| Autor: |
Pulito-Cueto V; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Rheumatology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Sebastián Mora-Gil M; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Rheumatology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Ferrer-Pargada D; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Remuzgo-Martínez S; Valdecilla Research Institute (IDIVAL), 39011 Santander, Spain., Genre F; Valdecilla Research Institute (IDIVAL), 39011 Santander, Spain., Lera-Gómez L; Department of Microbiology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Alonso-Lecue P; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Batista-Liz JC; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Rheumatology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Tello-Mena S; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Abascal-Bolado B; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Izquierdo S; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Ruiz-Cubillán JJ; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Armiñanzas-Castillo C; Department of Infectious Diseases, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Blanco R; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Rheumatology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., González-Gay MA; School of Medicine, University of Cantabria, 39011 Santander, Spain.; Department of Rheumatology, IIS-Fundación Jiménez Díaz, 28040 Madrid, Spain., López-Mejías R; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Rheumatology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain., Cifrián JM; Immunopathology Group, Marqués de Valdecilla University Hospital-Valdecilla Research Institute (IDIVAL), 39008 Santander, Spain.; Department of Pneumology, Marqués de Valdecilla University Hospital, 39008 Santander, Spain.; School of Medicine, University of Cantabria, 39011 Santander, Spain. |
| Abstrakt: |
The most critical forms of coronavirus disease 2019 (COVID-19) are associated with excessive activation of the inflammasome. Despite the COVID-19 impact on public health, we still do not fully understand the mechanisms by which the inflammatory response influences disease prognosis. Accordingly, we aimed to elucidate the role of polymorphisms in the key genes of the formation and signaling of the inflammasome as biomarkers of COVID-19 severity. For this purpose, a large and well-defined cohort of 377 COVID-19 patients with mild (n = 72), moderate (n = 84), severe (n = 100), and critical (n = 121) infections were included. A total of 24 polymorphisms located in inflammasome-related genes ( NLRP3 , NLRC4 , NLRP1 , CARD8 , CASP1 , IL1B , IL18 , NFKB1 , ATG16L1 , and MIF ) were genotyped in all of the patients and in the 192 healthy controls (HCs) (who were without COVID-19 at the time of and before the study) by RT-qPCR. Our results showed that patients with mild, moderate, severe, and critical COVID-19 presented similar allelic and genotypic distribution in all the variants studied. No statistically significant differences in the haplotypic distribution of NLRP3 , NLRC4 , NLRP1 , CARD8 , CASP1 , IL1B , and ATG16L1 were observed between COVID-19 patients, who were stratified by disease severity. Each stratified group of patients presented a similar genetic distribution to the HCs. In conclusion, our results suggest that the inflammasome polymorphisms studied are not associated with the worsening of COVID-19. |
