Background It is suggested that interferon-gamma (IFN-gamma), like other cy
tokines, is a mediator in the host inflammatory response, which could be of
importance in the pathophysiology of sepsis. The role of IFN-gamma in huma
n host inflammatory responses, however, has not been studied.
Design In a placebo-controlled trial we studied the acute effects of IFN-ga
mma administration on host inflammatory mediators in healthy men: i.e. the
cytokine/chemokine cascade system, acute-phase proteins, activation markers
of the innate cellular immunity and coagulation/fibrinolysis parameters.
Results IFN-gamma increased plasma levels of interleukin-6 (IL-6), IL-8 and
IFN-gamma -inducible protein-10 (IP-10) (P < 0.05), but did not affect pla
sma levels of other cytokines (IL-4, IL-10, tumour necrosis factor-<alpha>,
IL-12p40/p70). Plasma concentrations of C-reactive protein and secretory p
hospholipase A2 both increased (P < 0.05). Plasma levels of the leucocyte a
ctivation marker elastase-<alpha>1-antitrypsin complexes increased after IF
N-gamma administration (P < 0.05, IFN-<gamma> increased the percentage of h
igh-affinity Fc gamma -receptor (Fc gamma RI) -positive neutrophils (P < 0.
05), but did not affect the mean fluorescence intensity of Fc<gamma>RI on n
eutrophils. Procoagulant and profibrinolytic effects of IFN-gamma were evid
enced by increased plasma levels of prothrombin fragment F1+F2, tissue-plas
minogen activator and plasmin-alpha2-antiplasmin complexes (P < 0.05).
Conclusion We conclude that IFN-<gamma> selectively affects host inflammato
ry mediators in humans.