Tumor necrosis factor α induction in human monocytes

Misuno, Natalia I.; Osipovich, Oleg; Sudarikov, Andrey; Idel'son, G. L.; Kolesnikova, T. S.; Panyutich, Alexander V.; Voitenok, Nikolai N.

doi:10.1016/1043-4666(90)90056-y

Cited by 7 publications

(3 citation statements)

References 16 publications

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“…We have shown before that SAC is a potent stimulator of TNF‐α production in whole blood [22]. Since TNF‐α was shown to decrease the expression of CXCR2 on PMN [32], we explored the effects of anti‐TNF‐α on down‐regulation of neutrophil CXCR2 and CXCR1 caused by SAC or LPS in whole blood.…”

Section: Resultsmentioning

confidence: 99%

“…In the present study, we examined the effects of killed S. aureus (SAC) on the expression of the IL‐8 receptors CXCR1 and CXCR2 on PMN . Killed S. aureus possess a natural combination of staphylococcal toxins and have been shown to be potent inducers of TNF‐α and other cytokines [22,23]. We report here the ability of SAC to down‐regulate CXCR1 and CXCR2 expression on PMN in the whole blood and total blood leucocyte fraction containing PMN and monocytes.…”

Section: Introductionmentioning

confidence: 82%

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Down-regulation of CXCR1 and CXCR2 expression on human neutrophils upon activation of whole blood byS. aureusis mediated by TNF-α

Tikhonov¹,

Doroshenko²,

Chaly³

et al. 2001

Clinical and Experimental Immunology

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SUMMARYIt was suggested that bacterial products can inhibit the expression of leucocyte chemokine receptors during sepsis and affect leucocyte functions in septic syndrome. Superantigens and toxins produced by Staphylococcus aureus are capable of activating leucocytes via binding to MHC-II antigens on monocytes and T-cell receptor molecules on T lymphocytes. It was recently shown that staphylococcal enterotoxins directly down-regulate the expression of CC chemokine receptors on monocytes through binding to MHC class II molecules. We studied the effects of killed S. aureus on the expression of interleukin-8 receptors, CXCR1 and CXCR2, on polymorphonuclear leucocytes (PMN), which are known to lack the expression of MHC-II antigens. It was shown that S. aureus down-regulated the cellsurface expression of CXCR1 and CXCR2 on PMN in the whole blood and total blood leucocyte fraction containing PMN and monocytes, but did not modulate IL-8 receptor expression in purified PMN suspension. Antibody to TNF-a abrogated down-regulation of IL-8 receptors induced by S. aureus. In contrast, LPS reduced CXCR1 and CXCR2 expression in purified PMN and whole blood in a TNF-aindependent manner. We further showed that TNF-a-induced decrease of CXCR1 and CXCR2 expression was associated with lower IL-8 binding and lower CXCR1 and CXCR2 mRNA levels, and was abrogated by protease inhibitors. We suggest that during septicemia, S. aureus may inhibit neutrophil responsiveness to IL-8 and other CXC chemokines via TNF-a-mediated down-regulation of CXCR1 and CXCR2.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 82%

Down-regulation of CXCR1 and CXCR2 expression on human neutrophils upon activation of whole blood byS. aureusis mediated by TNF-α

Tikhonov¹,

Doroshenko²,

Chaly³

et al. 2001

Clinical and Experimental Immunology

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“…F'our types of antibodies were used for the depletion of cytokines from MNCS: (i) anti-TNF-a MoAb (0001 mg/ml antibody neutralized cytotoxic effect of 50 ng/ml rTNF-a on fibroblast line L-929 [15]); (ii) anti-IL-8 MoAb (0001 mg/ml antibody neutralized binding of 500 ng/ml IL-8 with iL-8 receptor on cell line U-937. treated by vitamin E [16]); (iii)anti-IL-l/J antibody (0001 mg/ml antibody neutralized activity of 100 ng/ml rIL-I/i.…”

Section: Depletion Of Cytokines From Mncsmentioning

confidence: 99%

Mononuclear cells from HIV-infected patients produce factors which enhance functional activity of polymorphonuclear neutrophils from healthy subjects

