scholarly journals Mast-cell products and heparin stimulate the production of mononuclear-cell factor by cultured human monocyte/macrophages

1985 ◽  
Vol 230 (1) ◽  
pp. 83-88 ◽  
Author(s):  
J R Yoffe ◽  
D J Taylor ◽  
D E Woolley

Purified mast cells derived from rat peritoneal fluids and dog mastocytomas were extracted with 1 M-NaCl and sonication techniques. The mast-cell products increased the production of mononuclear cell factor from human peripheral blood mononuclear cells in culture, as judged by the enhanced stimulation of prostaglandin E (2-5 fold) and collagenase (3-11-fold) production by cultured adherent synovial cells. Heparin alone (1-10 micrograms/ml) induced a similar stimulation of mononuclear-cell-factor production by monocyte cultures, whereas histamine (1-10 micrograms/ml) had no effect. The stimulatory effect of mast-cell products and heparin represented a direct effect on mononuclear cells; they did not potentiate the effect of monokine on the synovial cells. These results suggest that mast-cell-macrophage interactions may play a significant role in the pathogenesis of inflammation and connective-tissue degradation.

1981 ◽  
Vol 198 (2) ◽  
pp. 391-396 ◽  
Author(s):  
S M D'Souza ◽  
D J Englis ◽  
A Clark ◽  
R G Russell

1. Supernatant media from cultures of unstimulated human peripheral blood mononuclear cells contained one or more factors that increased by several hundred-fold the production of prostaglandin E by fibroblast-like cells derived from both inflamed and normal human gingival tissue. 2. This stimulation occurred in a dose-dependent manner and was completely inhibited by 14 microM-indomethacin. 3. Responsiveness to the factor declined as the age of the cell culture increased. 4. An increase in prostaglandin E production was first observed after a 2h exposure to the mononuclear cell factor(s) and could be prevented by cycloheximide. 5. Brief exposure (0.5 and 1.0 h) to mononuclear cell factor did not increase prostaglandin E production by the cells in a subsequent 72 h incubation in the absence of mononuclear cell factor. 6. Addition of arachidonate (10 microM and 15 microM) further enhanced stimulation of prostaglandin E production in response to mononuclear cell factor. 7. The stimulatory activity was resistant to digestion by trypsin, but was heat-labile, so that only 17% remained after treatment at 56 degrees C for 30 min.


2002 ◽  
Vol 80 (10) ◽  
pp. 1030-1033 ◽  
Author(s):  
David L Zhou ◽  
David D Kitts

North American ginseng (Panax quinquefolium) root extract (NAGE) with known ginsenosides composition was examined for its affinity to stimulate human tumour necrosis factor α (TNF-α) production in human peripheral blood mononuclear cells. Case studies were conducted in three donors, one that was diagnosed with an atopic allergy and two that were normal, healthy subjects. Cultured mononuclear cells were incubated with varying concentrations of NAGE for up to 72 h and culture media were tested for TNF-α concentration. Direct stimulation of mononuclear cell TNF-α production in vitro by NAGE occurred as early as 6 h with 200 μg NAGE/mL. The stimulation of TNF-α production was confirmed by TNF-α mRNA gene expression. These interesting results show the immunostimulating activity of NAGE components in reference to TNF-α production. This observation requires further investigation with more subjects to determine the affinity of ginseng in stimulating the human immune system. Moreover, the method of evaluating this response is very useful for standardizing ginseng extracts to a known bioactivity.Key words: North American ginseng extract, TNF-α, bioactivity.


Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1280-1283 ◽  
Author(s):  
E Dejana ◽  
F Breviario ◽  
G Balconi ◽  
V Rossi ◽  
G Remuzzi ◽  
...  

Abstract Supernatants were obtained from human peripheral blood mononuclear cells stimulated with phytohemagglutinin or in a mixed lymphocyte reaction. The effect of mononuclear cell products on vascular prostacyclin (PGI2) production was measured using cultured rat aortic smooth muscle cells (SMC) or aortic rings. PGI2 was measured by radioimmunoassay of its metabolite, 6-keto-PGF1 alpha. Supernatants containing mononuclear cell products induced PGI2 production in vascular tissue. Supernatant-induced PGI2 production of SMC was relatively slow, requiring more than six hours of incubation with supernatants, and was completely prevented by aspirin, a cyclooxygenase inhibitor. The regulation of arachidonic acid metabolism by products of stimulated mononuclear cells, which is critical to the physiology and pathology of blood vessels, may be an important aspect of the interaction between immunocompetent cells and vascular tissue.


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