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M Reale

Publications and source records attributed to M Reale.

100 records · Page 6Linked to original sources
PubMed1981

Determination of catecholamine permeability coefficients for passive diffusion across phospholipid vesicle membranes.

A convenient catecholamine transport assay has been developed which permits continuous, instantaneous monitoring of transmembrane flux. Epinephrine transport has been examined by spectrophotometrically monitoring adrenochrome formation resulting from the passive diffusion of catecholamine into unilamellar phospholipid vesicles containing entrapped potassium ferricyanide. Ferricyanide oxidation of epinephrine under the conditions employed is fast compared to membrane transport, which obviates the need for intravesicular concentration or volume determinations. Epinephrine transport data over a pH 6 to 7 range have been fitted to an integrated rate equation from which a permeability coefficient for neutral epinephrine of 2.7 1.5 X 10-6 cm/sec has been obtained.

Epinephrine↗
PubMedDate not supplied

Effect of the antirheumatic agent Tenidap on CD3, CD4, and CD8 expression and interleukin-1 and leukotriene B4 secretion in human peripheral blood mononuclear cells.

Thymocytes that express the complete CD3-T-cell receptor (TCR) complex are CD4- and CD8-. The CD4+ T-cell population can be subdivided into at least two quite distinct subsets, TH1 and TH2 cells, based upon cytokine expression. Interleukin-1 (IL-1) appears to be required for optimal proliferation of T cells in response to antigen and it seems that in the absence of IL-1, TH2 clones proliferate less in response to antigen. Tenidap is an antirheumatic agent that has an inhibitory effect on IL-1 production. In these studies, we show that isolated human peripheral blood mononuclear cells (PBMCs) treated in vitro with Tenidap (15 micrograms/mL) for 48-h incubations significantly (p < 0.05) enhanced the present of CD4+ expression compared with untreated cells (control), as determined by cytofluorimetric analysis. Lipopolysaccharide and Bacillus Calmette-Guérin were used as positive controls. When the cells were tested for CD3 or CD8 receptor expression, no differences were found between the untreated PBMCs and the treated (15 micrograms/mL Tenidap) cells. No change was found when cells were incubated for 72 h. Moreover, our data show a strong dose-dependent inhibitory effect of Tenidap (15 micrograms/mL) on IL-1 alpha, IL-1 beta, and leukotriene B4 secretion in PBMCs treated overnight. The increased CD4+ expression by Tenidap in PBMCs may suggest an important role for this new antirheumatic agent in immunity and may hold future therapeutic promise for diseases involving IL-1 and leukotriene B4 as mediators.

Antigens, CD↗
PubMedDate not supplied

Monocyte chemotactic protein 1 (MCP-1) is a mitogen for cultured rat vascular smooth muscle cells.

The involvement of inflammatory mechanisms in the progression of atherosclerosis has recently been suggested. Monocyte chemotactic protein 1 (MCP-1) is a soluble protein which is implicated in acute and chronic inflammatory processes, including atherosclerosis. We evaluated the effect of human recombinant MCP-1 on the in vitro proliferation of rat vascular smooth muscle cells (VSMCs). Incubation of VSMCs with MCP-1 (50-200 ng/ml) in the presence of 0.5% FCS significantly increased cell proliferation, [3H]-thymidine incorporation and the proliferative S fraction, measured by flow cytometry, compared to control cells. The proliferative effect of MCP-1 was specific, as shown by inhibition with a rabbit polyclonal serum to MCP-1. Moreover, the mitogenic effect of MCP-1 was significantly inhibited by downregulation of protein kinase C (PKC) activity and by incubation with H-7, a protein kinase inhibitor, suggesting the involvement of the PKC system. Verapamil, a Ca2+ channel blocker, also reduced the stimulatory effect of MCP-1 on cell proliferation. This study demonstrates that MCP-1 does not merely have a chemotactic activity, but also a mitogenic effect on cultured rat VSMCs.

Animals↗
PubMedDate not supplied

"In vitro" comparative immune effects of different titanium compounds.

