Cell-Bound C3b Stimulates Human Monocyte Release of Prostaglandin E and Thromboxane B2

1987 ◽  
Vol 41 (4) ◽  
pp. 363-366 ◽  
Author(s):  
David E. Fulford ◽  
R. Bruce Rutherford
Keyword(s):  
Human Monocyte ◽  
Thromboxane B2 ◽  
Prostaglandin E

Decreased systemic formation of prostaglandin E and prostacyclin, and unchanged thromboxane formation, in alcoholics during withdrawal as estimated from metabolites in urine

1987 ◽  
Vol 73 (3) ◽  
pp. 277-283 ◽  
Author(s):  
Ulrich Förstermann ◽  
Thomas J. Feuerstein
Keyword(s):  
Hydrolysis Product ◽  
Thromboxane A2 ◽  
Normal Subjects ◽  
Thromboxane B2 ◽  
Urinary Metabolite ◽  
Prostaglandin E ◽  
Dioic Acid ◽  
Control Subjects ◽  
Major Urinary Metabolite ◽  
Prostaglandins E1 And E2

1. The rates of secretion into the circulation of prostaglandin E, prostacyclin, and thromboxane A2 were estimated in male alcoholics on the third day of withdrawal and in control subjects by measuring appropriate metabolites in urine. 2. Urinary levels of tetranor-5,11-diketo-7α-hydroxyprostane-1,16-dioic acid (the major urinary metabolite of prostaglandins E1 and E2), of 2,3-dinor-6-ketoprostaglandin F1α (the major urinary metabolite of prostacyclin) and of 6-keto-prostaglandin F1α (the stable hydrolysis product of prostacyclin) were significantly different from the normal subjects in the alcoholic group. In contrast, 2,3-dinor-thromboxane B2 (the major urinary metabolite of thromboxane A2) and thromboxane B2 (the stable hydrolysis product of thromboxane A2) were not significantly different between the groups. 3. These data suggest that the ratio of the vasodilator prostanoids prostaglandin E and prostacyclin and the vasoconstrictor prostanoid thromboxane A2 is lower than in normal subjects, in alcoholics during withdrawal. This may be one causal factor for the higher incidence of hypertension observed in withdrawing alcoholics compared with control subjects.

PROSTAGLANDIN E, THROMBOXANE B2 AND 6-OXO-PROSTAGLANDIN F1α IN AMNIOTIC FLUID AND MATERNAL PLASMA OF RHESUS MONKEYS (MACACA MULATTA) DURING THE LATTER THIRD OF GESTATION

1979 ◽  
Vol 81 (3) ◽  
pp. 345-349 ◽  
Author(s):  
J. S. ROBINSON ◽  
R. NATALE ◽  
L. CLOVER ◽  
M. D. MITCHELL
Keyword(s):  
Rhesus Monkey ◽  
Amniotic Fluid ◽  
Macaca Mulatta ◽  
Rhesus Monkeys ◽  
Maternal Plasma ◽  
Thromboxane B2 ◽  
Prostaglandin E ◽  
Peripheral Plasma ◽  
Prostaglandin F ◽  
Serial Samples

The concentrations of prostaglandin E (PGE), thromboxane B2 (TXB2) and 6-oxo-prostaglandin F1α (6-oxo-PGF1α) were measured by radioimmunoassay in serial samples of amniotic fluid and maternal peripheral plasma in the latter third of pregnancy in rhesus monkeys (Macaca mulatta). The samples were collected under ketamine-induced anaesthesia. The concentration of PGE was undetectable in amniotic fluid until a few days before delivery when a large increase was observed in three of the five animals. There were small increases of TXB2 and 6-oxo-PGF1α in amniotic fluid before delivery. In maternal plasma the concentrations of PGE, TXB2 and 6-oxo-PGF1α were generally higher and more variable than in amniotic fluid and did not increase with advancing gestation. It is suggested that increased production of primary prostaglandins occurs before, and is involved in, the onset of parturition in the rhesus monkey.

scholarly journals Chlamydia pneumoniae Enhances Cytokine-Stimulated Human Monocyte Matrix Metalloproteinases through a Prostaglandin E2-Dependent Mechanism

2005 ◽  
Vol 73 (1) ◽  
pp. 632-634 ◽  
Author(s):  
Min P. Kim ◽  
Charlotte A. Gaydos ◽  
Billie Jo Wood ◽  
Justin P. Hardick ◽  
Yahong Zhang ◽  
...  
Keyword(s):  
Chlamydia Pneumoniae ◽  
Plaque Rupture ◽  
Human Monocyte ◽  
Prostaglandin E ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Atherosclerotic Plaque Rupture ◽  
Stimulating Factor ◽  
Necrosis Factor ◽  
Dependent Mechanism

ABSTRACT Exposure of human monocytes to Chlamydia pneumoniae resulted in a significant enhancement of matrix metalloproteinase (MMP) 1 and 9 production following stimulation with tumor necrosis factor alpha and granulocyte monocyte-colony stimulating factor. The effect of C. pneumoniae on monocyte MMPs was mediated through the induction of prostaglandin E2. These findings may have implications for atherosclerotic plaque rupture.

scholarly journals Cholera Toxin Indirectly Activates Human Monocyte-Derived Dendritic Cells In Vitro through the Production of Soluble Factors, Including Prostaglandin E2 and Nitric Oxide

2006 ◽  
Vol 13 (1) ◽  
pp. 106-115 ◽  
Author(s):  
Kenneth C. Bagley ◽  
Sayed F. Abdelwahab ◽  
Robert G. Tuskan ◽  
George K. Lewis
Keyword(s):  
Nitric Oxide ◽  
Dendritic Cells ◽  
Cholera Toxin ◽  
Human Monocyte ◽  
Prostaglandin E ◽  
Adjuvant Effects ◽  
Camp Levels ◽  
Dc Maturation

ABSTRACT Cholera toxin (CT) is a potent adjuvant that activates dendritic cells (DC) by increasing intracellular cyclic AMP (cAMP) levels. In vivo and in vitro, very small amounts of CT induce potent adjuvant effects and activate DC. We hypothesized that DC intoxicated by CT may release factors that enhance their own maturation and induce the maturation of toxin-free bystander DC. Through the use of mixed cultures and transwell cultures, we found that human monocyte-derived DC (MDDC) pulsed with CT or other cAMP-elevating agonists induce the maturation of bystander DC. Many DC agonists including CT increase the production of prostaglandin E2 (PGE2) and nitric oxide (NO). For this reason, we determined whether the actions of PGE2 or NO are involved in the maturation of MDDC induced by CT or dibutyryl-cAMP (d-cAMP). We found that blocking the production of PGE2 or blocking prostaglandin receptors inhibited MDDC maturation induced by CT and d-cAMP. Likewise, sequestering NO or blocking the downstream actions of NO resulted in the inhibition of MDDC maturation induced by CT and d-cAMP. These results indicate that endogenously produced factors including PGE2 and NO contribute to the maturation of DC induced by CT and that these factors participate in bystander DC maturation. The results of this study may help explain why bacterial toxins that elevate cAMP are such potent adjuvants.

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
Keyword(s):  
Mast Cell ◽  
Mononuclear Cell ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Human Monocyte ◽  
Prostaglandin E ◽  
Synovial Cells ◽  
Peripheral Blood Mononuclear ◽  
Tissue Degradation ◽  
Stimulation Of

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.

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