Gut Microbiota in Psoriasis: Evidence for Dysbiosis, Pathological Mechanisms, Causality, and Therapeutic Implications

Abstract: Psoriasis is a chronic inflammatory skin disease driven by genetic susceptibility, environmental triggers, and immune dysregulation, with a global prevalence of approximately 2%– 3%. In recent years, the gut microbiota has garnered increasing attention as a key interface linking environmental factors to host immunity in the pathogenesis of psoriasis. A growing body of research has revealed significant gut dysbiosis in patients with psoriasis, characterized by reduced microbial diversity, depletion of specific beneficial bacteria, and enrichment of opportunistic pathogens. Mechanistically, the gut microbiota participates in the pathological process of psoriasis through modulation of the Th17/IL-23 axis, induction of regulatory T cell dysfunction, disruption of the intestinal barrier leading to bacterial translocation, and imbalance of microbial metabolites. Regarding causal evidence, germ-free animal models, fecal microbiota transplantation experiments, and Mendelian randomization studies have provided multi-level support for causal relationships between specific microbial taxa and psoriasis. Therapeutically, microbiota-targeting strategies including probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation have shown potential to ameliorate psoriasis severity in preclinical and preliminary clinical studies. This review systematically synthesizes the above evidence, delineates the characteristics of dysbiosis, pathological mechanisms, the causal evidence chain, and therapeutic translation prospects, and highlights current limitations and future directions. Keywords: psoriasis, gut microbiota, dysbiosis, Th17, gut–skin axis, fecal microbiota transplantation, probiotics