Y H Lee1, S-C Bae2. 1. Division of Rheumatology, Department of Internal Medicine, Korea University College of Medicine, Seoul, Korea lyhcgh@korea.ac.kr. 2. Department of Rheumatology, Hanyang University Hospital for Rheumatic Diseases, Seoul, Korea.
Abstract
OBJECTIVE: This study determined whether NLRP3 polymorphisms rs35829419 C/A and rs10754558 C/G were associated with autoimmune and inflammatory diseases. METHODS: An association between the NLRP3 rs35829419 C/A and rs10754558 C/G polymorphisms and autoimmune and inflammatory diseases was determined by performing a meta-analysis by using (1) allele contrast, (2) recessive, (3) dominant, and (4) co-dominant models. RESULTS: Thirty comparative studies involving 8069 patients and 8824 controls were included in the meta-analysis. No association was observed between autoimmune and inflammatory diseases and NLRP3 rs35829419 C allele (OR = 1.020, 95% CI = 0.804-1.295, p = 0.869). Stratification by ethnicity showed no association between the NLRP3 rs35829419 C allele and autoimmune and inflammatory diseases in European, Latin American, and Polynesian populations. Stratification by disease type showed no association between the NLRP3 rs35829419 C allele and gout, SLE, RA, celiac disease, and Crohn's disease. Moreover, no association was observed between autoimmune and inflammatory diseases and the NLRP3 rs10754558 C allele (OR = 1.057, 95% CI = 0.950-1.177, p = 0.310). However, stratification by ethnicity showed an association between the NLRP3 rs10754558 C allele and autoimmune and inflammatory diseases in the Latin American (OR = 1.399, 95% CI = 1.201-1.630, p = 1.6 × 10-6) but not in European and Asian populations. Further, stratification by disease type showed a significant association of the NLRP3 rs10754558 C allele with SLE (OR = 1.465 95% CI = 1.144-1.875, p = 0.002) but not with gout and celiac disease. The same pattern was observed for the NLRP3 rs10754558 C allele in the recessive model. CONCLUSIONS: Our results indicated that the NLRP3 rs10754558 C/G polymorphism was associated with susceptibility to SLE and with autoimmune and inflammatory diseases in Latin American individuals.
OBJECTIVE: This study determined whether NLRP3 polymorphisms rs35829419 C/A and rs10754558 C/G were associated with autoimmune and inflammatory diseases. METHODS: An association between the NLRP3rs35829419 C/A and rs10754558 C/G polymorphisms and autoimmune and inflammatory diseases was determined by performing a meta-analysis by using (1) allele contrast, (2) recessive, (3) dominant, and (4) co-dominant models. RESULTS: Thirty comparative studies involving 8069 patients and 8824 controls were included in the meta-analysis. No association was observed between autoimmune and inflammatory diseases and NLRP3rs35829419 C allele (OR = 1.020, 95% CI = 0.804-1.295, p = 0.869). Stratification by ethnicity showed no association between the NLRP3rs35829419 C allele and autoimmune and inflammatory diseases in European, Latin American, and Polynesian populations. Stratification by disease type showed no association between the NLRP3rs35829419 C allele and gout, SLE, RA, celiac disease, and Crohn's disease. Moreover, no association was observed between autoimmune and inflammatory diseases and the NLRP3rs10754558 C allele (OR = 1.057, 95% CI = 0.950-1.177, p = 0.310). However, stratification by ethnicity showed an association between the NLRP3rs10754558 C allele and autoimmune and inflammatory diseases in the Latin American (OR = 1.399, 95% CI = 1.201-1.630, p = 1.6 × 10-6) but not in European and Asian populations. Further, stratification by disease type showed a significant association of the NLRP3rs10754558 C allele with SLE (OR = 1.465 95% CI = 1.144-1.875, p = 0.002) but not with gout and celiac disease. The same pattern was observed for the NLRP3rs10754558 C allele in the recessive model. CONCLUSIONS: Our results indicated that the NLRP3rs10754558 C/G polymorphism was associated with susceptibility to SLE and with autoimmune and inflammatory diseases in Latin American individuals.
Authors: Hector Gonzalez-Pacheco; Gilberto Vargas-Alarcon; Javier Angeles-Martinez; Carlos Martinez-Sanchez; Oscar Perez-Mendez; Gabriel Herrera-Maya; Marco Antonio Martinez-Rios; Marco Antonio Peña-Duque; Carlos Posadas-Romero; Jose Manuel Fragoso Journal: Immunol Res Date: 2017-08 Impact factor: 2.829