Kawasaki disease (KD) is an acute, immune-mediated medium-vessel vasculitis and the leading cause of acquired heart disease in children, yet its underlying etiology remains only partially defined. Emerging evidence implicates the gut microbiota as a key modulator of KD susceptibility, immune dysregulation, and therapeutic response. This narrative review aims to synthesise current insights linking gut microbial dysbiosis and microbial metabolites to the pathogenesis, clinical expression, and treatment of KD, and to explore microbiome-informed strategies with diagnostic and therapeutic potential. We conducted a comprehensive search of PubMed, Embase, Web of Science, and Google Scholar from database inception to April 2025 for English-language studies on Kawasaki disease and the gut microbiota, including terms related to microbiome, microbial dysbiosis, metabolites, pathogenesis, immunity, inflammation, and therapy. Reference lists of relevant articles and key reviews were also screened. Children with acute KD exhibit characteristic alterations in gut microbial composition, including an overrepresentation of Streptococcus species, depletion of short-chain fatty acid (SCFA)-producing taxa such as Faecalibacterium, Ruminococcus, and Roseburia, and a significant reduction in fecal butyrate. These changes have been associated with impaired intestinal barrier integrity, heightened NLRP3 inflammasome activation, and dysregulated cytokine signalling, contributing to systemic inflammation and vascular injury. Additional factors, such as antibiotic exposure and concurrent respiratory or oropharyngeal infections, can intensify dysbiosis and have been linked to resistance to intravenous immunoglobulin (IVIG) and an increased risk of coronary artery aneurysms. Conclusions: Gut microbial imbalance and metabolite disruption are likely associated with KD, potentially through interaction with host genetics and immune pathways. Microbiome-targeted approaches, including probiotics, dietary modulation, and metabolite-based therapies, hold promise for improving diagnostic precision, predicting treatment response, and guiding the development of targeted interventions in KD.
Mohsenzadeh et al. (Fri,) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: