scholarly journals Tumour necrosis factor α augments the inhibitory effects of CTLA‐4‐Ig on osteoclast generation from human monocytes via induction of CD80 expression

2019 ◽  
Vol 196 (3) ◽  
pp. 392-402
Author(s):  
K. Oi ◽  
T. Tokunaga ◽  
T. Kuranobu ◽  
K. Yukawa ◽  
H. Kohno ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Human Monocytes ◽  
Tumour Necrosis Factor Α ◽  
Inhibitory Effects ◽  
Factor Α ◽  
Necrosis Factor

Dietary beta-carotene supplementation modulates the production of tumour necrosis factor-α by human monocytes

1996 ◽  
Vol 24 (3) ◽  
pp. 387S-387S ◽  
Author(s):  
DAVID A. HUGHES ◽  
PAUL M. FINGLAS ◽  
ANTHONY J.A. WRIGHT ◽  
ABIGAEL C.J. PEERLESS ◽  
ANGELA L. BAILEY ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Beta Carotene ◽  
Human Monocytes ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Macrophage-mediated lysis of a β-cell line, tumour necrosis factor-α release from bacillus Calmette–Gue´rin (BCG)-activated murine macrophages and interleukin-8 release from human monocytes are dependent on extracellular glutamine concentration and glutamine metabolism

1999 ◽  
Vol 96 (1) ◽  
pp. 89-97
Author(s):  
Colin MURPHY ◽  
Philip NEWSHOLME
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Cytokine Production ◽  
Glutamine Metabolism ◽  
Human Monocytes ◽  
Tumour Necrosis Factor Α ◽  
Glutamine Concentration ◽  
Β Cell ◽  
Factor Α ◽  
Necrosis Factor

Macrophages and monocytes are cells with a large capacity for cytokine production. Cytokines produced by these cells are not preformed and released upon stimulation, but must be transcribed and translated. Although much is known concerning the regulation of the latter processes at the molecular level, the role of exogenous amino acids in the secretory process has not been actively investigated. Glutamine is utilized by macrophages at a much faster rate than any other amino acid. The role for high rates of glutamine utilization in macrophages or monocytes is not fully understood. We demonstrate here that the rates of lipopolysaccharide-stimulated tumour necrosis factor-α secretion from bacillus Calmette–Guérin (BCG)-activated murine peritoneal macrophages and lipopolysaccharide-stimulated interleukin-8 production from human monocytes are dependent upon extracellular glutamine concentration. We also demonstrate that potent inhibition of cytokine production can be achieved by incubating macrophages or monocytes in the presence of the glutaminase inhibitor 6-diazo-5-oxo-norleucine. On co-culture of BCG-activated macrophages and the clonal pancreatic β-cell line BRIN-BD11, macrophage-specific β-cell death was significantly reduced on prior exposure of macrophages to 6-diazo-5-oxo-norleucine. Thus glutamine metabolism may be essential for generation of cytotoxic products from macrophages, including tumour necrosis factor-α.

Paradoxical effects of tumour necrosis factor-α on rat granulosa cell DNA synthesis

2002 ◽  
Vol 14 (3) ◽  
pp. 133 ◽  
Author(s):  
Guillermo M. Lanuza ◽  
Patricia E. Saragüeta ◽  
Ursula A. Bussmann ◽  
J. Lino Barañao
Keyword(s):  
Dna Synthesis ◽  
Tumour Necrosis Factor ◽  
Granulosa Cell ◽  
Tumour Necrosis ◽  
Inhibitory Action ◽  
Tumour Necrosis Factor Α ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumour necrosis factor- α (TNF-α ) has been proposed as an intraovarian modulator of granulosa cell function. The effect of TNF-α on DNA synthesis in cultured rat granulosa cells was examined. Tumour necrosis factor-α stimulated thymidine incorporation when added in the presence of transforming growth factor-β (TGF-β). In contrast, the co-mitogenic effect of follicle-stimulating hormone (FSH) and TGF-β was inhibited in a dose-dependent manner by TNF-α . Inhibition of FSH-dependent DNA synthesis by TNF-α was also found when cultures were co-stimulated with activin A. The inhibitory action of TNF-α on FSH-treated cultures was not associated with changes in cell viability. The inhibitory effects of TNF-α could not be solely explained by a decrease in cAMP levels, since TNF-α was also able to inhibit the stimulation by dibutyryl-cAMP and TGF-β on granulosa cell DNA synthesis. These results suggest that TNF-α regulation of granulosa cell growth is elicited either independently or downstream from gonadotrophin-induced cAMP production. The actions of TNF-α could be only partially mimicked by a cell-permeable analogue of ceramide, thus indicating that actions of this cytokine can not be fully ascribed to an activation of sphingomyelinase. Data presented here indicate that, in addition to its previously demonstrated inhibitory effects on gonadotrophin-induced cell differentiation, TNF-α may also exert a marked inhibition on hormonally stimulated immature granulosa cell proliferation. In contrast to this inhibitory action, this cytokine could amplify the mitogenic action of putative intraovarian growth regulators such as TGF-β. These observations add further support to the notion that TNF-α plays a physiological role as a paracrine modulator of follicle development and may be also relevant to the alteration of ovarian function during physiopathological processes.

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