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Biomedical subjects

G Marone

Publications and source records attributed to G Marone.

221 records · Page 13Linked to original sources
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Antiinflammatory effects of oxatomide.

There is increasing evidence that histamine may have wider proinflammatory and immunomodulatory activities than previously reported. It may influence several functions of lymphocytes, monocytes, basophils and macrophages, modulating the release of inflammatory mediators and cytokines. These observations have aroused interest in the pharmacology and clinical applications of histamine H1 receptor antagonists and have led to the identification of novel antiinflammatory properties for this class of drugs. Oxatomide, initially characterized as an H1 antagonist, inhibits the secretion of several mediators of inflammation from human basophils and mast cells. In vitro oxatomide inhibits the release of both preformed (histamine and tryptase) and de novo synthesized mediators (leukotriene C4 and prostaglandin D2). The inhibitory effect is not restricted to basophils and mast cells but is also evident on other inflammatory cells such as the neutrophils. In this cell, oxatomide inhibits arachidonic acid mobilization, and leukotriene B4 and platelet-activating factor synthesis, presumably by reducing the activity of cytosolic phospholipase A2. These observations extend the pharmacological activities of oxatomide beyond H1 receptor antagonism and suggest that this drug influences a variety of biochemical events in human inflammatory cells. These antiinflammatory activities help to explain its beneficial effect in various allergic and inflammatory disorders, including urticaria, allergic rhinitis and bronchial asthma.

Animals↗
PubMedDate not supplied

The releasability of lysosomal enzymes from neutrophil leukocytes in patients with rheumatoid arthritis.

OBJECTIVE: To study the enzyme content and the "releasability" of lysosomal enzymes (lysozyme and beta-glucuronidase) in neutrophils purified from peripheral blood of patients with rheumatoid arthritis (RA) or normal subjects. METHODS: Neutrophils were obtained from 13 patients (10 women and 3 men) with rheumatoid arthritis and from 11 healthy subjects (8 women and 3 men). We measured: (1) lysosomal enzyme (lysozyme and beta-glucuronidase) content; (2) spontaneous enzyme release; (3) lysosomal enzyme release after cell challenge with different segretagogues (FMLP, C5a, aggregated IgG, zymosan and Ca2+ ionophore A23187). RESULTS: The lysosomal enzyme content was not statistically different in control subjects and in patients with RA (7.4 +/- 1.9 vs 6.3 +/- 0.8 micrograms/10(6) neutrophils for lysozyme; 102.9 +/- 16.4 vs 78.9 +/- 11.2 micrograms/10(6) neutrophils for beta-glucuronidase in control and RA subjects, respectively, p = NS). Unstimulated release of lysozyme was significantly lower in RA patients (3.8 +/- 1.1%) when compared to control subjects (9.5 +/- 2.1%) (p < 0.05). In contrast, spontaneous release of beta-glucuronidase did not differ in the two groups (5.5 +/- 0.9% and 3.8 +/- 1.1% in control and RA subjects, respectively). Enzyme release induced by FMLP (3 x 10(-9)-3 x 10(-7) M), C5a (10(-8)-10(-7) M), aggregated IgG (0.1-0.6 mg/ml), or Ca2+ ionophore A23187 (0.1-1 microgram/ml) did not differ statistically in the two groups of subjects. Neutrophil stimulation by serum-treated zymosan, at the concentration of 0.3 mg/ml, induced a release of lysozyme that was significantly higher in patients with RA when compared to control subjects (p < 0.05), whereas zymosan-activated beta-glucuronidase secretion was similar in the two donor populations. CONCLUSIONS: This study suggests that the contribution of leukocytes to the inflammatory processes typical of RA does not depend on an altered "releasability" of preformed mediators from peripheral blood neutrophils.

Adult↗