Polymorphisms in the NLRP3 gene and risk of primary gouty arthritis Corrigendum in /mmr/8/6/1888

Meng,Dong-Mei; Zhou,Yu-Jiao; Wang,Luan; Ren,Wei; Cui,Ling-Ling; Han,Lin; Qu,Zheng-Hai; Li,Chang-Gui; Zhao,Jia-Jun

doi:10.3892/mmr.2013.1429

Polymorphisms in the NLRP3 gene and risk of primary gouty arthritis

Corrigendum in: /mmr/8/6/1888

Authors:
- Dong-Mei Meng
- Yu-Jiao Zhou
- Luan Wang
- Wei Ren
- Ling-Ling Cui
- Lin Han
- Zheng-Hai Qu
- Chang-Gui Li
- Jia-Jun Zhao
View Affiliations

Affiliations: Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, P.R. China, Shandong Provincial Key Laboratory of Metabolic Diseases, Qingdao Key Laboratory of Common Disease Gout Laboratory, The Affiliated Hospital of Medical College, Qingdao University, Qingdao, Shandong 266003, P.R. China
Published online on: April 12, 2013 https://doi.org/10.3892/mmr.2013.1429
Pages: 1761-1766

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )

Metrics: Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )

Cited By (CrossRef): 0 citations Loading Articles...

Abstract

The aim of the present study was to investigate the association between genetic variants in 17 tagSNPs of the NLRP3 gene and the susceptibility to primary gouty arthritis. A genotype-phenotype analysis of 480 primary gout and 480 control patients was performed. Samples from all the patients were collected from The Affiliated Hospital of Medical College (Qingdao, China). Seventeen tagSNPs of the NLRP3 gene were amplified using polymerase chain reaction (PCR) and MassARRAY technology was used for single nucleotide polymorphism (SNP) genotyping. The genetic frequency of rs7512998 was significantly different between the gout and control patients (P<0.05), whereas no significant differences were identified for the remaining SNPs. The 17 SNPs conformed to the Hardy-Weinberg equilibrium (HWE) in the control group (P>0.05). The haplotype association among the 17 SNPs of the NLRP3 gene indicated that no individual SNP was significantly associated with primary gouty arthritis. CTATCAGCGCCCAGTGC was the most common haplotype in the case and control groups, with a frequency of 0.224 and 0.243, respectively. However, the odds ratios (ORs) of the 8 haplotypes were not identified to be significantly associated with gouty arthritis (P>0.05 for all the 8 haplotypes). To the best of our knowledge, this is the first study to investigate the association between SNPs of the NLRP3 gene and the risk of primary gouty arthritis, although no significant association was identified. Further clinical studies and functional analysis are required to explore the potential associations between NLRP3 gene polymorphisms and the risk of primary gouty arthritis.

