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Biomedical subjects

R Fantozzi

Publications and source records attributed to R Fantozzi.

At least 55 records · Page 3Linked to original sources
PubMed1986

FMLP-activated neutrophils evoke histamine release from mast cells.

Human neutrophils, having been activated by the chemotactic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP), evoke histamine release from rat serosal mast cells. The release is dependent on FMLP concentration and it can be inhibited by disodium cromoglycate and by a flavonoid, silymarin, which displays free radical scavenging properties. Silymarin inhibition of neutrophil-mediated histamine release is dose-dependent. These results further stress the concept of a neutrophil-mast cell interaction, which may be involved in inflammatory processes.

Adult↗
PubMed1986

The release of histamine by parasympathetic stimulation in guinea-pig auricle and rat ileum.

Two preparations, a segment of rat ileum and the vagally innerved guinea-pig auricles, have been used in an analysis of the responses to vagal or to electrical field stimulation. The responses to parasympathetic stimulation were depressed by atropine and by tetrodotoxin, and potentiated by eserine. Supramaximal stimulation (10-20 Hz) resulted in increased release of acetylcholine and histamine, both in rat ileum and guinea-pig auricles. The release of histamine after parasympathetic stimulation did not exhibit tachyphylaxis, and it was not reproduced by non-parasympathetic stimuli. In both preparations, atropine produced a significant, dose-related reduction of histamine measured in the bath fluid after stimulation, while eserine increased histamine output. A significant diminution of mast cell granules metachromasia was observed in guinea-pig auricles and in rat intestine after parasympathetic stimulation. The possibility is discussed that acetylcholine released by parasympathetic stimulation would in turn evoke the secretion of histamine from tissue mast cells.

Acetylcholine↗
PubMed1986

Upper aerodigestive neoplasm perpetuated in the nude mouse.

The ability to study and characterize squamous cell cancer of the upper aerodigestive system would be greatly facilitated by an in vivo model. The subsequent opportunity to observe cellular kinetics, membrane antigenicity and hence, potential response to chemotherapy, immunotherapy, radiotherapy, or a combination of these treatment modalities would most likely have early and significant clinical relevance. A multidisciplinary team of basic scientists and clinicians have developed a nude mouse colony for such investigational research. Melanoma and pulmonary squamous and pulmonary adenocarcinoma have been grown and successfully transferred. In addition, head and neck squamous cell carcinoma from multiple sites have also been successfully colonized. We present our experience with this interesting in vivo model and discuss problems in creating a nude mouse colony, techniques of successful tumor inoculation, ongoing maintenance of successful cell lines, and theoretical advantages for potential clinical investigations using this dynamic biologic system.

Adenocarcinoma↗
PubMed1985

Immunological modulation of cholinergic histamine release in isolated rat mast cells.

Isolated purified rat mast cells release histamine when exposed to acetylcholine according to different patterns of sensitivity. The degree of histamine release is correlated with the levels of reaginic antibodies presumably bound to the mast cell membrane. In fact, mast cells passively sensitized with mouse myeloma IgE against egg albumin or DNP2-lysine, react to acetylcholine with a release of histamine, which is proportional to the IgE concentration in the incubation medium. The histamine release induced by acetylcholine is due to the stimulation of a muscarinic receptor. Accordingly, acetylthiocholine is unable to evoke histamine release and preincubation of sensitized cells with atropine fully inhibits the cholinergic histamine release. The histamine release evoked by acetylcholine is potentiated by the exposure of sensitized cells to the specific antigen. The present results suggest that sensitization of mast cells is a crucial factor in modulating their sensitivity to acetylcholine.

Acetylcholine↗
PubMed1985

Mast cell and neutrophil interactions: a role for superoxide anion and histamine.

Histamine inhibits superoxide anion (O-2) production from human neutrophils stimulated by N-formylmethionyl-leucyl-phenylalanine (FMLP). The effects of histamine are dose-dependent and competitively antagonized by cimetidine. When passively sensitized rat serosal mast cells and human neutrophils are mixed together, O-2 production from FMLP-activated granulocytes is significantly reduced, following mast cell degranulation by acetylcholine. These inhibitory effects can be counteracted by cimetidine. Exposure of non-sensitized rat mast cells to FMLP-stimulated human neutrophils causes histamine release. These results suggest bidirectional control mechanisms between mast cells and neutrophils, that further stress the role of histamine in regulating inflammatory processes.

