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Tumour necrosis factor and eicosanoid production from monocytes exposed to HTV in vitro
Author(s) -
SKØT J.,
KABRIT P.,
HANSEN J.E. S.,
NIELSEN J. O.,
LUNDGREN J. D.,
NIELSEN L.
Publication year - 1994
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1699-0463.1994.tb05210.x
Subject(s) - proinflammatory cytokine , tumor necrosis factor alpha , eicosanoid , lipopolysaccharide , in vitro , incubation , monocyte , immunology , chemistry , medicine , endocrinology , biology , inflammation , arachidonic acid , biochemistry , enzyme
We investigated the hypothesis that exposure of monocytes to human immunodeficiency virus (HIV) augments production of proinflammatory mediators. The production of tumour necrosis factor a (TNF‐α) 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‐α 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‐α and PGE 2 production concomitantly, but this might be due to toxicity. HIV‐1 IIIB had no effect on either TNF‐α or PGE 2 production. Calcium ionophore‐stimulated LTB 4 production was doubled by HIV‐l 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.