ABSTRACT
Objective To explore the polymorphism of-592C/A of IL-10 gene promoter region in children with bronchial asthma and its relationship with serum concentration of IL-10.Methods Ninety-two children with bronchial asthma and 92 healthy children were selected for study,polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) were used for the analysis of-592C/A of IL-10 promoter region polymorphism.The frequencies of genotypes of IL-10 gene-592 locus (CC,CA and AA) and alleles were accounted respectively,and x2 test was used to analyze the difference between the groups.Enzyme-linked immunosorbent assay (ELISA) was used to measure the concentration of the serum IL-10,and F test and q test were used for statistical analysis.Results Compared with the healthy control group,there were significant differences in-592C/A polymorphism of IL-10 gene in asthma group.The frequencies of AA genotypes (56.5％) and A allele (73.9％) in asthma group were higher than those (34.8％,58.7％)in the control group,there were significant differences(x2 =9.32,P ＜ 0.01 ;x2 =8.87,P ＜ 0.005,respectively).The individuals with AA genotype and A allele were 3.25 (95 ％ CI:1.28-8.28,P ＜ 0.05) and 1.99 (95 ％ CI:1.28-3.08,P ＜0.01) times susceptible to asthma compared with CC genotype and C allele.The serum concentration of IL-10 in asthma group was significantly lower than that in healthy control group,whether in attacking-stage or remission-stage,and there were significant differences (all P ＜ 0.01).The individuals with AA genotypes had lower serum IL-10 concentration than those with CC genotypes (P ＜ 0.05) . Conclusions The IL-10 gene-592C/A polymorphism is different significantly between children with bronchial asthma and healthy ones,and this polymorphism influences the concentration of IL-10.The individuals with AA genotype have relatively lower IL-10 concentration,and A allele may be one of genetic susceptibility factor of bronchial asthma in children.
ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the association of serum leptin concentrations and polymorphisms of G1019A and A223G of leptin receptor gene (LEPR) with severe pre-eclampsia. MEHTODS: A case-control study was carried out in 207 patients with severe pre-eclampsia (SPE group) and 252 healthy pregnant women (control group) during the third trimester of pregnancy. The serum leptin was determined by enzyme-linked immunosorbent assay. The polymorphisms of LEPR gene G1019A and A223G were detected by polymerase chain reaction restriction-fragment length polymorphism (PCR-RFLP) analysis. Miettinen's test was used to estimate the odds ratios (OR) and 95% confidence intervals (CI).</p><p><b>RESULTS</b>(1) In severe pre-eclampsia group, serum leptin levels and rate of premature infant birth were significantly higher than that in normal pregnant women, and birth weight was lower than that in controls (P<0.01). (2) The frequencies of GA genotype and G allele for LEPR gene G1019A in SPE group (33.8% and 20.3%) were markedly higher than that in controls (19.8% and 15.1%) (P<0.01), and the carriers of GA genotype and G allele were more frequent in SPE group than in control group, resulting in an OR 2.04 (95%CI: 0.77-5.42) and 1.43 (95%CI: 1.02-2.01) to develop severe pre-eclampsia, compared with carriers of AA genotype and A allele. (3) AG genotype and A allele frequencies of LEPR gene A223G in SPE group (19.3% and 12.6%) were significantly lower than that in controls (34.5% and 19.2%) (P<0.01), resulting in an OR of 0.46 (95%CI: 0.30-0.71) and 0.60 (95%CI: 0.42-0.87) to develop severe pre-eclampsia, compared with subjects with GG genotype and G allele. (4) The "1019AA+223AG" genotype frequency was significantly lower in SPE group (6.8%) than in controls (24.6%) (P<0.01), resulting in an OR of 0.22 (95%CI: 0.12-0.39) to develop severe pr-eclampsia, while the "1019AA+223AG" was significantly higher in SPE group (22.2%) than in controls (11.9%) (P<0.05), resulting in an OR of 2.10 (95%CI: 0.78-3.45) to develop severe pre-eclampsia. (5) No significant differences were found in SBP, DBP, BMI and serum leptin levels in subjects with different genotypes in the two groups (P>0.05).</p><p><b>CONCLUSION</b>Elevated serum leptin level and LEPR gene G1019A and A223G polymorphisms might play a role in severe pre-eclampsia, while the level of serum leptin was not associated with genotypes of LEPR gene G1019A and A223G polymorphisms. The genotypes GA and "1019AA+223AG"of G1019A may be genetic susceptibility factors to severe pre-eclampsia.</p>