Function is Dissociated From Activation-Related Immunophenotype on Phagocytes From Patients With SIRS/Sepsis Syndrome

ABSTRACTSepsis is a life-threatening condition associated with failure of at least one organ in the presence of infection. Along with SIRS, the acute systemic inflammatory syndrome without documented infection, sepsis represents a main health problem in intensive care units around the world. Hypercy...

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Veröffentlicht in:Shock (Augusta, Ga.) Ga.), 2019-11, Vol.52 (5), p.e68-e75
Hauptverfasser: Flores-Mejía, Luis A, Cabrera-Rivera, Graciela L, Ferat-Osorio, Eduardo, Mancilla-Herrera, Ismael, Torres-Rosas, Rafael, Boscó-Garate, Ilka B, López-Macías, Constantino, Isibasi, Armando, Cérbulo-Vazquez, Arturo, Arriaga-Pizano, Lourdes A
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Sprache:eng
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Zusammenfassung:ABSTRACTSepsis is a life-threatening condition associated with failure of at least one organ in the presence of infection. Along with SIRS, the acute systemic inflammatory syndrome without documented infection, sepsis represents a main health problem in intensive care units around the world. Hypercytokinemia and overexpression of activation-markers on leukocytes are frequently reported in SIRS/sepsis. Leukocyte functions including antibody mediated-phagocytosis, pathogen recognition, and migration appear to be disabled in SIRS/septic patients. Our aim was to evaluate the so-called activation immunophenotype and functions related to infection contention in phagocytes from patients with sepsis. We analyzed blood samples from 44 patients with SIRS/sepsis and 14 healthy volunteers. CD16, CD69, CD64, CCR7, and TREM-1 levels were determined on the surface of neutrophils and monocytes. Phagosome maturation and p38, STAT3, and STAT5 phosphorylation were evaluated in these phagocytes. As expected, sepsis and SIRS patients had increased serological levels of pro- and anti-inflammatory cytokines. E coli internalization was not increased in monocytes from patients with SIRS/sepsis, despite increased numbers of circulating neutrophils and monocytes (P 
ISSN:1073-2322
1540-0514
DOI:10.1097/SHK.0000000000001314