Animals↗
PubMed1985

Mast cell heterogeneity in response to cholinergic stimulation.

Mast cell heterogeneity in response to acetylcholine has been evidentiated by the virtual lack of sensitivity or by the full reaction to nanomolar concentrations of acetylcholine, observed in samples of serosal mast cells isolated from the same animal species. The incubation with IgE of isolated rat mast cells renders the originally heterogeneous response homogeneous, the release of histamine evoked by acetylcholine being proportional to the IgE concentration. The histamine release induced by acetylcholine is due to the activation of muscarinic receptors, since it is blocked by atropine, not reproduced by acetylthiocholine and potentiated by exposure of the cells to the specific antigen.

Acetylcholine↗
PubMed1985

Sjogren's syndrome: a persistent clinical problem.

One hundred sixty patients with Sjogren's syndrome have been evaluated and managed at Scripps Clinic. Objective diagnosis has relied heavily on rose-bengal vital staining and corneal slit lamp examination to establish the presence of KCS and lip biopsy. The role of the head and neck surgeon in evaluating the patient with "dry mouth" is discussed. Usually Sjogren's syndrome is managed nonsurgically, but problems of abscess, recurrent infection, disfigurement, and malignant transformation may result in the need for total parotidectomy with nerve preservation. Radiation for Sjogren's syndrome is rarely, if ever, indicated. The etiology of Sjogren's syndrome may be closely tied to the homogeneous genetic background of its patients and the presence of a chronic immunogenic stimulus well recognized in the secondary form but less clear in the primary.

Diagnosis, Differential↗
PubMed1985

Drug modulation of superoxide anion production from human neutrophils.

The effects of drugs on the production of superoxide anion from neutrophils stimulated by N-formylmethionyl-leucyl-phenylalanine (FMLP) were examined. Drugs acting on specific receptors, such as beta-adrenergic agonists (e.g. fenoterol, salbutamol) inhibited FMLP-evoked superoxide in a dose-dependent fashion. The order of activity: isoprenaline greater than fenoterol greater than salbutamol is the same as that found by assaying their effects on lysosomal enzyme release. Superoxide production from human neutrophils can also be affected in different manners, such as by a scavenging mechanism. A new non-steroidal anti-inflammatory drug, imidazole 2-hydroxybenzoate, by forming complexes with copper, displayed a significant superoxide dismutase activity which would contribute to explain its anti-inflammatory effect in vivo.

Adrenergic beta-Agonists↗
PubMed1984

Inhibition of the cardiac response to sympathetic nerve stimulation by opioid peptides and its potentiation by morphine and methadone.

[D-Ala2,D-Leu5]enkephalin (1-10 microM) and [Met5]enkephalin-Arg-Phe (1-10 microM) produced concentration-dependent inhibition of the cardiac response to field stimulation of the adrenergic nerve terminals in preparations pretreated with peptidase inhibitors (captopril 10 microM, bestatin 10 microM, thiorphan 0.3 microM and L-leucyl-L-leucine 2 mM). The inhibitory response to the opioid agonists was evident in preparations superfused with solutions containing 1.8 mM calcium, but not in those containing 3.6 mM calcium. Moreover the inhibition was antagonized by naloxone 10 microM. [D-Ala2,Met5]enkephalinamide (1-3 microM) and beta-endorphin (1-3 microM) did not significantly affect the sympathetic response. The cardiac response to sympathetic stimulation was not inhibited but, on the contrary, was potentiated by morphine (3-10 microM) and methadone (3-10 microM). It is suggested that the depressant effect of the opioid peptides was due to stimulation of presynaptic inhibitory opiate receptors on adrenergic nerve terminals of the heart, and that the potentiation of the sympathetic response by morphine and methadone was probably attributable to an unspecific inhibitory effect on the neuronal uptake of noradrenaline.

Animals↗
PubMed1984

Mediator release from isolated rat ileum in response to field stimulation.

