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<p>Kawasaki disease (KD) is an acute, self-limiting systemic vasculitis of early childhood and remains the leading cause of acquired heart disease in developed nations. Despite decades of investigation, its etiology and immunopathogenesis are still not fully understood. This review integrates nearly six decades of histopathological, epidemiological, and immunological research to examine infection-driven mechanisms underlying KD. Current evidence indicates that KD may result from a convergence of microbial and host factors: viral infections can trigger mucosal IgA-mediated immune activation; superantigens may induce T-cell receptor (TCR) Vβ–skewed cytokine release; conventional antigens appear to elicit oligoclonal adaptive immune responses consistent with infection-associated vasculitis; and gut microbiota dysbiosis may amplify systemic inflammation through disruption of intestinal barrier integrity and short-chain fatty acid metabolism. Rather than a single-pathogen infection, KD likely reflects infection-triggered immune dysregulation in genetically susceptible children. By contrasting these mechanistic hypotheses, this review highlights the need for longitudinal, multi-omics studies integrating metagenomic, transcriptomic, and serologic analyses to delineate causal microbial signatures, identify diagnostic biomarkers, and guide precision immunomodulatory strategies for this complex pediatric vasculitis.</p>

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Potential Mechanisms and Hypotheses for Pathogenic Microorganisms Triggering Kawasaki Disease

  • 期刊论文

  • 发表日期：

    2025年12月22日

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  • Jinhan Yu,
  • Linlin Cheng,
  • Haoting Zhan,
  • Yuan Huang,
  • Siyu Wang,
  • Haolong Li,
  • Yongmei Liu,
  • Yingchun Xu,
  • Ye Guo,
  • Yongzhe Li

摘要

Kawasaki disease (KD) is an acute, self-limiting systemic vasculitis of early childhood and remains the leading cause of acquired heart disease in developed nations. Despite decades of investigation, its etiology and immunopathogenesis are still not fully understood. This review integrates nearly six decades of histopathological, epidemiological, and immunological research to examine infection-driven mechanisms underlying KD. Current evidence indicates that KD may result from a convergence of microbial and host factors: viral infections can trigger mucosal IgA-mediated immune activation; superantigens may induce T-cell receptor (TCR) Vβ–skewed cytokine release; conventional antigens appear to elicit oligoclonal adaptive immune responses consistent with infection-associated vasculitis; and gut microbiota dysbiosis may amplify systemic inflammation through disruption of intestinal barrier integrity and short-chain fatty acid metabolism. Rather than a single-pathogen infection, KD likely reflects infection-triggered immune dysregulation in genetically susceptible children. By contrasting these mechanistic hypotheses, this review highlights the need for longitudinal, multi-omics studies integrating metagenomic, transcriptomic, and serologic analyses to delineate causal microbial signatures, identify diagnostic biomarkers, and guide precision immunomodulatory strategies for this complex pediatric vasculitis.