Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.

J Skøt; P Kabrit; J E Hansen; Jens Ole Nielsen; Lars Nørregaard Nielsen; Jens Dilling Lundgren

Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.

Bidragets oversatte titel: Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.

J Skøt, P Kabrit, J E Hansen, Jens Ole Nielsen, Lars Nørregaard Nielsen, Jens Dilling Lundgren

Institut for Klinisk Medicin

3 Citationer (Scopus)

Abstract

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 PGE2 and LTB4 from human monocytes was evaluated after exposure to two strains of HIV (SSI-002 or HIV-1IIIB). After 16 h incubation with low doses of SSI-002, lipopolysaccharide-stimulated TNF-alpha production was enhanced 70-85% while PGE2 production was decreased. Heat-inactivated virus failed to alter the production of these mediators. Higher viral doses tended to decrease TNF-alpha and PGE2 production concomitantly, but this might be due to toxicity. HIV-1IIIB had no effect on either TNF-alpha or PGE2 production. Calcium ionophore-stimulated LTB4 production was doubled by HIV-1IIIB, but significantly decreased by SSI-002. Three or seven days after exposure to both HIV strains, increased PGE2 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.

Bidragets oversatte titel	Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.
Originalsprog	Engelsk
Tidsskrift	Acta Pathologica Microbiologica et Immunologica Scandinavica
Vol/bind	102
Udgave nummer	8
Sider (fra-til)	603-611
Antal sider	9
ISSN	0903-4641
Status	Udgivet - 1994

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http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7946262&query_hl=10

Citationsformater

Skøt, J., Kabrit, P., Hansen, J. E., Nielsen, J. O., Nielsen, L. N., & Lundgren, J. D. (1994). Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro. Acta Pathologica Microbiologica et Immunologica Scandinavica, 102(8), 603-611. http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7946262&query_hl=10

Skøt, J, Kabrit, P, Hansen, JE, Nielsen, JO, Nielsen, LN & Lundgren, JD 1994, 'Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.', Acta Pathologica Microbiologica et Immunologica Scandinavica, bind 102, nr. 8, s. 603-611. <http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7946262&query_hl=10>

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title = "Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.",

abstract = "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 PGE2 and LTB4 from human monocytes was evaluated after exposure to two strains of HIV (SSI-002 or HIV-1IIIB). After 16 h incubation with low doses of SSI-002, lipopolysaccharide-stimulated TNF-alpha production was enhanced 70-85% while PGE2 production was decreased. Heat-inactivated virus failed to alter the production of these mediators. Higher viral doses tended to decrease TNF-alpha and PGE2 production concomitantly, but this might be due to toxicity. HIV-1IIIB had no effect on either TNF-alpha or PGE2 production. Calcium ionophore-stimulated LTB4 production was doubled by HIV-1IIIB, but significantly decreased by SSI-002. Three or seven days after exposure to both HIV strains, increased PGE2 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.",

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year = "1994",

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T1 - Tumour necrosis factor and eicosanoid production from monocytes exposed to HIV in vitro.

AU - Skøt, J

AU - Kabrit, P

AU - Hansen, J E

AU - Nielsen, Jens Ole

AU - Nielsen, Lars Nørregaard

AU - Lundgren, Jens Dilling

PY - 1994

Y1 - 1994

N2 - 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 PGE2 and LTB4 from human monocytes was evaluated after exposure to two strains of HIV (SSI-002 or HIV-1IIIB). After 16 h incubation with low doses of SSI-002, lipopolysaccharide-stimulated TNF-alpha production was enhanced 70-85% while PGE2 production was decreased. Heat-inactivated virus failed to alter the production of these mediators. Higher viral doses tended to decrease TNF-alpha and PGE2 production concomitantly, but this might be due to toxicity. HIV-1IIIB had no effect on either TNF-alpha or PGE2 production. Calcium ionophore-stimulated LTB4 production was doubled by HIV-1IIIB, but significantly decreased by SSI-002. Three or seven days after exposure to both HIV strains, increased PGE2 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.

AB - 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 PGE2 and LTB4 from human monocytes was evaluated after exposure to two strains of HIV (SSI-002 or HIV-1IIIB). After 16 h incubation with low doses of SSI-002, lipopolysaccharide-stimulated TNF-alpha production was enhanced 70-85% while PGE2 production was decreased. Heat-inactivated virus failed to alter the production of these mediators. Higher viral doses tended to decrease TNF-alpha and PGE2 production concomitantly, but this might be due to toxicity. HIV-1IIIB had no effect on either TNF-alpha or PGE2 production. Calcium ionophore-stimulated LTB4 production was doubled by HIV-1IIIB, but significantly decreased by SSI-002. Three or seven days after exposure to both HIV strains, increased PGE2 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.

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