The effect of electrical field stimulation on mediator release from the isolated rat ileum was evaluated by recording the muscle responses and by measuring acetylcholine and histamine appearing in the perfusion fluid. In the presence of cholinesterase inhibitors, supramaximal field stimulation (10 Hz) resulted in twitch responses accompanied by an increased release of acetylcholine. The resting output of histamine was measurable also in the absence of inhibition of cholinesterases, and neatly increased during electrical stimulation. Atropine produced a dose-related decrease in the release of histamine from electrically stimulated muscle, while eserine extends the time-course of the contractile response and of the histamine release as well. The results are discussed in the context of the role ascribed to acetylcholine as a physiological modulator of histamine release.

Acetylcholine↗
PubMed1984

Autacoid and beta-adrenergic agonist modulation of N-formylmethionyl-leucyl-phenylalanine evoked lysosomal enzyme release from human neutrophils.

Isoprenaline, histamine and PGE1 inhibit N-formylmethionyl-leucyl-phenylalanine evoked lysosomal enzyme release from human neutrophils. Their effects are dose-dependent and potentiated by 3-isobutyl-1-methylxanthine pretreatment of the cells. The order of activity is PGE1 greater than isoprenaline greater than histamine. The maximum of inhibition afforded by each agonist depends on the amount of the secretory stimulus, since it is higher at lower concentrations of the secretagogue. Isoprenaline effects are competitively antagonized by propranolol and are mimicked by fenoterol and salbutamol. These results suggest that human neutrophil functions are modulated by endogenous control mechanisms, that can also be activated by drugs acting on the same receptors as the endogenous mediators.

1-Methyl-3-isobutylxanthine↗
PubMed1983

Histamine release by vagal stimulation.

The content of acetylcholine and histamine in the effluent of isolated, vagally innerved guinea-pig auricles was determined. Spontaneous or stimulation-induced overflow of acetylcholine was detected only in the presence of acetylcholinesterase inhibitors. The histamine overflow was measurable also in the absence of inhibition of cholinesterase, and neatly increased during vagal stimulation. The vagally evoked histamine overflow was blocked by atropine and potentiated by eserine. The stimulation-induced histamine overflow in the effluent is discussed, presumably assuming that acetylcholine may release histamine from cardiac histamine stores.

Acetylcholine↗
PubMed1983

N-Formylmethionyl-leucyl-phenylalanine: Different releasing effects on human neutrophils and rat mast cells.

N-Formylmethionyl-leucyl-phenylalanine (FMLP) is a synthetic chemotactic peptide which induced beta-glucuronidase and lysozyme release from human neutrophils treated with cytochalasin B. FMLP-releasing effects were rapid and dose dependent. Unlike other secretagogues of neutrophils (e.g., zymosan and immune complexes), FMLP secretory activity was not modulated by acetylcholine, which by itself did not release lysosomal enzymes from human neutrophils. Isolated rat mast cells did not respond to FMLP, which has been demonstrated to release histamine from human neutrophils. Two markers of rat mast cell secretory granules, histamine and beta-glucuronidase, were assayed, but the results were negative for both. In the same experimental conditions, 48/80 released histamine and the enzyme: the ratio of the net percentage release of beta-glucuronidase to the net percentage release of histamine was congruent 0.4.

Acetylcholine↗
PubMed1983

Muscarinic cholinergic receptor binding in rat mast cells.

Specific [3H]-QNB binding was present in isolated, purified, intact rat mast cells and in crude membrane preparations. The binding is saturable, time- and temperature-dependent. Cholinergic agents inhibit selectively the binding: atropine is the most effective of the antagonists while oxotremorine is the most potent of the muscarinic agonists. It is concluded that rat mast cells are provided with muscarinic cholinergic receptors.

Animals↗
PubMed1983

The amine oxidase of human blood lymphocytes and granulocytes.

The deamination of some monoamines in human blood lymphocytes and granulocytes is dependent on the presence of two different enzymes: a mitochondrial (type B) monoamine oxidase and a "benzylamine oxidase" similar to the plasma BAO which is inhibited by semicarbazide and resistant to clorgyline.

Benzylamine Oxidase↗