Tumor necrosis factor and eicosanoid production from monocytes infected with HIV in vitro.

Important note: Information in this article was accurate in 1993. The state of the art may have changed since the publication date.

Tumor necrosis factor and eicosanoid production from monocytes infected with HIV in vitro.

Int Conf AIDS. 1993 Jun 6-11;9(1):174 (abstract no. PO-A13-0239). Unique Identifier : AIDSLINE MED/93333673
Skot J; Kabrit P; Hansen JE; Nielsen JO; Arendrup M; Lundgren JD; Dept. of Infectious Diseases, Hvidovre Hospital, Denmark.

Abstract: OBJECTIVE: Investigate changes in production of inflammatory mediators (TNF and eicosanoid (prostaglandin E2 (PGE2) and leukotriene B4 (LTB4)) from human monocytes infected with HIV in vitro. METHODS: Monocytes were separated from healthy blood donors, and infected with different doses of HIV (JC10). TNF levels in supernatant after 16 h of coincubation with LPS (1 microgram/ml) and HIV were assayed by a cytotoxic assay (L929). Levels of eicosanoids in supernatant were assayed by radioimmunoassay--1/2 and 16 h post-HIV infection--after a 1 1/2 h incubation with fresh media. LTB4 production was induced by the calcium ionophore A23187 (0.5 microM). RESULTS: JC10 at concentrations of 1.5 and 15 CCID50/ml JC10 caused an increase in TNF production compared to controls (% increase (mean +/- SEM): 92% +/- 20 and 70% +/- 18, respectively), whereas 1500 CCID50/ml of JC10 tended to depress the TNF production (-38% +/- 24). Eicosanoid production was not affected by JC10 1/2 h post-HIV infection. However, 16 h post-HIV infection, 15 and 1500 CCID50/ml of JC10 both suppressed PGE2 production by 60% compared to controls, whereas only the lower concentration of JC10 suppressed LTB4 production. Heat-inactivated JC10 failed to influence TNF or eicosanoid production. CONCLUSIONS: Acute active infection of monocytes with low doses of JC10 stimulated TNF but suppressed eicosanoid production. Since PGE2 may suppress TNF production in monocytes, our data suggests that HIV prevents PGE2 synthesis leading to enhanced TNF production from monocytes. HIV at high doses suppressed the production of inflammatory mediators.

Keywords: *Eicosanoids/BIOSYNTHESIS *HIV Infections/METABOLISM *Monocytes/METABOLISM *Tumor Necrosis Factor/BIOSYNTHESIS
931130
M93B5423

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