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首页> 外文期刊>International journal of immunogenetics >Polymorphisms in the promoter region of iNOS predispose to rheumatoid arthritis in south Indian Tamils
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Polymorphisms in the promoter region of iNOS predispose to rheumatoid arthritis in south Indian Tamils

机译：南印度泰米尔人in Inos启动子区的多态性易燃对类风湿性关节炎

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Nitric oxide synthase (NOS) catalyses the production of nitric o x ide (NO) from L-Arginine, which participates in diverse biological processes including inflammation and apoptosis. Macrophages, chondrocytes, osteoblasts and osteoclasts e x press inducible NOS (iNOS) at the site of synovial inflammation. NO produced at the inflamed joint may contribute to peri-articular bone loss, mediate apoptosis and regulate Th1/Th2 balance in rheumatoid arthritis (RA). Variations in the promoter region of NOS gene regulate the nitric o x ide synthase e x pression and iNOS (NOS2) polymorphisms have been associated with susceptibility to autoimmune disorders. Hence, this study was conducted to identify the possible contributions of NOS2 -1659G/A, -1026C/A, -277A/G promoter polymorphisms towards development of RA in South Indian Tamils. A total of 242 (219 females, 23 males) patients with RA (mean age 41.2 +/- 10.9years, disease duration 8.5 +/- 4.3years) and 279 age- and se x -matched healthy individuals of South Indian Tamil ethnicity were genotyped for NOS2 -1659C/T, -1026G/T and -277A/G promoter polymorphisms by TaqMan chemistry. Nature of disease (erosive or nonerosive), the presence of e x tra-articular manifestations, seropositivity for rheumatoid factor and anticyclic citrullinated peptide, serum C-reactive protein (CRP) level and response to therapy were assessed for all patients. The three single nucleotide polymorphisms (SNPs) were in Hardy-Weinberg equilibrium. The frequency of GG genotype and G allele of NOS2-277 was higher in patients (pc = 5.7 x 10(-9), OR = 6.09, 95% CI = 3.09-12.8 and pc = 4 x 10(-13), OR = 2.37, 95% CI = 2.06-3.62, respectively) compared to controls. Similarly, the frequency of NOS2-1026 (rs2779249) GT genotype and the T allele was higher in patients with RA (pc = .01, OR = 1.61, 95% CI = 1.09-2.36, and pc = .04, OR = 1.40, 95% CI = 1.02-1.91, respectively). However, no significant difference in frequency of NOS2-1659C/T polymorphism was observed between patients and controls. None of the studied SNPs were associated with erosive disease, seropositivity or e x tra-articular manifestations. The -277A/G and -1026G/T promoter polymorphisms in iNOS may confer susceptibility to RA in South Indian Tamils.
机译：一氧化氮合酶（NOS）催化了来自L-精氨酸的硝酸o X IDE（NO）的产生，该硝酸含量从L-精氨酸参与不同的生物过程，包括炎症和细胞凋亡。巨噬细胞，软骨细胞，成骨细胞和骨质糖细胞E X在滑膜炎症部位压诱导NoS（InOS）。在发炎的关节中没有产生可能有助于围关节骨质损失，介导细胞凋亡并调节类风湿性关节炎（RA）中的TH1 / TH2平衡。 NoS基因的启动子区域的变化调节硝酸o ide合酶E X压力和InOS（NOS2）多态性与自身免疫疾病的易感性有关。因此，该研究进行了鉴定NOS2 -1659G / A，-1026C / A，-277A / g启动子多态性对南印度泰米尔岛的发育的可能贡献。共有242名（219名女性，23名男性）患者（平均41.2 +/- 10.9年，疾病持续时间8.5 +/- 4.3years）和279岁和SE X-Matched Healthy的南印度泰米尔种族的健康个体Taqman化学的NOS2 -1659C / T，-1026g / t和-277A / g启动子多态性的基因分型。对所有患者评估了所有患者的疾病（腐蚀性或不整形），e X TRA关节表现的存在，类风湿因子和反应性蛋白质（CRP）水平和对治疗反应的血清阳性。三种单核苷酸多态性（SNPs）在Hardy-Weinberg平衡中。患者的GG基因型和G等位基因的频率较高（PC = 5.7×10（-9），或= 6.09,95％CI = 3.09-12.8和PC = 4×10（-13），或与对照相比，分别为2.37,95％CI = 2.06-3.62。类似地，NOS2-1026的频率（RS2779249）GT基因型和T等位基因在RA（PC = 0.01，或= 1.61,95％CI = 1.09-2.36和PC = .04，或= 1.40 ，95％CI = 1.02-1.91分别）。然而，在患者和对照之间观察到NOS2-1659C / T多态性的频率频率没有显着差异。没有研究的SNP与糜烂性疾病，血清阳性或E X TRA关节表现有关。 Inos中的-277A / g和-1026g / t启动子多态性可能会赋予南印度泰米尔岛的Ra。

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