Lin Kun, Zhang Linyuan, Wang Yishuai, Li Jinqing, Xu Yufen, Che Di, Mai Hanran, Yu Hongyan, Fu Lanyan, Wei Bing, Jiang Zhiyong, Pi Lei, Gu Xiaoqiong
Department of Clinical Biological Resource Bank, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 510623, People's Republic of China.
Department of Blood Transfusion and Clinical Lab, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong, 510623, People's Republic of China.
J Inflamm Res. 2021 Jun 21;14:2633-2640. doi: 10.2147/JIR.S311956. eCollection 2021.
A large number of studies demonstrated that the key to the occurrence and development of Kawasaki disease (KD) is the over-activation of immune cells and the generation of various inflammatory factors, leading to the imbalance of the immune system. Recently, mutations in the FNDC1 gene have been shown to be associated with inflammatory responses. However, there have been no reports on the relationship between FNDC1 gene and KD so far.
We enrolled 1611 controls and 1459 patients with KD, including 372 patients with coronary artery aneurysm (CAA) and 179 patients with coronary artery lesion (CAL). The relationship between FNDC1 rs3003174 polymorphism and KD with CAA or without CAA was investigated.
This study showed no evidence that the association between FNDC1 rs3003174 C>T polymorphism and KD susceptibility was statistically significant (CT versus CC: adjusted odds ratio (OR) =0.897, 95% confidence interval (CI) =0.769-1.045, P=0.162; TT versus CC: adjusted OR=0.995, 95% CI=0.786-1.260, P=0.968; dominant model: adjusted OR=0.916, 95% CI=0.792-1.059, P=0.235; and recessive model: adjusted OR=1.055, 95% CI=0.845-1.316, P=0.638). However, our further stratified analysis in the control and KD group bore out that the incidence of TT genotype of FNDC1 rs3003174 C > T polymorphism was higher than that of CC/CT genotype in KD patients stratified by CAA (adjusted OR=1.437, 95% CI=1.034-1.996, P=0.031). Moreover, a stratified analysis of age and gender in KD patients indicated that the rs3003174 TT genotype increased the risk of CAA formation in aged ≦60 months (CC/CT vs TT: adjusted OR=1.580, 95% CI=1.106-2.259, P=0.012) and male (CC/CT vs TT: adjusted OR=1.653, 95% CI=1.101-2.481, P=0.015) KD patients.
The results of this study demonstrated that the FNDC1 rs3003174 C>T polymorphism may be a hazard factor in the formation of CAA in KD patients that was not disclosed before.
大量研究表明，川崎病（KD）发生发展的关键在于免疫细胞过度激活及多种炎症因子产生，导致免疫系统失衡。近期研究显示，FNDC1基因的突变与炎症反应相关。然而，目前尚无关于FNDC1基因与KD关系的报道。
我们纳入了1611名对照者和1459名KD患者，其中包括372例冠状动脉瘤（CAA）患者和179例冠状动脉病变（CAL）患者。研究了FNDC1 rs3003174多态性与伴有或不伴有CAA的KD之间的关系。
本研究未发现FNDC1 rs3003174 C>T多态性与KD易感性之间存在统计学显著关联的证据（CT与CC相比：调整后的优势比（OR）=0.897，95%置信区间（CI）=0.769-1.045，P=0.162；TT与CC相比：调整后的OR=0.995，95%CI=0.786-1.260，P=0.968；显性模型：调整后的OR=0.916，95%CI=0.792-1.059，P=0.235；隐性模型：调整后的OR=1.055，95%CI=0.845-1.316，P=0.638）。然而，我们在对照组和KD组中进一步分层分析发现，在按CAA分层的KD患者中，FNDC1 rs3003174 C>T多态性的TT基因型发生率高于CC/CT基因型（调整后的OR=1.437，95%CI=1.034-1.996，P=0.031）。此外，对KD患者的年龄和性别进行分层分析表明，rs3003174 TT基因型增加了年龄≤60个月（CC/CT与TT相比：调整后的OR=1.580，95%CI=1.106-2.259，P=0.012）和男性（CC/CT与TT相比：调整后的OR=1.653，95%CI=1.101-2.481，P=0.015）KD患者发生CAA的风险。
本研究结果表明，FNDC1 rs3003174 C>T多态性可能是KD患者中CAA形成的一个此前未被揭示的危险因素。
