| A mysterious source is the cause of Kawasaki disease(KD),a type of short-term,self-limited vasculitis.The activation of certain inflammatory factors and immunoactive substances is the main source of inflammation in small and medium vessels,especially in children under 5 years of age.Acquired heart disease in children is most often caused by KD,and it is a possible risk factor for ischemic heart disease and sudden cardiac death in adults.Consequently,the physical and mental damage,as well as the financial strain,inflicted upon children and families is immense.Therefore,early detection and prompt treatment are crucial.The source of KD’s emergence is still a mystery.Research has demonstrated a correlation between the emergence and growth of KD and lipid metabolism disorder.Bioactive cytokines,secreted by adipose tissue,can stimulate the production of a variety of inflammatory cytokines and foster KD vascular inflammation.Leptin(LEP)is a pro-inflammatory adipocytokine,and more and more studies have shown that LEP is associated with systemic inflammatory response,immune system and vascular endothelial disease.Studies have found that high levels of leptin are observed during infection and inflammation.Leptin also maintains the balance of T cells,activates T cells,and triggers T cell differentiation to Th1.Polymorphism of leptin(LEP)gene rs2167270 is associated with pain in patients with osteoarthritis,which may play a role in the pathogenesis of atopic dermatitis,and leptin receptor(LEPR)gene rs1137100homozygous G/G genotype is significantly associated with an increased risk of cardiovascular disease.This study aims to investigate the potential association between LEP and LEPR levels and their gene polymorphisms and KD,and explore the genetic susceptibility mechanism of KD and its relationship with KD from the perspective of genetics.ObjectiveThis study aims to investigate the changes and clinical significance of LEP and LEPR levels in patients with KD,and explore the relationship between LEP gene rs2167270 A/G,LEPR gene rs 1137100 A/G gene polymorphism and susceptibility to KD,so as to provide scientific and reliable basis for the comprehensive prevention and treatment of KD and the study of pathogenesis.MethodsA case-control study was carried out.53 Han KD patients aged 6 months to 5 years old who were admitted in Zhuzhou Central Hospital from January 2021 to July 2022were selected as the KD group,and 53 Han children who underwent physical examination during the same period were selected as the control group.Serum levels of LEP and LEPR were measured by enzyme-linked immunosorbent assay(ELISA).The polymorphism of LEP gene rs 2167270 A/G and LEPR gene rs 1137100 A/G in each group was analyzed by polymerase chain reaction-restriction fragment length polymorphism analysis(PCR-RFLP),and their relationship with susceptibility to KD was investigated.Results1.The distribution frequency of AG genotype on LEPrs2167270 was significantly different between KD test group and control group(χ~2=6.334,P=0.021<0.05),and the difference was statistically significant(OR=3.380,95%CI:1.272～8.982,P=0.021).The AA genotype distribution frequency of LEP rs 2167270 was significantly lower than that of control group(χ~2=4.970,P=0.023<0.05),and the difference was statistically significant(OR=0.205,95%CI:0.054～0.776).There was no significant difference in the distribution of A and G alleles on LEP rs2167270 between KD test group and control group(P>0.05);2.There were no significant differences in genotype AA,AG,GG and allele distribution at LEPR rs1137100 between experimental group and control group(P>0.05).3.There were no statistical significance in serum LEP levels between LEPrs2167270 and LEPRrs1137100 SNP genotypes and alleles.4.There were no statistical significance in serum LEPR levels between LEPrs2167270 and LEPRrs1137100 SNP genotypes and alleles.5.LEP level in KD group was significantly higher than that in control group(0.290±0.055ng/m L VS 0.209±0.039ng/m L),and the difference was statistically significant by independent sample T-test(t=8.043,P<0.001).6.LEPR level in KD group was significantly higher than that in control group(10.951±2.53ng/m L VS 7.238±1.78ng/m L),and the difference was statistically significant by independent sample T-test(t=8.043,P<0.001).Conclusion1.LEP rs2167270 A/G locus gene polymorphism is associated with susceptibility to KD.GA genotype may be a risk factor,which may increase the incidence of KD,while AA genotype may be a protective factor,which may reduce the incidence of KD.2.There is no correlation between LEPR rs1137100 A/G polymorphism and KD.3.There was no correlation between the serum leptin(LEP)level and the genotypes of LEPrs2167270 and LEPRrs1137100 SNPs.4.There was no correlation between the serum leptin receptor(LEPR)level and the genotypes of LEPrs2167270 and LEPRrs1137100 SNPs.5.The concentrations of LEP and LEPR in KD group are significantly higher than those in control group,which may indicate that cytokines released in the pathogenesis of KD can stimulate the synthesis of LEP.At the same time,elevated LEP can directly act on immune cells to cause the proliferation and activation of cells(such as T lymphocytes),and high concentrations of LEP can directly affect peripheral blood mononuclear cells and activate immune cells through LEPRs.Certain inflammatory cytokines are secreted in direct proportion to the LEPR expression rate.High levels of LEP and LEPR may be a marker of inflammatory response activation in KD patients. |