Exposure to Ti compounds is today an occupational and environmental health hazard. Object of this study was to determine "in vitro" effects of different Ti salts on cultured human peripheral blood mononuclear cells (PBMC) proliferation and cytokine release. 10(-4) and 10(-7) M Ti compounds did not modify spontaneous PBMC proliferation. Ti dioxide (a biocompatible material and sunscreen component) did not exert effects on phytoemagglutinin (PHA) stimulated PBMC proliferation and on PHA stimulated IFN-gamma and TNF-alpha release from PBMC. On the other hand, 10(-4) M Ti oxalate (with wide industrial applications) and Ti ascorbate (used mainly in agriculture) inhibited about 70% the PHA stimulate PBMC proliferation; both these Ti compounds at 10(-4) and 10(-7) M concentrations significantly inhibited TNF-alpha release, while only Ti oxalate inhibited that of IFN-gamma. Titanocene (used in chemotherapy) did no exert effects on PBMC proliferation but markedly inhibited IFN-gamma and TNF-alpha release. On the whole, this study demonstrates that Ti dioxide is not immunotoxic; Ti oxalate shows marked immunotoxicity; titanocene exerts selective toxicity on cytokine release but not on PBMC proliferation, while Ti ascorbate affects TNF-alpha release from PBMC but not iFN-gamma release. In conclusion, the data show that immunotoxicity fo Ti depends on speciation.

Adult↗
PubMedDate not supplied

Chemokines in inflammatory states.

Chemokines probably mediate inflammation in asthma by acting on endothelial cells, alveolar cells, neutrophils, eosinophils, basophils, mast cells, monocytes, and lymphocytes, which are inhibited by corticosteroids. In 1995, we found that MCP-1 provokes mast cell aggregation and [3H]5HT-release in cultured mast cells. In another study, MCP-1 and RANTES revealed to have a potent chemoattractive effect on basophilic cells originating from the rat skin. In this inflammatory model, RANTES also attracted eosinophils and macrophages along with basophilic cells. The effect of RANTES on inducing HDC mRNA was dose dependent. MCP-1 and RANTES provoked histamine release in intradermal mast cells and prostaglandin D2 generation. These effects clearly show that RANTES and MCP-1 are mediators of acute inflammatory responses. In chronic inflammatory reactions, MCP-1 is also present as we show in a study recently published by our group. In this paper, we found that MCP-1, strongly mediates the recruitment of mononuclear cells in the granuloma formed by KMnO4. In addition, MCP-1 mediated a parasitic infection caused by Trichinella spiralis in mice. Our data strongly demonstrate that chemokines, such as RANTES and MCP-1, mediate acute inflammatory response.

Animals↗
PubMedDate not supplied

Effects of 50 Hz sinusoidal electromagnetic fields on MCP-1 and RANTES generated from activated human macrophages.

Extremely low frequency electromagnetic fields (ELF-EMF) induce cellular changes and modulate signal transduction pathways, and may be beneficial in the treatment of inflammatory diseases. In this paper we studied two inflammatory chemokines, MCP-1 and RANTES produced by human cultured isolated monocytes from peripheral blood, with or without PHA and in the absence or presence of 50 Hz magnetic field of 1.0 mT for 24 h. The production of MCP-1 and RANTES was determined by ELISA method. Here, we found that ELF-EMF strongly inhibited the production of these chemokines stimulated by PHA, while the control was not affected. Since MCP-1 and RANTES exert chemoattraction for several populations inflammatory leukocytes, the inhibitory effect of these chemokines could be one of the mechanisms by which ELF-EMF is therapeutic in inflammatory diseases.

Journal Article↗
PubMedDate not supplied

"In vitro" effects of different arsenic compounds on PBMC (preliminary study).

Aim of this investigation was to compare the effects of 10(-4) M and 10(-7) M As compounds on spontaneous and PHA stimulated PBMC proliferation and IFN-gamma and TNF-alpha release. The inhibitory effect of the 10(-4) M As salts was in the following order: momo-methyl-arsinous acic (MMAs(III)) > sodium arsenite (As(III)) > tetraphenyl arsonium chloride (As(V)) > sodium arsenate (As(V)) > potassium- and sodium-esa-fluorum arsenate (As(V)) > dimethyl arsinic acid (DMAs(V)), while monomethyl-arsonic-acid (MMAs(V)) and arsenobetaine did not exert immune effects. 10(-7) M MMAs(III) stimulated the spontaneous PBMC proliferation, while As(III) and DMAs(V) enhanced the PHA stimulated PBMC proliferation. This study shows that the immune effects of As salts depends on speciation; moreover, the immunotoxicity of inorganic arsenic in part depends on the intracellular bio-synthesis of MMAs(III) from MMAs(V).

Animals↗