Wang Ji-Gan, Dou Hui-Hong, Liang Qiong-You
Department of Pediatrics, Maternal and Child Health Hospital of Guangxi Zhuang Autonomous Region, Guangxi Clinical Research Center for Pediatric Diseases, Nanning, China.
Pediatr Res. 2025 Feb 10. doi: 10.1038/s41390-025-03911-7.
This study investigates the causal relationship between gut microbiota, inflammatory cytokines, and Kawasaki disease (KD), and whether cytokines mediate the effect of gut microbiota on KD.
A Mendelian randomization analysis using the inverse-variance weighted method assessed the causal effects of gut microbiota and inflammatory cytokines on KD and explored potential mediation.
The study found causal links between 20 types of gut microbiota and KD. Ten types increased KD risk, notably Francisellales (OR = 27.82, P = 0.0309). Ten types provided protection, with Fusobacteriaceae showing the strongest effect (OR = 0.0424, P = 0.002). Five inflammatory cytokines were significantly associated with KD; adenosine deaminase was most protective (OR = 0.7447, P = 0.0037), while Fractalkine indicated higher risk (OR = 2.0448, P = 0.0315). Mediation analysis revealed that the Interleukin-10 receptor subunit beta mediates the effect of Bifidobacterium adolescentis on KD, with a mediation effect of -0.0237 (4.75% ratio). Interleukin-20 mediates the effect of Faecalicatena lactaris on KD, with a mediation effect of -0.1168 (15.30% ratio).
The findings indicate a causal relationship among gut microbiota, inflammatory cytokines, and KD, suggesting that the gut microbiome influences KD through specific cytokines.
The study confirmed a causal relationship between 20 types of gut microbiota and Kawasaki disease, finding that 10 types increase the risk of Kawasaki disease, particularly Francisellales. Five inflammatory cytokines were significantly associated with Kawasaki disease, with adenosine deaminase showing a protective effect, while Fractalkine increased the risk. Mediation analysis indicated that specific inflammatory cytokines (such as Interleukin-10 receptor subunit beta and Interleukin-20) play a significant mediating role between gut microbiota and Kawasaki disease.
本研究调查肠道微生物群、炎性细胞因子与川崎病（KD）之间的因果关系，以及细胞因子是否介导肠道微生物群对KD的影响。
采用逆方差加权法进行孟德尔随机化分析，评估肠道微生物群和炎性细胞因子对KD的因果效应，并探索潜在的中介作用。
该研究发现20种肠道微生物群与KD之间存在因果联系。10种增加了KD风险，特别是弗朗西斯菌目（OR = 27.82，P = 0.0309）。10种具有保护作用，其中梭杆菌科的作用最强（OR = 0.0424，P = 0.002）。5种炎性细胞因子与KD显著相关；腺苷脱氨酶的保护作用最强（OR = 0.7447，P = 0.0037），而趋化因子表明风险更高（OR = 2.0448，P = 0.0315）。中介分析显示，白细胞介素-10受体亚基β介导青春双歧杆菌对KD 的影响，中介效应为-0.0237（比例为4.75%）。白细胞介素-20介导乳酸粪球菌对KD的影响，中介效应为-0.1168（比例为15.30%）。
研究结果表明肠道微生物群、炎性细胞因子与KD之间存在因果关系，提示肠道微生物组通过特定细胞因子影响KD。
该研究证实了20种肠道微生物群与川崎病之间的因果关系，发现10种会增加川崎病风险，尤其是弗朗西斯菌目。5种炎性细胞因子与川崎病显著相关，腺苷脱氨酶具有保护作用，而趋化因子增加风险。中介分析表明，特定炎性细胞因子（如白细胞介素-10受体亚基β和白细胞介素-20）在肠道微生物群和川崎病之间起重要中介作用。
