@Article{,
AUTHOR = {Mirrin J. Dorresteijn, Peter Pickkers, Mihai G. Netea, Johannes G. Van der Hoeven},
TITLE = {IFN-γ is not induced through increased plasma concentrations of interleukin-12/interleukin-18 during human endotoxemia},
JOURNAL = {European Cytokine Network},
VOLUME = {16},
YEAR = {2005},
NUMBER = {3},
PAGES = {191--193},
URL = {http://www.techscience.com/ECN/v16n3/66212},
ISSN = {1952-4005},
ABSTRACT = {Endotoxin administration to animals and humans is an accepted experimental model of Gramnegative
sepsis, and endotoxin is believed to play a major role in triggering the activation of cytokines. In septic
patients, the IL-12/IL-18/IFN-γ axis is activated and correlates with mortality. Our aim was to investigate the
effects of endotoxin administration in humans on the activation of the IL-12/IL-18/IFN-γ axis. Seven healthy
volunteers received <i>E. coli</i> endotoxin (O:113). Hemodynamics, temperature and the course of plasma concentrations
of TNF-α, IL-1β, IL-12, IL-18 and IFN-γ were determined. Endotoxin administration resulted in the
expected flu-like symptoms, a temperature of 38.8 ± 0.3℃ (p < 0.003), a decrease in mean arterial blood pressure
of 14.8 ± 1.8 mmHg (p < 0.0002) and an increase in heart rate of 27.5 ± 4.8 bpm (p < 0.002) compared to baseline
values. TNF-a increased from 16.6 ± 8.2 to 927 ± 187 pg/mL (p < 0.003). IL-1b increased from 8.6 ± 0.5 to
25.3 ± 2.0 pg/mL (p < 0.0001). IL-12 showed no significant increase (8.2 ± 0.2 to 9.3 ± 0.8 pg/mL, p = 0.13), and all
IL-18 measurements remained below the level of detection. In contrast, IFN-γ showed an increase from
106.6 ± 57.1 to 152.7 ± 57.8 (p < 0.005). These results indicate that pathways other than the IL-12/IL-18 axis may
induce IFN-γ production in human endotoxemia.},
DOI = {}
}