title: Solute carrier family 11 member A1 gene polymorphisms in reactive arthritis.
abstract: To investigate the role of SLC 11A1 polymorphisms in the development of reactive arthritis, 91 patients with reactive arthritis and 163 healthy controls were enrolled in this study. The SLC 11A1 polymorphisms were determined by the method of polymerase chain reaction/restriction fragment length polymorphism. The genotype distributions of SLC 11A1 274, 823, 1703, and 1729+ 55 del 4 were significantly different between the patients with reactive arthritis and controls. The genotype frequency of SLC 11A1 274C/C was significantly decreased in the patients with reactive arthritis when compared with that of the controls. In contrast, the SLC 11A1 274C/T showed a significant association with reactive arthritis. The patients with reactive arthritis have a significantly higher frequency of SLC 11A1 823C/C than the controls. However, SLC 11A1 823T/T was resistant to the development of reactive arthritis. The allele frequencies of SLC 11A1 274T and 823C were significantly increased in the patients with reactive arthritis in comparison with those of the controls, independent of HLA-B27. On the contrary, the allele frequencies of SLC 11A1 274C and 823T were significantly decreased in the patients with reactive arthritis. The estimated haplotype frequency of SLC 11A1 274C 823T 1703G 1729+55del 4 TGTG+ was significantly decreased in the patients with reactive arthritis when compared with that of the controls. In contrast, the estimated haplotype frequency of SLC 11A1 274T 823C 1703G 1729+55 del 4 TGTG+ was significantly increased in the patients with reactive arthritis. This study shows that the SLC 11A1 274T and 823C alleles are associated with susceptibility to reactive arthritis independently of HLA-B27 in Taiwan. The SLC 11A1 274T 823C 1703G 1729+55 del 4 TGTG+ haplotype is associated with the development of reactive arthritis in Taiwan. In contrast, the SLC 11A1 274C 823T 1703G 1729+55 del 4 TGTG+ haplotype may be a protective factor.
authors.affiliation: Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.
authors.forename: Yi-Jing
authors.initials: YJ
authors.lastname: Chen
authors.forename: Chia-Hui
authors.initials: CH
authors.lastname: Lin
authors.forename: Tsan-Teng
authors.initials: TT
authors.lastname: Ou
authors.forename: Cheng-Chin
authors.initials: CC
authors.lastname: Wu
authors.forename: Wen-Chan
authors.initials: WC
authors.lastname: Tsai
authors.forename: Hong-Wen
authors.initials: HW
authors.lastname: Liu
authors.forename: Jeng-Hsien
authors.initials: JH
authors.lastname: Yen
mesh_terms: D016918:Arthritis, Reactive / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology; D027682:Cation Transport Proteins / Q000235:genetics* / Q000276:immunology; D002690:Chlamydia Infections / Q000453:epidemiology / Q000235:genetics* / Q000276:immunology; D002692:Chlamydia trachomatis; D005260:Female; D005787:Gene Frequency; D005819:Genetic Markers; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006239:Haplotypes; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics; D008297:Male; D012150:Polymorphism, Restriction Fragment Length; D012307:Risk Factors; D013624:Taiwan / Q000453:epidemiology; D000099173:Natural Resistance-associated Macrophage Protein 1
chemical_list: D027682:Cation Transport Proteins; D005819:Genetic Markers; D000099173:Natural Resistance-associated Macrophage Protein 1