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L Ceccatelli

Publications and source records attributed to L Ceccatelli.

30 records · Page 2Linked to original sources
PubMed1985

Adenosine inhibits polymorphonuclear leukocyte in vitro activation: a possible role as an endogenous calcium entry blocker.

Adenosine is able to in vitro inhibit FMLP-dependent activation of polymorphonuclear leukocytes as evaluated by enzyme release, superoxide anion generation and chemiluminescence production. The inhibiting effect is more relevant when A23187 is employed as stimulating agent. In this case the effect is significantly reversed by increasing concentrations of extracellular calcium. Since A23187-dependent activation is strictly dependent on Ca++ influx into the cell, the hypothesis is suggested that adenosine could act by regulatory mechanisms involving membrane calcium transport.

Adenosine↗
PubMed1985

Platelet-dependent granulocyte activation in vitro: effect of ticlopidine.

The presence of platelets or platelet release products is known to augment the injury of endothelial cells caused by stimulated neutrophils (PMN leukocytes). In our in vitro studies, platelet-rich or platelet-poor plasma (PRP or PPP) was placed in one compartment and a PMN suspension in the other of a modified Boyden chamber divided by a dialysis membrane. The addition of the aggregating substance (ADP, collagen) to PRP but not to PPP was followed by PMN activation as shown by enzyme release and O-2 generation. The in vivo treatment with ASA completely prevented the platelets from triggering PMN activation. The in vitro addition of a thromboxane synthetase inhibitor (imidazole 10(-3) M) or a lipoxygenase inhibitor (NDGA 10(-6) M) did not show any effect on platelet-dependent PMN activation, thus suggesting that neither TxA2 nor lipoxygenase by-products are involved. Finally, in vitro and in vivo treatment with ticlopidine blunted the stimulating activity of the platelets on PMN. Our data further support the hypothesis that a sequential platelet-PMN interaction may occur, and that the therapeutic effect of some antiplatelet drugs may be partly due to a protective effect against platelet-dependent PMN-mediated vascular damage.

Adenosine Diphosphate↗
PubMed1985

Polymorphonuclear leucocytes as a model of Ca++ and Mg++-dependent cellular activation. Effect of calcium entry blockers.

Flunarizine inhibited FMLP- and A23187-induced aggregation, enzyme release and O2- generation from human PMN as a function of its concentration. A23187-dependent PMN aggregation was also studied in media devoid of Ca++ or Mg++. Flunarizine (2.4 X 10(-5)M) significantly affected not only Ca++-supported but also Mg++-sustained PMN aggregation. The inhibiting effect of the drug was reversed by increasing the level of Ca++ (1.2 mM) or Mg++ (2 mM). Nifedipine, another Ca++-entry blocker, was shown to inhibit enzyme release and O2- generation induced by FMLP and A23187 as a function of its concentration, but only slightly affected PMN aggregation at very high concentration (10(-4)M). A role for flunarizine as a specific Mg++-entry blocker is suggested.

Calcimycin↗
PubMed1984

Heparin inhibition of polymorphonuclear leukocyte activation in vitro. A possible pharmacological approach to granulocyte-mediated vascular damage.

The "in vitro" effects of heparin on different functions of human polymorphonuclear leukocytes were studied. Granulocyte aggregation, enzyme release induced by FMLP and zymosan-activated serum and superoxide anion and chemiluminescence generated by FMLP were assessed. Heparin (25-500 micrograms/ml) was able to inhibit in a dose-dependent way cellular aggregation and degranulation induced either by FMLP or by zymosan-activated serum. FMLP-dependent superoxide anion generation and chemiluminescence were specifically inhibited by heparin at the concentration of 25 micrograms/ml. Our results showed that heparin "in vitro" inhibits all the aspects of the functional and metabolic granulocyte activation. A possible protecting effect of the drug on leukocyte-mediated tissue injury and vascular damage is discussed.

Cell Aggregation↗
PubMed1984

Polymorphonuclear leukocyte as a model of Ca++ and Mg++-dependent cellular activation. Effect of flunarizine.

