Polymorphisms of interleukin 6 and interleukin 10 in Egyptian people with Behcet's disease.
Cytokines play critical roles in the pathogenesis of Behçet's disease (BD). They mediated many of the effectors and regulatory functions of immune and inflammatory responses. Many studies have linked Interleukin-6 (IL-6) and Interleukin-10 (IL-10) pathologically to BD. Thus, this study aimed to investigate the associations between IL-6 and IL-10 promoter single-nucleotide polymorphisms (SNPs) and the susceptibility to BD and their implication on plasma levels. We genotyped IL-6 -174 G/C (rs1800795) using Mutagenically Separated Polymerase Chain Reaction PCR (MS-PCR) and IL-10 -1082 G/A (rs1800896) and -819 C/T (rs1800871) using Sequence Specific Primer PCR (SSP-PCR) in 87 Egyptian patients and 97 controls. The plasma levels of IL-6 and IL-10 were measured using Enzyme-linked Immunosorbent Assay (ELISA). Significant increase in the frequency of -1082 GG genotype (P<0.05, OR=2.25, 95%CI=1.03-4.91) and significant decrease in the frequency of -1082 GA genotype (P<0.05, OR=0.53, 95%CI=0.29-0.96) was demonstrated in BD patients compare to controls. Patients with genital ulcer had significantly lower frequency of -1082 GG (P<0.05, OR 0.2, 95% CI=0.04-0.99) and G allele (P<0.05, OR=0.28, 95%CI=0.08-0.93), while patients with ocular manifestations had significantly higher frequency of -1082 G allele (P<0.01, OR=2.28, 95%CI=1.19-4.36). BD patients had significantly higher level of IL-6 (P<0.001) and significantly lower level of IL-10 (P<0.001) compared to controls. The changes in the level of cytokines were independent of any genotype of IL-6 or any genotype/haplotype of IL-10. Patients with active disease state had significantly higher level of IL-6 compared to patients in remission (P<0.05). In conclusion, our preliminary study indicates that the polymorphism at IL-10 -1082 G/A may play a role in BD susceptibility. The significant increase in IL-6 level and the significant decrease in IL-10 level in BD patients were independent of any particular genotype in IL-6 or any particular genotype/haplotype in IL-10.
Molecular Biology Department, Genetic Engineering and Biotechnology Research Institute (GEBRI), University of Sadat City, Egypt. Electronic address: Robamtalaat@yahoo.com.
Roba M
RM
Talaat
Molecular Biology Department, Genetic Engineering and Biotechnology Research Institute (GEBRI), University of Sadat City, Egypt; Center of Genomics, Helmy Institute, Zewail City of Science and Technology, Giza, Egypt.
Mohamed E
ME
Ashour
Rheumatology and Rehabilitation Department, Faculty of Medicine, Cairo University, Cairo, Egypt.
Iman H
IH
Bassyouni
National Liver Institute (NLI), Menufia University, Egypt.
Ahmed A
AA
Raouf
D000328:Adult; D001528:Behcet Syndrome / Q000235:genetics / Q000276:immunology*; D004252:DNA Mutational Analysis; D018450:Disease Progression; D004534:Egypt; D005260:Female; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics*; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics*; D008297:Male; D020641:Polymorphism, Single Nucleotide; D011401:Promoter Regions, Genetic / Q000235:genetics; D055815:Young Adult
D015850:Interleukin-6; D016753:Interleukin-10
Behçet's disease; Cytokines; IL-10; IL-6; Polymorphism; SNP