Angiotensin-converting-enzyme inhibitors suppress synthesis of tumour necrosis factor and interleukin 1 by human peripheral blood mononuclear cells

Cytokine ◽  
1995 ◽  
Vol 7 (6) ◽  
pp. 526-533 ◽  
Author(s):  
Ralf Schindler ◽  
Charles A. Dinarello ◽  
Karl-M. Koch
Keyword(s):  
Tumour Necrosis ◽  
Mononuclear Cells ◽  
Enzyme Inhibitors ◽  
Human Peripheral Blood ◽  
Interleukin 1 ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor

scholarly journals Ricin induces the production of tumour necrosis factor-α and interleukin-1 β by human peripheral-blood mononuclear cells

1993 ◽  
Vol 294 (2) ◽  
pp. 517-520 ◽  
Author(s):  
F Licastro ◽  
M C Morini ◽  
A Bolognesi ◽  
F Stirpe
Keyword(s):  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Tumour Necrosis ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Interleukin 1 ◽  
Tnf Alpha ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Necrosis Factor

Ricin induced the release of tumour necrosis factor-alpha (TNF-alpha) and interleukin-1 beta by human peripheral-blood mononuclear cells in a dose- and time-dependent manner. The inhibition induced by ricin upon the phytohaemagglutinin (PHA)-driven lymphocyte proliferation was greater in cultures of mononuclear cells than that observed in monocyte-free cultures of lymphocytes, and was decreased after addition of an anti-TNF-alpha antibody to PHA-activated cultures. Low levels of TNF-alpha were detected in plasma from rats poisoned with ricin. These results suggest that ricin induced the release of macrophage-derived cytokines which may have a role in the pathogenesis of ricin toxic effects.

scholarly journals Immunomodulating Properties of the Antibiotic Novobiocin in Human Monocytes

1998 ◽  
Vol 42 (8) ◽  
pp. 1911-1916 ◽  
Author(s):  
Anja Lührmann ◽  
Jürgen Thölke ◽  
Ingrid Behn ◽  
Jens Schumann ◽  
Gisa Tiegs ◽  
...  
Keyword(s):  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Interleukin 1 ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Adp Ribosylation ◽  
Surface Molecules ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor

ABSTRACT We show that the coumeromycin antibiotic novobiocin, a potent inhibitor of ADP ribosylation, prevents lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-α), interleukin-1 (IL-1), IL-6, and IL-10 secretion in human peripheral blood mononuclear cells. It shares these cytokine-suppressing properties with other inhibitors of ADP ribosylation. We found that novobiocin prevents TNF-α production by inhibiting translation of the TNF-α mRNA. Elevated TNF-α levels in mice treated withd-galactosamine (GalN)-LPS or GalN-TNF were not reduced by novobiocin; however, the drug exhibited hepatoprotective properties. Novobiocin causes downregulation of the surface molecules on monocytes, among which CD14 was the most affected. The diminished expression of surface molecules was not observed on T and B lymphocytes. Similar to other inhibitors of ADP ribosylation, novobiocin prevents LPS-induced phosphate labelling of γ-actins.

Investigation of the Influenza-Like Symptoms Associated with Recombinant Human Erythropoietin Therapy

1997 ◽  
Vol 25 (3) ◽  
pp. 127-134 ◽  
Author(s):  
A Takemasa ◽  
N Yorioka ◽  
M Yamakido
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Recombinant Human Erythropoietin ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Tumour Necrosis Factor Α ◽  
Peripheral Blood Mononuclear ◽  
Human Erythropoietin ◽  
Factor Α ◽  
Necrosis Factor

The mechanism by which fever and influenza-like symptoms occur, after the administration of recombinant human erythropoietin (rHuEPO) to patients on continuous ambulatory peritoneal dialysis, was investigated. Peripheral blood mononuclear cells, obtained from two patients with fever and/or influenza-like symptoms related to the administration of rHuEPO for the treatment of anaemia were cultured with or without rHuEPO (100, 200, and 300 U/ml). Production of interleukin-1 β and tumour necrosis factor-α was higher in cultures with rHuEPO than in cultures without rHuEPO, although the dose relationships were not clear. These findings suggest that increased production of interleukin-1 β and tumour necrosis factor-α, induced by administration of rHuEPO, may cause fever and influenza-like smptoms.

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