Yeh Yao-Tsung, Chen Kuang-Den, Huang Cheng-Hsieh, Tsai Jia-Rong, Kuo Ho-Chang
Aging and Diseases Prevention Research Center, Fooyin University, Kaohsiung, Taiwan.
Department of Medical Laboratory Science and Biotechnology, Fooyin University, Kaohsiung, Taiwan.
Virulence. 2025 Dec;16(1):2512401. doi: 10.1080/21505594.2025.2512401. Epub 2025 May 31.
Kawasaki Disease (KD) is a multisystemic vasculitis of unknown aetiology in children. The incidence of KD varies by geographic area and correlates with differences in gut microbiota patterns, with the highest incidence in Asian. This study aimed to investigate alterations in faecal microbiota and assess their relationship with systemic inflammation in KD patients. A total of 59 patients and 55 matched controls were included. Fecal samples were collected at the onset of KD. The V3/V4 regions of 16S rDNA were sequenced using the MiSeq platform. PICRUSt 2 was used to analyse the potential functional pathways involved in gut dysbiosis. Alpha ( < 0.042) and beta ( < 0.001) diversity in KD were significantly decreased when compared to the control group. After multivariate regression, among the seven critical microbes, increased ( = 0.016) and decreased Bacteroides ovatus ( = 0.014) could also predict KD risk using receiver operating characteristic curve (ROC) analysis (: area under the ROC curve, AUC = 0.841, odds ratio = 23.956; Bacteroides ovatus: AUC = 0.816, odds ratio = 31.365). Notably, was positively correlated with blood segment cells ( = 0.006), but negatively correlated with blood lymphocytes ( = 0.013). After multivariate regression, flavone and flavonol biosynthesis decreased in children with KD ( < 0.001). Our results indicated that both and may deregulate flavone and flavonol biosynthesis, consequently modulating immune cells and potentially triggering KD. This study suggests that alterations in the gut microbiota are closely associated with immune responses and provides a new perspective on the aetiology, pathogenesis, and treatment of KD.
川崎病（KD）是一种病因不明的儿童多系统血管炎。KD的发病率因地理区域而异，与肠道微生物群模式的差异相关，亚洲地区发病率最高。本研究旨在调查KD患者粪便微生物群的变化，并评估它们与全身炎症的关系。共纳入59例患者和55例匹配的对照。在KD发病时采集粪便样本。使用MiSeq平台对16S rDNA的V3/V4区域进行测序。PICRUSt 2用于分析肠道生态失调所涉及的潜在功能途径。与对照组相比，KD组的α（<0.042）和β（<0.001）多样性显著降低。多因素回归分析后，在七种关键微生物中，使用受试者工作特征曲线（ROC）分析，[微生物名称未给出]增加（P=0.016）和卵形拟杆菌减少（P=0.014）也可预测KD风险（[微生物名称未给出]：ROC曲线下面积，AUC=0.841，比值比=23.956；卵形拟杆菌：AUC=0.816，比值比=31.365）。值得注意的是，[微生物名称未给出]与血液中的分段细胞呈正相关（P=0.006），但与血液淋巴细胞呈负相关（P=0.013）。多因素回归分析后，KD患儿中黄酮和黄酮醇生物合成减少（P<0.001）。我们的结果表明，[微生物名称未给出]和[微生物名称未给出]都可能失调黄酮和黄酮醇生物合成，从而调节免疫细胞并可能引发KD。本研究表明肠道微生物群的改变与免疫反应密切相关，并为KD的病因、发病机制和治疗提供了新的视角。
