The association of NLRP3 and TNFRSF1A polymorphisms with risk of ankylosing spondylitis and treatment efficacy of etanercept

被引:23
作者
Zhao, Shengchun [1 ]
Chen, Hongwei [2 ]
Wu, Guolin [2 ]
Zhao, Chen [3 ]
机构
[1] Yiwu City Cent Hosp, Dept Orthopaed 2, Yiwu, Zhejiang, Peoples R China
[2] Yiwu City Cent Hosp, Dept Orthopaed, Yiwu, Zhejiang, Peoples R China
[3] Zhejiang Prov Peoples Hosp, Dept Orthopaed, Hangzhou, Zhejiang, Peoples R China
关键词
ankylosing spondylitis; etanercept; NLRP3; single nucleotide polymorphism; TNFRSF1A; CROHNS-DISEASE; RHEUMATOID-ARTHRITIS; HIV-1; INFECTION; GENE; SUSCEPTIBILITY; INFLAMMASOME; MANIFESTATIONS; POPULATION; PREDICTORS; VARIANTS;
D O I
10.1002/jcla.22138
中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
BackgroundTo discover how NLRP3 and TNFRSF1A polymorphisms affect the efficacy of traditional medicine and etanercept for ankylosing spondylitis (AS) patients. MethodsSingle nucleotide polymorphism (SNP) and haplotype analyses were conducted based on determined NLRP3 and TNFRSF1A among AS patients. We subsequently analyzed the relationship between relevant clinical indexes and polymorphisms of NLRP3 and TNFRSF1A. ResultsThe 4 SNP loci on NLRP3 and 3 SNP loci on TNFRSF1A showed significant linkage disequilibrium, respectively. The T allele of NLRP3 rs4612666 and the T allele of TFRSF1A rs4149570 are both associated with AS (P<.05). The T-A-C-T haplotype of NLRP3 as well as the G-C-C, T-C-C, T-C-T, and T-T-T haplotypes of TFRSF1A are associated with AS (P<.05). The morning stiffness time, BASDAI scoring, and ESR of patients receiving etanercept were significantly higher than those receiving traditional medicine. T allele of NLRP3 rs4612666 had a significantly greater negative impact on the ASAS20 improvement than C allele. Whereas the A allele of NLRP3 rs3806268 had a significantly greater positive impact on the ASAS20 improvement than G allele. There is no significant association between SNP and efficacy of traditional medicine in the treatment of AS. ConclusionNLRP3 and TFRSF1A (rs4149570) are associated with AS susceptibility. There is a significant association between NLRP3 polymorphisms and treatment of etanercept.
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页数:13
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共 46 条
[21]   Associations of functional NLRP3 polymorphisms with susceptibility to food-induced anaphylaxis and aspirin-induced asthma [J].
Hitomi, Yuki ;
Ebisawa, Motohiro ;
Tomikawa, Morimitsu ;
Imai, Takanori ;
Komata, Takatsugu ;
Hirota, Tomomitsu ;
Harada, Michishige ;
Sakashita, Masafumi ;
Suzuki, Yoichi ;
Shimojo, Naoki ;
Kohno, Yoichi ;
Fujita, Kimie ;
Miyatake, Akihiko ;
Doi, Satoru ;
Enomoto, Tadao ;
Taniguchi, Masami ;
Higashi, Noritaka ;
Nakamura, Yusuke ;
Tamari, Mayumi .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 2009, 124 (04) :779-785
[22]   The benefit/risk profile of TNF-blocking agents: Findings of a consensus panel [J].
Hochberg, MC ;
Lebwohl, MG ;
Plevy, SE ;
Hobbs, KF ;
Yocum, DE .
SEMINARS IN ARTHRITIS AND RHEUMATISM, 2005, 34 (06) :819-836
[23]   Predictors of response to anti-TNF-α therapy among patients with rheumatoid arthritis:: results from the British Society for Rheumatology Biologics Register [J].
Hyrich, K. L. ;
Watson, K. D. ;
Silman, A. J. ;
Symmons, D. P. M. .
RHEUMATOLOGY, 2006, 45 (12) :1558-1565
[24]   Genetic variation in proteins of the cryopyrin inflammasome influences susceptibility and severity of rheumatoid arthritis (The Swedish TIRA project) [J].
Kastbom, A. ;
Verma, D. ;
Eriksson, P. ;
Skogh, T. ;
Wingren, G. ;
Soederkvist, P. .
RHEUMATOLOGY, 2008, 47 (04) :415-417
[25]   Genetic variants in CARD8 but not in NLRP3 are associated with ankylosing spondylitis [J].
Kastbom, A. ;
Klingberg, E. ;
Verma, D. ;
Carlsten, H. ;
Forsblad-d'Elia, H. ;
Wesamaa, J. ;
Cedergren, J. ;
Eriksson, P. ;
Soderkvist, P. .
SCANDINAVIAN JOURNAL OF RHEUMATOLOGY, 2013, 42 (06) :465-468
[26]   Expansion of Immunologically-Relevant E. Coli in the Intestinal Microbiota of Patients with IBD-Associated Spondyloarthritis Promotes Mucosal RORgt-Dependent Immunity [J].
Kivolowitz, Charles ;
Abdulhamid, Ahmed ;
Victorio, Daniel ;
Castellanos, Jim ;
Simpson, Kenneth ;
Scherl, Ellen ;
Longman, Randy .
INFLAMMATORY BOWEL DISEASES, 2016, 22 :S3-S3
[27]   Autoinflammatory gene mutations in Behcet's disease [J].
Kone-Paut, I. ;
Sanchez, E. ;
Le Quellec, A. ;
Manna, R. ;
Touitou, I. .
ANNALS OF THE RHEUMATIC DISEASES, 2007, 66 (06) :832-834
[28]   Cardiomyopathy in Ankylosing Spondylitis [J].
Lui, Nai Lee ;
Thumboo, Julian ;
Inman, Robert .
ARTHRITIS CARE & RESEARCH, 2011, 63 (04) :564-569
[29]   The inflammasome:: A molecular platform triggering activation of inflammatory caspases and processing of proIL-β [J].
Martinon, F ;
Burns, K ;
Tschopp, J .
MOLECULAR CELL, 2002, 10 (02) :417-426
[30]   ANTI-TNF-α INHIBITORS: A NEW THERAPEUTIC APPROACH FOR INFLAMMATORY IMMUNE-MEDIATED DISEASES: AN UPDATE UPON EFFICACY AND ADVERSE EVENTS [J].
Murdaca, G. ;
Colombo, B. M. ;
Puppo, F. .
INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY, 2009, 22 (03) :557-565