Details

Autor(en) / Beteiligte

• de la Fuente, Amanda
• López-Sánchez, Jaime
• Vaquero-Roncero, Luis Mario
• Merino García, María
• Sánchez Barrado, María Elisa
• Sánchez-Hernández, Miguel Vicente
• Garcia-Mateo, Nadia
• Rico-Feijoo, Jesús
• Muñoz-Bellvís, Luis
• González de Castro, Rafael
• Tedim, Ana P.
• Ortega, Alicia
• Abdel-lah Fernández, Omar
• Suárez-de-la-Rica, Alejandro
• Maseda, Emilio
• Trejo González, Ignacio
• García Carrera, Geovanna Liszeth
• Marcos-Vidal, José Miguel
• Nieto Arranz, Juan Manuel
• Chiscano-Camón, Luis
• Ferrer, Ricard
• Ruiz-Rodríguez, Juan Carlos
• González-López, Juan José
• Vila Fernández, José Alberto
• Prieto Carballo, Regina
• Lopez-Izquierdo, Raul
• Garrosa, Sonsoles
• Barón, Beatriz
• Esteban-Velasco, Carmen
• Aldecoa, César
• Bermejo-Martin, Jesús F.

Titel

Synergistic impact of innate immunity hyper-activation and endothelial dysfunction on the magnitude of organ failure in the infection-sepsis continuum

Ist Teil von

• International journal of infectious diseases, 2024-09, Vol.146, p.107142, Article 107142

Ort / Verlag

Canada: Elsevier Ltd

Erscheinungsjahr

2024

Quelle

EZB Electronic Journals Library

Beschreibungen/Notizen

• •We identified the biomarkers most associated with organ failure in infection.•The combination of lipocalin-2, interleukin-15, triggering receptor expressed on myeloid cells-1, angiopoietin-2 (Dys-4) score combined innate immunity and endothelial dysfunction biomarkers.•Dys-4 showed a greater impact on organ failure than individual biomarkers.•Dys-4 could help to detect and monitor organ failure in infection. Identifying host response biomarkers implicated in the emergence of organ failure during infection is key to improving the early detection of this complication. Twenty biomarkers of innate immunity, T-cell response, endothelial dysfunction, coagulation, and immunosuppression were profiled in 180 surgical patients with infections of diverse severity (IDS) and 53 with no infection (nIDS). Those better differentiating IDS/nIDS in the area under the curve were combined to test their association with the sequential organ failure assessment score by linear regression analysis in IDS. Results were validated in another IDS cohort of 174 patients. C-reactive protein, procalcitonin, pentraxin-3, lipocalin-2 (LCN2), tumoral necrosis factor-α, angiopoietin-2, triggering receptor expressed on myeloid cells-1 (TREM-1) and interleukin (IL)-15 yielded an area under the curve ≥0.75 to differentiate IDS from nIDS. The combination of LCN2, IL-15, TREM-1, angiopoietin-2 (Dys-4) showed the strongest association with sequential organ failure assessment score in IDS (adjusted regression coefficient; standard error; P): Dys-4 (3.55;0.44; <0.001), LCN2 (2.24; 0.28; <0.001), angiopoietin-2 (1.92; 0.33; <0.001), IL-15 (1.78; 0.40; <0.001), TREM-1(1.74; 0.46; <0.001), tumoral necrosis factor-α (1.60; 0.31; <0.001), pentraxin-3 (1.12; 0.18; <0.001), procalcitonin (0.85; 0.12; <0.001). Dys-4 provided similar results in the validation cohort. There is a synergistic impact of innate immunity hyper-activation (LCN2, IL-15, TREM-1) and endothelial dysfunction (angiopoietin-2) on the magnitude of organ failure during infection. [Display omitted]