The gut–skin axis in chronic urticaria: Role of gut dysbiosis in understanding of urticaria and its management

Chronic spontaneous urticaria (CSU) affects 0.5-1% of adults and involves mast cell degranulation leading to chronic hives and angioedema. Up to 40% of patients are resistant to conventional antihistamine therapy, necessitating alternative treatment strategies. Recent evidence implicates gut dysbiosis, characterized by altered microbial composition and reduced diversity, in the pathogenesis of CSU through the gut-skin axis. This review systematically examines the role of gut dysbiosis in CSU, including mechanistic pathways, associations with related gastrointestinal disorders, diagnostic biomarkers, and emerging microbiome-targeted therapeutic interventions. A comprehensive literature review was conducted using PubMed and additional scientific databases, covering studies published between 2010 and 2025. Search terms included “gut microbiota,” “chronic urticaria,” “dysbiosis,” “gut-skin axis,” “probiotics,” “biomarkers,” and “short-chain fatty acids.” Both mechanistic studies and clinical trials were included. Dysbiosis in CSU is characterized by reduced microbial a-diversity, depletion of short-chain fatty acid-producing bacteria ( Roseburia, Faecalibacterium ), and enrichment of pathogenic Proteobacteria ( Klebsiella pneumoniae, Escherichia coli ). These changes correlate with increased intestinal permeability, elevated serum lipopolysaccharide, and T-helper cell (Th)2/Th17-skewed immune responses. Associations with inflammatory bowel disease, irritable bowel syndrome, and Helicobacter pylori infection highlight shared inflammatory mechanisms. Therapeutic interventions targeting dysbiosis, including probiotics, prebiotics, fecal microbiota transplantation, and adjunctive dietary modifications, demonstrate clinical efficacy, with multi-strain probiotics reducing the urticaria activity score 7 (UAS7)by up to 60% in randomized controlled trials. Evidence supports dysbiosis as a significant contributor to CSU pathogenesis through immune dysregulation, barrier dysfunction, and metabolic alterations. Microbiome-targeted therapies offer promise as adjunctive treatment strategies, though large-scale, long-term clinical trials remain necessary to optimize therapeutic protocols, identify responder phenotypes, and establish clinical endpoints.