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Biomedical subjects

D Fumarola

Publications and source records attributed to D Fumarola.

At least 91 records · Page 5Linked to original sources
PubMed1982

Legionella pneumophila and related organisms induce the generation of procoagulant activity by peripheral mononuclear cells in vitro.

We investigated the in vitro effect of various members of the genus Legionella on human peripheral mononuclear cells. All the strains tested induced the generation of strong procoagulant activity (tissue factor) when incubated for a prolonged period of time with pure mononuclear cell suspensions. This effect was dependent on the number of bacteria. The production of mononuclear cell procoagulant activity was also observed after the addition of bacteria to citrated whole blood. Escherichia coli 0111:B4 showed similar activity, but Staphylococcus aureus was much less effective. These findings suggest that the presence of endotoxin-like substance(s) in the outer cell wall of Legionellae could contribute to the stimulation of mononuclear cells. The production of tissue factor, a potent trigger of blood clotting, by these cells could help us to understand the mechanism(s) responsible for the activation of intravascular coagulation associated with severe legionellosis.

Escherichia coli↗
PubMed1982

In vitro modulation of cell-mediated immunity by prostaglandin E2. I. Enhancing-inhibitory effects on antibody-dependent cellular cytotoxicity.

The modulating effects of Prostaglandin E2, solubilized in medium, were observed in the antibody-dependent cytotoxic system. The pretreatment of effector cells with PGE2 up to 5 hours increased significantly the cytotoxic activity. The enhancement was distributed in both Non-T and T lymphocyte fractions suggesting a more pronounced activation of K cells. The effect was abrogated by pretreating lymphocyte suspensions with Indomethacin before exposure to prostaglandin. On the other hand, the addition of PGE2 during the test led to an inhibition of the cytotoxic capacity. Taken together, these results imply either a relationship between endogenously produced PGE2 and the concentration of exogenous PGE2 or the influence of PGE2 on microenvironment (i. e. exchange of calcium and magnesium through the cell membrane) during the cytolytic phenomenon.

Antibody-Dependent Cell Cytotoxicity↗
PubMed1982

In vitro modulation of cell-mediated immunity by prostaglandin E2. II. Enhancement of spontaneous plaque-forming cell generation.

The effect of the pretreatment of human peripheral blood lymphocytes by Prostaglandin E2 (dissolved in medium) on the spontaneous Plaque-Forming Cell generation has been evaluated. A significant enhancement of immunoglobulin production, markedly increased by the addition of further PGE2 to the pretreated cells, has been demonstrated. Experiments carried out with indomethacin have shown an inhibition of plaque formation, thus indicating that the content of endogenous prostaglandin E2 may play an important role in the enhancement of antibody synthesis, previously described. Results obtained with populations of rosetting and non-rosetting lymphocytes pointed out that non-rosetting cells are exclusively responsive to prostaglandin treatment.

Dinoprostone↗
PubMed1982

Cardiovascular effects of Shigella sonnei endotoxin in the rat.

Shigella sonnei lipopolysaccharide (LPS), either in phase I (extracted from the smooth strains), or in phase II (extracted from the rough strains) reduced mean arterial pressure and heart rate following a 640 micrograms/Kg intravenous (iv) bolus injection in the urethane-anesthetized rat. Lower doses were without significant effects. Escherichia coli LPS (640 micrograms/Kg iv) produced a greater and more prolonged hypotension, however the negative chronotropic effect was less severe. The iv injection of the lipid A moiety of the LPS molecule of Shigella sonnei resulted in a more pronounced hypotensive effect than that obtained with the parent LPS, thus showing that lipid A is the vasodilatating fraction of the molecule. When lipid A was injected in rats pretreated with aspirin or with naloxone, the hypotensive effect was significantly reduced and the decrease in heart rate was reverted in tachycardia. In atropine-pretreated, surgically bivagotomized rats, iv injection of lipid A was followed by a long-lasting pressor effect. The date indicate that Shigella sonnei endotoxin has cardiovascular effects, mainly due to its lipid A moiety of the molecule. The hypotensive effect involves a wide range of mechanisms.

Animals↗
PubMed1982

Effects of bacterial lipopolysaccharides (LPS) on leukocytes and platelets. Recent views on the pathophysiological role of LPS in the host.

Some effects of bacterial endotoxin on leukocytes and platelets are reviewed. The release of two mediators, Leukocyte Inhibiting Factor (LIF) and Tissue Factor (TF) from human mononuclear cells are described. These factors may play either beneficial effects (LIF) or noxious activities (TF liberation in certain pathological conditions). Regarding the activities of LPS on platelets the AA. report some personal data about the electrokinetic modification of platelets due to endotoxin. This LPS effect can be performed directly or via a lymphokine release, Platelet Slowing Factor (PSF). In the light of all the mentioned considerations, a scheme of interaction LPS/platelets is suggested.

Animals↗
PubMed1982

In vitro effect of endotoxin from Shigella sonnei. phase I on human blood platelets and mononuclear leucocytes: comparison of "free endotoxin" with cell-extracted preparations.

The in vitro effect of a purified endotoxin preparation from culture fluids of Shigella sonnei, phase I (purified free endotoxin, PFE) and of three endotoxin preparations chemically extracted from the intact parent cells on human blood mononuclear leucocytes and platelets was investigated. PFE, like cell-extracted preparations, caused generation of strong procoagulant activity (tissue factor) by human mononuclear cells. PFE-stimulated cells, however, developed significantly greater activity than cells stimulated by the other endotoxins. they had about 4-fold more activity. Neither free nor cell-extracted preparations induced aggregation in human citrated or heparinized platelet-rich plasma (PRP) or unmasking of platelet factor 3 (PF3). These findings suggest that free endotoxin from Shigella sonnei, phase I resembles endotoxin extracted from cells by conventional procedures in their interaction with human platelets and mononuclear leucocytes. In view of the possible contribution of free endotoxin to endotoxemia in human and experimental gram-negative sepsis, our data that free endotoxin stimulates human mononuclear leucocytes to produce a potent trigger of blood coagulation (tissue factor) may be relevant to the understanding of the mechanism(s) responsible for the initiation of intravascular coagulation in severe human infections.

Blood Platelets↗
PubMed1981

Platelet aggregation and stimulation of leucocyte procoagulant activity by rickettsial lipopolysaccharides in rabbits and in man.

The effects in vitro of 4 purified lipopolysaccharide (LPS) preparations from Rickettsiae on platelets and leucocytes were studied in rabbits and in man. All LPS induced aggregation in rabbit platelet-rich plasma but to differing degrees. This activity was abolished by inactivation of complement. None of the preparations induced aggregation of human platelets. Both rabbit and human leucocytes, when incubated with each of the rickettsial LPS preparations, generated a potent procoagulant activity (tissue factor). These findings add further support to the concept that rickettsial LPS behave as typical LPS from gram-negative bacteria and may be relevant to the understanding of the mechanism(s) responsible for triggering intravascular coagulation in rickettsial diseases.

Animals↗