, and Streptococcus, may also act as environmental triggers through overlapping inflammatory pathways.

The review also described a bidirectional relationship between psoriasis therapies and the microbiome. Biologic treatments can produce drug-specific microbiome changes that may correlate with clinical normalization, although associated infection risks require consideration. Microbiome-directed strategies, including specific probiotics, have shown potential, but methodological inconsistencies currently limit their application.

The authors emphasized that establishing causality remains a key research challenge. “Future breakthroughs require a shift from correlation to mechanism,” they wrote.

Reference
Wang B, Zhang Y, Lin L, Wang S, Yang S. Psoriasis: microbiome dysbiosis and pathogenic mechanisms. Front Immunol. 2026;17:1714515. doi:10.3389/fimmu.2026.1714515