Psoriasis: microbiome dysbiosis and pathogenic mechanisms

Psoriasis is a chronic immune-mediated inflammatory disease whose pathogenesis is a triad of genetic predisposition, immune dysregulation, and environmental triggers. 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. We move beyond cataloging microbial shifts to construct a detailed mechanistic framework of the gut-skin axis. Gut dysbiosis; characterized by reduced diversity, a diminished Bacteroidetes/Firmicutes ratio, and depleted SCFA producers, compromises intestinal barrier integrity, reduces systemic immunoregulatory tone via diminished SCFA signaling, and promotes Th17 polarization. This systemic inflammation is directly communicated to the skin. Concurrently, cutaneous dysbiosis, featuringdominance and fungal alterations, disrupts the local barrier, provides chronic antigenic stimulation, and amplifies IL-17-driven inflammation, creating a self-sustaining loop. Crucially, we analyze how specific infections () act as environmental triggers by sharing or activating these very pathways. The bidirectional relationship with therapy is dissected: while biologics induce drug-specific microbiome shifts that often correlate with clinical normalization, they also carry infection risks that must be strategically managed. Emerging microbiome-targeted interventions like specific probiotics show promise but are hampered by methodological inconsistencies. This review uniquely highlights the causality gap and proposes that future breakthroughs require a shift from correlation to mechanism. We conclude that the microbiome is a dynamic interface between genes and environment in psoriasis; its successful integration into diagnostic and therapeutic paradigms demands standardized multi-omics approaches, functional validation, and personalized medicine strategies that target this critical axis.Staphylococcus aureusHCV, H. pylori, Streptococcus