View Figures

View References

1	Roddy E, Zhang W and Doherty M: The changing epidemiology of gout. Nat Clin Pract Rheumatol. 3:443–449. 2007. View Article : Google Scholar
2	Terkeltaub R: Gout in 2006: the perfect storm. Bull NYU Hosp Jt Dis. 64:82–86. 2006.PubMed/NCBI
3	Falasca GF: Metabolic diseases: gout. Clin Dermatol. 24:498–508. 2006. View Article : Google Scholar
4	Zaka R and Williams CJ: New developments in the epidemiology and genetics of gout. Curr Rheumatol Rep. 8:215–223. 2006. View Article : Google Scholar : PubMed/NCBI
5	Becker MA and Jolly M: Hyperuricemia and associated diseases. Rheum Dis Clin North Am. 32:275–293. 2006. View Article : Google Scholar : PubMed/NCBI
6	Mikuls TR and Saag KG: New insights into gout epidemiology. Curr Opin Rheumatol. 18:199–203. 2006. View Article : Google Scholar : PubMed/NCBI
7	Masseoud D, Rott K, Liu-Bryan R and Agudelo C: Overview of hyperuricaemia and gout. Curr Pharm Des. 11:4117–4124. 2005. View Article : Google Scholar : PubMed/NCBI
8	Choi HK, Ford ES, Li C and Curhan G: Prevalence of the metabolic syndrome in patients with gout: the Third National Health and Nutrition Examination Survey. Arthritis Rheum. 57:109–115. 2007. View Article : Google Scholar : PubMed/NCBI
9	Choi HK, De Vera MA and Krishnan E: Gout and the risk of type 2 diabetes among men with a high cardiovascular risk profile. Rheumatology (Oxford). 47:1567–1570. 2008. View Article : Google Scholar : PubMed/NCBI
10	Taniguchi A and Kamatani N: Control of renal uric acid excretion and gout. Curr Opin Rheumatol. 20:192–197. 2008. View Article : Google Scholar : PubMed/NCBI
11	Shima Y, Teruya K and Ohta H: Association between intronic SNP in urate-anion exchanger gene, SLC22A12, and serum uric acid levels in Japanese. Life Sci. 79:2234–2237. 2006. View Article : Google Scholar : PubMed/NCBI
12	Vázquez-Mellado J, Jiménez-Vaca AL, Cuevas-Covarrubias S, Alvarado-Romano V, Pozo-Molina G and Burgos-Vargas R: Molecular analysis of the SLC22A12 (URAT1) gene in patients with primary gout. Rheumatology (Oxford). 46:215–219. 2007.PubMed/NCBI
13	Miao ZM, Zhao SH, Yan SL, Li CG, Wang YG, Meng DM, Zhou L and Mi QS: NALP3 inflammasome functional polymorphisms and gout susceptibility. Cell Cycle. 8:27–30. 2009. View Article : Google Scholar : PubMed/NCBI
14	Miao ZM, Zhao SH, Wang YG, Li CG, Wang ZC, Chen Y, Chen XY and Yan SL: Epidemiological survey of hyperuricemia and gout in coastal areas of Shandong Province. Chin J Endocrinol Metab. 22:421–425. 2006.(In Chinese).
15	Jin C and Flavell RA: Molecular mechanism of NLRP3 inflammasome activation. J Clin Immunol. 30:628–631. 2010. View Article : Google Scholar : PubMed/NCBI
16	Agostini L, Martinon F, Burns K, McDermott MF, Hawkins PN and Tschopp J: NALP3 forms an IL-1beta-processing inflammasome with increased activity in Muckle-Wells autoinflammatory disorder. Immunity. 20:319–325. 2004. View Article : Google Scholar : PubMed/NCBI
17	Martinon F and Tschopp J: Inflammatory caspases: linking an intracellular innate immune system to autoinflammatory diseases. Cell. 117:561–574. 2004. View Article : Google Scholar : PubMed/NCBI
18	Miao Z, Li C, Chen Y, Zhao S, Wang Y, Wang Z, Chen X, Xu F, Wang F, Sun R, Hu J, Song W, Yan S and Wang CY: Dietary and lifestyle changes associated with high prevalence of hyperuricemia and gout in the Shandong coastal cities of Eastern China. J Rheumatol. 35:1859–1864. 2008.PubMed/NCBI
19	Martinon F: Mechanisms of uric acid crystal-mediated autoinflammation. Immunol Rev. 233:218–232. 2010. View Article : Google Scholar : PubMed/NCBI
