Interleukin-10-induced HIV-1 expression is mediated by induction of both membrane-bound tumour necrosis factor (TNF)-α receptor type 1 in a promonocytic cell line

Barcellini, Wilma; Gp, Rizzardi; Jb, Marriott; Fain, C.; Rj, Shattock; Meroni, P.L.; Poli, Guido; Ag, Dalgleish

doi:10.1097/00002030-199607000-00006

Cited by 21 publications

(14 citation statements)

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“…We now report that high enough DA concentrations in the cell cytosol enable the cell to express TNF-R1 receptors and TNFa factor. A simultaneous overexpression of TNFa and TNF-R1, as a mechanism of possible autocrine cell control, was previously reported in other treatments, such as that of interleukine-10 in a promonocytic cell line [17] and, similarly, increased TNF-R1 expression preceding the upregulation of TNFa reported as an effect of bilirubin in astrocytes [18]. Treatment with 500 mM DA decreased cell viability by 40% after 12 h and this effect was attenuated to 20% by neutralizing TNFa with anti-TNFa.…”

Section: Discussionsupporting

confidence: 53%

Dopamine induces TNFα and TNF-R1 expression in SH-SY5Y human neuroblastoma cells

Gómez-Santos

Francisco²,

Giménez-Xavier³

et al. 2007

NeuroReport

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Cytotoxic concentrations of dopamine (100-500 microM DA) induce expression of tumour necrosis factor receptor-1 (TNF-R1) and tumour necrosis factor-alpha (TNFalpha) in SH-SY5Y human neuroblastoma cells. TNFalpha expression is dose-dependent and can also be detected after 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenylpyridinium iodide (MPP) treatment. The expression of TNF-R1 is also dose-dependent, but was not observed in 6-OHDA or MPP-treatment. Cells not expressing TNF-R1 were insensitive to TNFalpha, whereas those treated with DA showed a further decrease in viability when subsequently treated with TNFalpha. Thus, DA treatment confers sensitivity to TNFalpha. The decrease of cell viability caused by DA was in part prevented by neutralizing TNFalpha with anti-TNFalpha. As TNF-R1 is increased in substantia nigra of Parkinsonian brains, we suggest that nonvesiculated DA might also play a role in inducing TNF-R1 expression and predispose the neuron to the action of cytokines released in a microglia-mediated inflammatory response.

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Section: Discussionsupporting

confidence: 53%

Dopamine induces TNFα and TNF-R1 expression in SH-SY5Y human neuroblastoma cells

Gómez-Santos

Francisco²,

Giménez-Xavier³

et al. 2007

NeuroReport

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“…TNF bioactivity may be present in cultures despite the absence of detectable TNF protein. Induction of membrane-bound TNF has been observed in U1 cells, and cell surface-bound TNF may be functional by a juxtacrine mechanism despite the absence of measurable TNF (15). Therefore, we stimulated HIV synthesis in U1 cells with IL-1␤ in the presence or absence of the TNF inhibitor TNFbp.…”

Section: Resultsmentioning

confidence: 99%

Role of p38 mitogen-activated protein kinase in HIV type 1 production in vitro

Shapiro

Heidenreich

Meintzer

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

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The proinf lammatory cytokines interleukin (IL)-1 and tumor necrosis factor (TNF) promote HIV type 1 viral replication in vitro. In the present studies, HIV production was increased in the macrophagic U1 cell line expressing the HIV genome after exposure to IL-1␤, osmotic stress, or surface adhesion, suggesting a conf luence of signaling pathways for proinf lammatory cytokines and cell stressors. The p38 mitogen-activated protein kinase (MAPK) mediates both cytokine and stress responses; thus the role of this kinase in HIV production was investigated. HIV production as measured by p24 antigen correlated with changes in the expression of a specific (non-alpha) isoform of p38 MAPK. In the presence of a specific p38 MAPK inhibitor (p38 inh), IL-1␤-induced HIV production was suppressed by more than 90% and IL-1␤-induced IL-8 production was suppressed completely, both with IC 50 of 0.01 M. p38 inhibition blocked cell-associated p24 antigen and secreted virus to a similar extent. The p38 inh also decreased constitutive HIV production in freshly infected peripheral blood mononuclear cells by up to 50% (P < 0.05). Interruption of p38 MAPK activity represents a viable target for inhibition of HIV.

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“…Therefore, IL-18-induced TNF activity in U1 cells may be caused by cellsurface-associated TNF. Increased bioactive cell-surface TNF expression in IL-10-stimulated U1 cells has been documented by flow cytometry (43).…”

Section: Discussionmentioning

confidence: 98%