Flunarizine, a calcium entry blocker drug, concentration-dependently inhibited FMLP and A23187-induced aggregation, enzyme release and superoxide anion generation from human granulocytes. A23187-dependent granulocyte aggregation was also studied in media devoided of Ca++ or Mg++. Flunarizine (2.4 x 10(-5) M) significantly affected not only Ca++-supported but also Mg++-sustained granulocyte aggregation. The inhibiting effect of the drug was reversed by increasing extracellular level of Ca++ (1.2 mM) or Mg++ (2 mM). In this "in vitro" model, the role of flunarizine as a specific Mg++ entry blocker was suggested.

Calcimycin↗
PubMed1984

In vitro inhibition of granulocyte function by timegadine, a new anti-inflammatory agent.

Timegadine, a new non-acidic anti-inflammatory agent, inhibits in a concentration-dependent way the FMLP-induced release of beta-glucuronidase and lysozyme from human granulocytes. Superoxide generation and directed migration are also inhibited. As this effect on granulocytes occurs at drug concentrations inhibiting the lipoxygenase pathway of arachidonic acid metabolism, the hypothesis that these two phenomena could be related is discussed.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1983

Heparin inhibits FMLP and Con-A dependent activation of human polymorphonuclear leucocytes in vitro.

The effects in vitro of heparin on different functions of human neutrophilic leucocytes were assessed. Granulocyte aggregation, enzyme release and superoxide anion generation induced by FMLP (10(-6) M), ConA (30 micrograms/ml), and A 23187 (5 microM) were evaluated. Heparin was able to inhibit, in a dose-dependent way, FMLP-mediated and ConA-mediated granulocyte activation. Heparin inhibited cellular aggregation at the final concentration of 100-500 micrograms/ml, while the inhibiting effect on enzyme release and superoxide anion production was present at lower concentrations (10-100 micrograms/ml). No activity was observed on A 23187-induced granulocyte stimulation. The inhibiting effect of heparin on FMLP-induced granulocyte activation proved to be time-dependent. The hypothesis that an interaction of heparin with cells may possibly initiate the inhibitory effect is proposed.

Calcimycin↗
PubMed1980

Pharmacological induced depression of E-rosette forming cells (RFC) of normal healthy subjects. Restoration by levamisole and thymopoietin pentapeptide.

The authors describe a pharmacological inhibition of E-Rosette formation by the "in vitro" addition of adenosine and theophylline. In the same experimental conditions TP5 and levamisole are able to reverse this inhibiting activity. The role of the cyclic nucleotides (cAMP and cGMP) in the regulation of the lymphocytes response is discussed.

Adenosine↗
PubMedDate not supplied

Captopril-induced granulocyte aggregation. A possible complement mediated mechanism of peripheral leukopenia.

Captopril, competitive inhibitor of angiotensin converting enzyme, is clinically employed for its antihypertensive activity and drug-dependent granulocytopenia or agranulocytosis have been seldom observed during treatment. In previous unpublished studies an activating effect of the drug on the complement alternate pathway has been demonstrated. In this paper we demonstrate that captopril-treated serum is able to "in vitro" induce granulocyte activation and aggregation. Granulocyte aggregation was shown by the turbidimetric method and cellular activation was confirmed by the release of the granule associated enzyme lysozyme and beta-glucuronidase. On this basis complement-mediated leukoaggregation and leukosequestration in vivo could be proposed as the effector mechanism of peripheral leukopenia.

Captopril↗
PubMedDate not supplied

Isradipine inhibits PMN leukocyte function. A possible interference with the adenosine system.

The dihydropyridine derivative isradipine is able to inhibit PMN leukocyte function, such as enzyme release and free radical generation, following the activation with specific stimuli. Moreover, the drug prevents calcium influx into the cells as detected by the specific fluorescent dye FURA 2/acetoxymethylester. The specific adenosine receptor antagonist theophylline is able to partially remove the inhibiting activity, thus suggesting a possible interference of isradipine with the adenosine system. Such a cell-protecting activity adds further rationale to the employment of isradipine in those conditions, such as acute and chronic ischaemia and reperfusion damage, in which PMN leukocyte-dependent tissue injury represents a relevant pathogenetic mechanism.

Adenosine↗