Interleukin-18 promoter gene polymorphisms in Chinese patients with systemic lupus erythematosus: association with CC genotype at position -607

<p><b>INTRODUCTION</b>Interleukin-18 (IL-18) is a Th1 cytokine, which is postulated to play a role in systemic lupus erythematosus (SLE). Two single nucleotide polymorphisms (SNPs) in the IL-18 promoter gene region were found to influence the quantitative expression of the IL-18 protein. The aim of this study was to determine whether IL-18 promoter gene polymorphisms are associated with SLE.</p><p><b>MATERIALS AND METHODS</b>One hundred and thirteen Chinese SLE patients and 218 Chinese healthy individuals were recruited. Genomic DNA was extracted from peripheral venous blood. Sequence-specific primer PCR and restriction fragment length polymorphism (RFLP) analysis were used to genotype the DNA samples for SNP-137 and SNP- 607. The following genotypes were obtained: SNP(-607) AA, AC, CC and SNP(-137) GG, GC, CC. Plasma IL-18 concentrations of patients and control subjects were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>the frequency of SNP-607/CC genotype was significantly higher in SLE patients (Pc < 0.05) while genotype SNP-607/AC was significantly decreased in SLE patients compared to the control group (Pc <0.05). Plasma IL-18 concentrations were significantly higher in SLE patients than in control subjects (P <0.05). Both patients and control subjects with CC and AC genotypes have significantly higher IL-18 concentrations than those with AA genotype.</p><p><b>CONCLUSION</b>The IL-18 promoter gene polymorphism SNP-607 C allele is associated with SLE and may result in the enhanced production of IL-18 protein in SLE and normal individuals.</p>

In vivo pro- and anti-inflammatory cytokines in normal and patients with rheumatoid arthritis

<p><b>INTRODUCTION</b>Rheumatoid arthritis (RA) is a chronic, deforming arthritis that can lead to disabilities and poor quality of life. Cytokines are protein mediators of inflammation and are produced as a result of the activation of various cellular reactions. They are the final mediators and/or regulators of the inflammatory process.</p><p><b>MATERIALS AND METHODS</b>The sera from 64 RA patients were assayed for both Th-1 and Th-2 related cytokines and soluble TNF-alpha receptors (IFN-gamma, TGF-beta, TNF-alpha, IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, sTNF-R1 and sTNFR2) using ELISA.</p><p><b>RESULTS</b>The pro-inflammatory cytokines (IL-1, IL-6, IL-8, IL-18 and TNF- alpha) were significantly elevated in RA patients, while TGF-beta, an immunomodulatory cytokine, was elevated in control individuals. When the RA patients were categorised as active or inactive based on DAS scores, similar cytokines profiles were observed in both RA sub-groups. However, assays of sTNF-R1 and sTNFR-2 were noted to be significantly elevated in inactive RA patients when compared to active patients.</p><p><b>CONCLUSION</b>Our findings indicate that local production of cytokine inhibitors is capable of diminishing disease activity and cytokine activity.</p>