Inflammasome Genes Polymorphisms and Susceptibility to Gout. Is There a Link?

• Denise Clavijo Cornejo ^[7] ; Alberto G. López Reyes ^[8] ; E. Cruz Arenas ^[9] ; Leonor Jacobo Albavera ^[1] ; Daniel Rivera Tlaltzicapa ^[2] ; Adriana Francisco Balderas ^[3] ; Mayra Domínguez Pérez ^[4] ; Pablo Romero Morelos ^[5] ; Janitzia Vázquez Mellado ^[6] ; Luis H. Silveira Torre ^[10] ; Carlos Pineda Villaseñor ^[7] ; Gabriela A. Martínez-Nava ^[10] ; Marwin Gutiérrez ^[7]
  1. [1] Instituto Nacional de Medicina Genómica

     Instituto Nacional de Medicina Genómica

     México

     
  2. [2] Universidad Autónoma Metropolitana

     Universidad Autónoma Metropolitana

     México

     
  3. [3] Instituto Politécnico Nacional

     Instituto Politécnico Nacional

     México

     
  4. [4] Universidad Estatal del Valle de Ecatepec

     Universidad Estatal del Valle de Ecatepec

     México

     
  5. [5] Hospital General de México

     Hospital General de México

     México

     
  6. [6] Instituto Nacional de Cardiología

     Instituto Nacional de Cardiología

     México

     
  7. [7] Division of Musculoskeletal and Rheumatic Diseases. Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City
  8. [8] Gerosciences Laboratory, and 3Hospital Epidemiological Surveillance Unit, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City
  9. [9] Hospital Epidemiological Surveillance Unit, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City
  10. [10] Synovial Fluid Laboratory, Instituto Nacional de Rehabilitación LGII, Mexico City, Mexico

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• Localización: Revista de investigación clínica, ISSN 0034-8376, ISSN-e 2564-8896, Vol. 74, Nº. 3, 2022, págs. 147-155
• Idioma: inglés
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• Resumen

  • Background: The inflammatory response in gout disease is induced by the activation of NLR family pyrin domain-containing 3 (NLPR3) signaling pathway mediated by IL-1β release. Objective: The objective of the study was to determine the association between single nucleotide polymorphisms (SNPs) within NLRP3 inflammasome genes and gout susceptibility. Methods: Mexican patients with gout from the National Rehabilitation Institute and General Hospital of Mexico were enrolled. A healthy control group was also included. We analyzed the frequency and allelic distribution of eight SNPs from seven different genes within the NLRP3 inflammasome signaling pathway: TLR4 rs2149356, CD14 rs2569190, NLRP3 rs3806268, NLRP3 rs10754558, CARD8 rs2043211, IL-1β rs1143623, P2RX7 rs3751142, and PPARGC1B rs45520937 SNPs. Results: We found that the SNP rs45520937 of PPARGC1B was associated with the risk of developing gout when it was analyzed using the dominant model (Odds ratio [OR] = 2.30; 95% confidence interval [CI]: 1.09-4.86; p = 0.030), and it is proposed that the adaptor molecule CD14 rs2569190 polymorphism could be associated with a lower risk of gout under an additive model (OR= 0.41;95% CI: 0.16-1.05; p = 0.064). No significant associations were identified for the remaining SNPs. Conclusion: Our findings suggest that the PPARGC1B rs45520937 SNP is associated with gout susceptibility.