20	Hoffman HM, Mueller JL, Broide DH, Wanderer AA and Kolodner RD: Mutation of a new gene encoding a putative pyrin-like protein causes familial cold autoinflammatory syndrome and Muckle-Wells syndrome. Nat Genet. 29:301–305. 2001. View Article : Google Scholar : PubMed/NCBI
21	Church LD, Cook GP and McDermott MF: Primer: inflammasomes and interleukin 1beta in inflammatory disorders. Nat Clin Pract Rheumatol. 4:34–42. 2008. View Article : Google Scholar : PubMed/NCBI
22	Pétrilli V and Martinon F: The inflammasome, autoinflammatory diseases, and gout. Joint Bone Spine. 74:571–576. 2007.PubMed/NCBI
23	Masters SL, Lobito AA, Chae J and Kastner DL: Recent advances in the molecular pathogenesis of hereditary recurrent fevers. Curr Opin Allergy Clin Immunol. 6:428–433. 2006. View Article : Google Scholar : PubMed/NCBI
24	Stojanov S and Kastner DL: Familial autoinflammatory diseases: genetics, pathogenesis and treatment. Curr Opin Rheumatol. 17:586–599. 2005. View Article : Google Scholar : PubMed/NCBI
25	Kastner DL: Hereditary periodic fever syndromes. Hematology Am Soc Hematol Educ Program. 74–81. 2005. View Article : Google Scholar
26	Wallace SL, Robinson H, Masi AT, Decker JL, McCarty DJ and Yü TF: Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheum. 20:895–900. 1977. View Article : Google Scholar : PubMed/NCBI
27	Barrett JC, Fry B, Maller J and Daly MJ: Haploview: analysis and visualization of LD and haplotype maps. Bioinformatics. 21:263–265. 2005. View Article : Google Scholar : PubMed/NCBI
28	Nakamura Y, Kambe N, Saito M, Nishikomori R, Kim YG, Murakami M, Núñez G and Matsue H: Mast cells mediate neutrophil recruitment and vascular leakage through the NLRP3 inflammasome in histamine-independent urticaria. J Exp Med. 206:1037–1046. 2009. View Article : Google Scholar : PubMed/NCBI
29	Mason DR, Beck PL and Muruve DA: Nucleotide-binding oligomerization domain-like receptors and inflammasomes in the pathogenesis of non-microbial inflammation and diseases. J Innate Immun. 4:16–30. 2012. View Article : Google Scholar : PubMed/NCBI
30	Yang CS, Shin DM and Jo EK: The Role of NLR-related Protein 3 Inflammasome in Host Defense and Inflammatory Diseases. Int Neurourol J. 16:2–12. 2012. View Article : Google Scholar : PubMed/NCBI
31	Villani AC, Lemire M, Fortin G, Louis E, Silverberg MS, et al: Common variants in the NLRP3 region contribute to Crohn’s disease susceptibility. Nat Genet. 41:71–76. 2009.
32	Vandanmagsar B, Youm YH, Ravussin A, Galgani JE, Stadler K, et al: The NLRP3 inflammasome instigates obesity-induced inflammation and insulin resistance. Nat Med. 17:179–188. 2011. View Article : Google Scholar : PubMed/NCBI
33	Serlin DM, Kuang PP, Subramanian M, O’Regan A, Li X, Berman JS and Goldstein RH: Interleukin-1beta induces osteopontin expression in pulmonary fibroblasts. J Cell Biochem. 97:519–529. 2006. View Article : Google Scholar : PubMed/NCBI
34	Qu Y, Ramachandra L, Mohr S, Franchi L, Harding CV, Nunez G and Dubyak GR: P2X7 receptor-stimulated secretion of MHC class II-containing exosomes requires the ASC/NLRP3 inflammasome but is independent of caspase-1. J Immunol. 182:5052–5062. 2009. View Article : Google Scholar : PubMed/NCBI
35	Eisenbarth SC, Colegio OR, O’Connor W, Sutterwala FS and Flavell RA: Crucial role for the Nalp3 inflammasome in the immunostimulatory properties of aluminium adjuvants. Nature. 453:1122–1126. 2008. View Article : Google Scholar
36	Wynn TA: Fibrotic disease and the T(H)1/T(H)2 paradigm. Nat Rev Immunol. 4:583–594. 2004. View Article : Google Scholar : PubMed/NCBI