Increased nuclear factor kappa B activation in critically ill patients whodie

Citation
Rl. Paterson et al., Increased nuclear factor kappa B activation in critically ill patients whodie, CRIT CARE M, 28(4), 2000, pp. 1047-1051
Citations number
26
Categorie Soggetti
Aneshtesia & Intensive Care
Journal title
CRITICAL CARE MEDICINE
ISSN journal
00903493 → ACNP
Volume
28
Issue
4
Year of publication
2000
Pages
1047 - 1051
Database
ISI
SICI code
0090-3493(200004)28:4<1047:INFKBA>2.0.ZU;2-Q
Abstract
Objectives: To determine nuclear factor kappa B (NF kappa B) activation in mononuclear and neutrophils from critically ill patients and to compare NF kappa B activation with circulating concentrations of interleukin (IL)-6, I L-8, and soluble intercellular adhesion molecule (sICAM)-1. Design: Observational study. Setting: University Teaching Hospital, eight-bed intensive care unit in nor theast Scotland. Patients: Ten patients admitted to the intensive care unit who fulfilled th e criteria for systemic inflammatory response syndrome were studied at 0, 2 4, 48, and 72 hrs. Six healthy volunteers were also studied. Interventions: None. Measurements and Main Results: NF kappa B activation was significantly high er in patients compared to healthy volunteers in both neutrophils (p =.001) and mononuclear leukocytes (p =.013). In the six patients who survived to 96 hrs, the level of NF kappa B activation in mononuclear cells remained co nstant (p =.9). However, in the four patients who died before 96 hrs, monon uclear cell NF kappa B activation increased markedly and was significantly higher before death than in those who survived to 96 hrs (p =.0105). NF kap pa B activation in neutrophils similarly remained constant in patients who survived to 96 hrs (p =.4) but did not show the same increase before death. Circulating concentrations of IL-6, IL-8, and sICAM-1 were elevated but we re unrelated to leukocyte NF kappa B activation. Conclusions: We found NF kappa B activation in mononuclear and neutrophils in patients with systemic inflammatory response syndrome, which increased m arkedly before death in mononuclear leukocytes and was not related to plasm a IL-6, IL-8, and sICAM-1 concentrations. These data support the need for f urther study of the role of NF kappa B activation in mortality from systemi c inflammatory response syndrome and sepsis.