Enhancement of plasma levels of tumor necrosis factor alpha but not interleukin-6 following endotoxin injection of Friend leukemia virus infected mice.

Friend leukemia virus complex (FLC) infection of BALB/c mice causes a rapid, progressive suppression of most immune functions. In the present study, FLC infection resulted in increased induction by bacterial lipopolysaccharide (LPS) of tumor necrosis factor alpha (TNF alpha) but not IL-6. TNF alpha levels were significantly elevated beginning 11 days post infection and increasing levels were measured through day 21. The highest TNF alpha levels in FCL-infected mice were as much as 100-fold higher than in LPS treated non-infected mice. Peak plasma levels of TNF alpha were seen between 1 and 2 hr after LPS induction, as compared to a peak at 1 hr in controls. The ability of LPS to stimulate TNF alpha was concentration dependent over a range of 0.005 to 50 micrograms per mouse. Using anti-TNF alpha antiserum, cytotoxic activity of plasma was shown to be due specifically to TNF alpha. These data suggest that induction of TNF alpha and IL-6 is regulated by different mechanisms in FLC-infected mice.