Gabrilovich

Shepeleva

Serebrovskaya

et al. 1992

Clinical and Experimental Immunology

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SUMMARYThe influence of mononuclear cell supernatants (MNCS) from nine healthy donors and 35 HIVinfected patients (1.7 with lymphoadenopathy syndrome (LAS), 15 with ARC and three with AIDS) on functional activity of polymorphonuclear neutrophils (PMN) from healthy donors was investigated. MNC after short-term cultivation (24 h) produced factors which enhanced chemiluminescence (CL) and chemotaxis of PMN. This augmentation did not depend on stimulation of MNC by mitogens (lipopolysaccharide Escherichia coli (LPS) and concanavalin A (Con A)) or on activation of PMN by FMLP. After 48 h of cultivation only MNC stimulated by LPS produced these factors. MNCS from HIV-infected patients provoked a more pronounced augmentation of PMN CL compared with MNCS from healthy subjects. This enhancement was observed in patients at all stages of infection, but was more pronounced in patients with LAS. MNCS impact on PMN CL was not connected with proliferative activity of MNC but was correlated with the level of CD4 cells. It was shown that removal of adherent cells from MNC fraction resulted in decreased MNCS impact. Treatment of MNCS by antibody to IL-Ip, IL-8, interferon-alpha (IFN-oc) and tumour necrosis factor-alpha (TNF-a) did not decrease MNCS impact on PMN CL.

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A Leishmania protein that modulates interleukin (IL)‐12, IL‐10 and tumor necrosis factor‐α production and expression of B7‐1 in human monocyte‐derived antigen‐presenting cells

et al. 1997

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LeIF, a gene homologue of the eukaryotic initiation factor 4A was first described as a leishmanial antigen that induced a Th1-type T cell response in peripheral blood mononuclear cells (PBMC) from leishmaniasis patients. Moreover, the interferon (IFN)-gamma production by PBMC was found to be interleukin (IL)-12 dependent. Herein, we characterize the effects of LeIF on cytokine production and expression of surface molecules by normal human monocytes as well as by monocyte-derived macrophages and dendritic cells (MoDC). LeIF was a strong inducer of IL-12 and, to a lesser extent, of IL-10 and tumor necrosis factor (TNF)-alpha in macrophages and MoDC. IL-12 production did not require CD40 triggering, confirming that the ability of LeIF to induce IL-12 was not mediated through an effect on T cells. However, addition of soluble CD40 ligand (L) synergistically augmented IL-12 production in macrophages and MoDC. The cytokine-inducing activity of LeIF is located in the N-terminal portion of the molecule and was both proteinase K sensitive and polymyxin B resistant. LeIF, lipopolysaccharide and fixed Staphylococcus aureus all induced comparable amounts of IL-12, validating the potent cytokine-inducing effects of LeIF. Moreover, of these stimuli, LeIF had the highest IL-12/IL-10 and IL-12/TNF-alpha ratio demonstrating the preference of LeIF for IL-12 induction. Studies investigating the expression of surface molecules showed that LeIF up-regulated B7-1 and CD54 (ICAM-1) on macrophages and MoDC. To our knowledge this is the first report describing IL-12 production, up-regulation of co-stimulatory and intercellular adhesion molecules by monocytic antigen-presenting cells in response to a protein from a pathogenic microorganism. These immunomodulatory characteristics of LeIF might be excellent properties for a Th1-type adjuvant.

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Tumor necrosis factor α induction in human monocytes

Cited by 7 publications

References 16 publications

Down-regulation of CXCR1 and CXCR2 expression on human neutrophils upon activation of whole blood byS. aureusis mediated by TNF-α

Down-regulation of CXCR1 and CXCR2 expression on human neutrophils upon activation of whole blood byS. aureusis mediated by TNF-α

Mononuclear cells from HIV-infected patients produce factors which enhance functional activity of polymorphonuclear neutrophils from healthy subjects

A Leishmania protein that modulates interleukin (IL)‐12, IL‐10 and tumor necrosis factor‐α production and expression of B7‐1 in human monocyte‐derived antigen‐presenting cells

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