川崎病（Kawasaki disease, KD）是一种以全身性中小血管炎为核心病理特征的急性发热性疾病，好发于儿童期，其病因及发病机制尚未阐明。研究显示，肠道菌群失调可通过减少短链脂肪酸生成、激活核苷酸结合结构域富含亮氨酸重复序列和含热蛋白结构域受体3炎症小体等途径，加剧血管内皮损伤及系统性炎症反应；抗生素的应用可能进一步破坏菌群稳态，降低KD患者静脉注射免疫球蛋白的治疗应答率，并增加冠状动脉病变的发生风险。该文系统综述肠道菌群在KD中的特征性改变，以及抗生素通过“肠-血管轴”影响疾病预后的相关机制，为靶向菌群的干预策略提供理论依据。

Kawasaki disease (KD) is an acute febrile illness characterized by systemic vasculitis predominantly affecting small- and medium-sized arteries in children, and its etiology and pathogenesis remain unclear. Studies show that gut microbiota dysbiosis can aggravate vascular endothelial injury and systemic inflammation by reducing short-chain fatty acid production and activating the nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 inflammasome. Antibiotic use may further disrupt microbial homeostasis, decrease the response rate to intravenous immunoglobulin therapy in KD, and increase the risk of coronary artery lesions. This review systematically summarizes the characteristic alterations of the gut microbiota in KD and the mechanisms by which antibiotics influence disease prognosis via the gut-vascular axis, and provides a theoretical basis for microbiota-targeted interventions.