Interferon-gamma, interleukin-1 and tumour necrosis factor-alpha synthesis during experimental murine staphylococcal infection.

Several exotoxins of Staphylococcus aureus were shown to modulate the host immune system by stimulation of monokine release. BALB/c mice infected intravenously (i.v.) with live cells if S. aureus, strain Cowan 1, had a detectable serum level of TNF-alpha at 3, 4 and 5 h after injection. When S. epidermidis (strain E3380, clinical isolate) was used to infect mice, the level of TNF-alpha was lower (the detection limit of the cytotoxicity assay with WEHI cells was 40 pg ml-1). Kinetics of TNF synthesis was different from that observed in experimental infections caused by Gram-negative bacteria. Similarly to TNF-alpha, IL-1 alpha appears in a measurable level at 3 h after i.v. injection of bacteria. The highest serum level of IFN-gamma was observed 12 h after infection with both S. aureus and S. epidermidis. A quantity ten times more of S. epidermidis than of S. aureus cells was required to induce similar levels of TNF-alpha and IFN-gamma. Recombinant IFN-gamma administered in vivo in four daily doses followed by infection of S. aureus resulted in increased elimination of bacteria from the spleen, liver and peritoneal cavity of mice.