Gut microbiota–host immunity crosstalk in psoriasis: from dysbiosis to cutaneous inflammation

Abstract

Psoriasis is a chronic inflammatory skin disease driven by the IL-23/IL-17 axis. Evidence accumulated over the past decade indicates that its pathogenesis extends beyond the skin and involves bidirectional communication between the intestinal microbiota and host immunity. This narrative review organizes current evidence along a proposed sequence running from gut dysbiosis and intestinal barrier damage, through altered microbial metabolites, to reprogrammed host immune responses and cutaneous inflammation. We summarize the gut microbiota changes reported in patients with psoriasis and the clinical evidence for impaired intestinal permeability. We describe how microbiota-derived metabolites—short-chain fatty acids (SCFAs), tryptophan/kynurenine metabolites, and bile acids—modulate Th17/Treg balance and innate immunity through the aryl hydrocarbon receptor (AhR) and G protein-coupled receptors. We then review clinical data on microbiome-directed interventions, chiefly probiotics and fecal microbiota transplantation (FMT), and close with the outstanding issues in causal inference, methodological heterogeneity, and standardization of interventions. The current evidence is consistent with the gut–skin axis hypothesis. The direction of causality between the microbiota and psoriasis, the dose-response relationship, and the clinical benefit of microbiome-directed therapy nonetheless remain to be confirmed in prospective cohorts and well-designed randomized controlled trials.