| Autor: |
Palacios Y; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Ruiz A; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Ramón-Luing LA; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Ocaña-Guzman R; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Barreto-Rodriguez O; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Sánchez-Monciváis A; Laboratorio de Inmunología, Escuela Militar de Graduados de Sanidad, SEDENA, Mexico City 11200, Mexico., Tecuatzi-Cadena B; Laboratorio de Inmunología, Escuela Militar de Graduados de Sanidad, SEDENA, Mexico City 11200, Mexico., Regalado-García AG; Laboratorio de Inmunología, Escuela Militar de Graduados de Sanidad, SEDENA, Mexico City 11200, Mexico., Pineda-Gudiño RD; Hospital Central Militar, SEDENA, Mexico City 11200, Mexico., García-Martínez A; Hospital Central Militar, SEDENA, Mexico City 11200, Mexico., Juárez-Hernández F; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Farias-Contreras JP; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Fricke-Galindo I; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Pérez-Rubio G; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Falfán-Valencia R; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Buendia-Roldan I; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico., Medina-Quero K; Laboratorio de Inmunología, Escuela Militar de Graduados de Sanidad, SEDENA, Mexico City 11200, Mexico., Chavez-Galan L; Instituto Nacional de Enfermedades Respiratorias Ismael Cosío Villegas, Mexico City 14080, Mexico. |
| Abstrakt: |
Overproduction of inflammatory cytokines is a keystone event in COVID-19 pathogenesis; TNF and its receptors (TNFR1 and TNFR2) are critical pro-inflammatory molecules. ADAM17 releases the soluble (sol) forms of TNF, TNFR1, and TNFR2. This study evaluated TNF, TNFRs, and ADAM17 at the protein, transcriptional, and gene levels in COVID-19 patients with different levels of disease severity. In total, 102 patients were divided into mild, moderate, and severe condition groups. A group of healthy donors (HD; n = 25) was included. Our data showed that solTNFR1 and solTNFR2 were elevated among the COVID-19 patients ( p < 0.0001), without increasing the transcriptional level. Only solTNFR1 was higher in the severe group as compared to the mildly ill ( p < 0.01), and the level was higher in COVID-19 patients who died than those that survived ( p < 0.0001). The solTNFR1 level had a discrete negative correlation with C-reactive protein ( p = 0.006, Rho = -0.33). The solADAM17 level was higher in severe as compared to mild disease conditions ( p < 0.01), as well as in COVID-19 patients who died as compared to those that survived ( p < 0.001). Additionally, a potential association between polymorphism TNFRSF1A :rs767455 and a severe degree of disease was suggested. These data suggest that solTNFR1 and solADAM17 are increased in severe conditions. solTNFR1 should be considered a potential target in the development of new therapeutic options. |
