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.

Effect of the antirheumatic agent Tenidap on CD3, CD4, and CD8 expression and interleukin-1 and leukotriene B4 secretion in human peripheral blood mononuclear cells

1994 ◽  
Vol 72 (9-10) ◽  
pp. 397-402 ◽  
Author(s):  
Pio Conti ◽  
Marcella Reale ◽  
Renato C. Barbacane ◽  
Stephano Stuard ◽  
Fernanda Placido
Keyword(s):  
T Cell ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Interleukin 1 ◽  
Inhibitory Effect ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Antirheumatic Agent

Thymocytes that express the complete CD3−T-cell receptor (TCR) complex are CD4− and CD8−. The CD4+ T-cell population can be subdivided into at least two quite distinct subsets, TH1 and TH2 cells, based upon cytokine expression. Interleukin-1 (IL-1) appears to be required for optimal proliferation of T cells in response to antigen and it seems that in the absence of IL-1, TH2 clones proliferate less in response to antigen. Tenidap is an antirheumatic agent that has an inhibitory effect on IL-1 production. In these studies, we show that isolated human peripheral blood mononuclear cells (PBMCs) treated in vitro with Tenidap (15 μg/mL) for 48-h incubations significantly (p < 0.05) enhanced the present of CD4+ expression compared with untreated cells (control), as determined by cytofluorimetric analysis. Lipopolysaccharide and Bacillus Calmette-Guérin were used as positive controls. When the cells were tested for CD3 or CD8 receptor expression, no differences were found between the untreated PBMCs and the treated (15 μg/mL Tenidap) cells. No change was found when cells were incubated for 72 h. Moreover, our data show a strong dose-dependent inhibitory effect of Tenidap (15 μg/mL) on IL-1α, IL-1β, and leukotriene B4 secretion in PBMCs treated overnight. The increased CD4+ expression by Tenidap in PBMCs may suggest an important role for this new antirheumatic agent in immunity and may hold future therapeutic promise for diseases involving IL-1 and leukotriene B4 as mediators.Key words: Tenidap, lymphocyte receptors, leukotriene B4, interleukin-1, lipopolysaccharide.

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