4.6 Article

Protective Effect of TNFRSF11A rs7239667 G > C Gene Polymorphism on Coronary Outcome of Kawasaki Disease in Southern Chinese Population

Journal

FRONTIERS IN GENETICS
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fgene.2021.691282

Keywords

Kawasaki disease (KD); coronary artery lesion (CAL); tumor necrosis factor receptor superfamily; single nucleotide polymorphisms (SNP); tumor necrosis factor superfamily

Funding

  1. Guangdong Natural Science Fund, China [2019A1515012061, 2021A1515011207]
  2. Guangzhou Science and Technology Program Project, China [201904010486, 202102010197]
  3. Guangzhou Service Center for Scholarly Exchange, China [011302026]
  4. Guangzhou Institute of Pediatrics, Guangzhou Women and Childrens Medical Center [3001127]
  5. Guangzhou Institute of Pediatrics/Guangzhou Women and Childrens Medical Center Fund, China [GCP-2019-003, GCP-2019-006, YIP-2019-050]

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The study found that the TNFRSF11A rs7239667 G > C polymorphism is not associated with susceptibility to KD, but the CC genotype may be a protective genetic factor for KD coronary artery damage. This protective effect is more significant in children with KD <= 60 months.
Background: The main symptoms of Kawasaki disease (KD) are inflammatory vasculitis characterized by fever lasting 1-2 weeks, failure to respond to antibiotic treatment, conjunctivitis, redness of the lips and mouth, strawberry tongue, and painless enlargement of the neck lymph nodes. Studies have been shown that tumor necrosis factor (TNF) and TNF receptor family members are abnormally expressed in the acute phase of Kawasaki disease, also revealing that these two play a significant role in the pathogenesis of KD. The purpose of our study is to determine the relationship between TNFRSF11A rs7239667 and the pathogenesis of KD and Coronary artery lesions in KD. Methods and Results: In this study, TNFRSF11A (rs7239667) genotyping was performed in 1396 patients with KD and 1673 healthy controls. Our results showed that G > C polymorphism of TNFRSF11A (rs7239667) was not associated with KD susceptibility. In addition, the patients with KD were divided into CAA and NCAA groups according to whether they had coronary artery aneurysm (CAA) or not, and the TNFRSF11A rs7239667 genotyping was performed in the two groups. After gender and age calibration, We found that genotype CC of TNFRSF11A may be a protective factor in KD coronary artery damage (adjusted OR = 0.69 95% CI = 0.49-0.99 P = 0.0429) and is more significant in children with KD <= 60 months (adjusted OR = 0.49 95% CI = 0.49-0.93 P = 0.0173). Conclusion Our study suggests that TNFRSF11A rs7239667 G > C polymorphism maybe play a protective gene role for the severity of KD coronary artery injury and is related to age, which has not been previously revealed.

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