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It is currently being understood that most of the agents modulating host response in sepsis have failed because they act to refrain an over-exaggerated immune response whereas immunoparalysis takes place on the time of their administration. The effect of IFNγ on immunoparalysis of monocytes in sepsis was assessed.
Blood was isolated within the first 24 hours from the advent of signs of sepsis from 10 healthy donors and from 33 patients; 14 with sepsis and 19 with severe sepsis/shock. Peripheral blood mononuclear cells (PBMCs) were isolated and stimulated with 10 ng/ml LPS; 5 μg/ml Pam3Cys; and heat-killed isolates of Candida albicans, multidrug-resistant Pseudomonas aeruginosa and methicillin-resistant Staphylococcus aureus (MRSA). Stimulations were done in the absence and presence of 10 ng/ml IFNγ. Concentrations of cytokines were estimated in supernatants by an enzyme immunoassay.
Effects of IFNγ on the release of TNFα are shown in Figure Figure1.1. Open bars represent stimulation in the absence of IFNγ and solid bars stimulation in the presence of IFNγ. Asterisks signify differences compared with the absence of IFNγ. IL-6 and IL-1β had similar kinetics to TNFα.
IFNγ reverses in vitro sepsis-induced immunoparalysis of monocytes. The type of affected cytokine depends on the agonist and probably reflects the mechanism of action of IFNγ.