TUMOR-NECROSIS-FACTOR AND EICOSANOID PRODUCTION FROM MONOCYTES EXPOSED TO HIV IN-VITRO

We investigated the hypothesis that exposure of monocytes to human immunodeficiency virus (HIV) augments production of proinflammatory mediators. The production of tumour necrosis factor alpha (TNF-alpha) and the eicosanoids PGE(2) and LTB(4) from human monocytes was evaluated after exposure to two strains of HIV (SSI-002 or HIV-1(IIIB)). After 16 h incubation with low doses of SSI-002, lipopolysaccharide-stimulated TNF-alpha production was enhanced 70-85% while PGE(2) production was decreased. Heat-inactivated virus failed to alter the production of these mediators. Higher viral doses tended to decrease TNF-alpha and PGE(2) production concomitantly, but this might be due to toxicity. HIV-1(IIIB) had no effect on either TNF-alpha or PGE(2) production. Calcium ionophore-stimulated LTB(4) production was doubled by HIV-1(IIIB) but significantly decreased by SSI-002 Three or seven days after exposure to both HIV strains, increased PGE(2) production was found. In conclusion, HIV only modestly altered the production of mediators from monocytes. The effects were strain-specific. In most experiments a second stimulus was required to demonstrate differences.