PubMed Health⌕ Search

Biomedical subjects

L Armetti

Publications and source records attributed to L Armetti.

7 recordsLinked to original sources
PubMed2000

Activation and inhibition of mast cells degranulation affect their morphometric parameters.

Activation of mast cells, the key cells of allergic inflammation, causes typical morphological changes associated with an increase in volume, that is a function of area and perimeter. The purpose of this study was to evaluate the effect of mast cell activation to degranulate, carried out by the secretagogue Compound 48/80, and of inhibition of this activation carried out by Nedocromil sodium, a mast cell stabilizing drug, on mast cell area, perimeter and shape factor by a computerized image analyzer. Mast cells were isolated and purified by peritoneal lavage of rats (purity >98%) and co-cultured with mouse 3T3 fibroblasts to which they adhere. Cultures were incubated for 10 min at 37 degrees C with culture medium alone (Enriched Medium) or Enriched Medium containing either Nedocromil (10(-4) M) or Compound 48/80 (0.3 microg/ml) or Compound 48/80 and Nedocromil (0.3 microg/ml and 10(-4) M respectively). Supernatants were then assessed for histamine release, as a marker of mast cell activation and the cell monolayers were fixed and stained with an alcoholic-acidic toluidine blue solution and examined with a computerized image analyzer connected with a light microscope. Mast cells incubated in Enriched Medium or Nedocromil possessed similar morphometric parameters. Mast cells activated with Compound 48/80 (70% histamine release) had a significant increase in area and perimeter and a decrease in shape factor in comparison to mast cells in Enriched Medium alone. Simultaneous incubation of mast cells with Compound 48/80 and Nedocromil significantly inhibited their histamine release (36% histamine release) and the increase in area and perimeter, but did not affect significantly their shape factor, in comparison with mast cells incubated with Compound 48/80 alone. These data clearly show that there is a relationship between mast cell activation, consequent histamine release and changes in cell area, perimeter and shape factor and that Nedocromil not only inhibits mast cell histamine release but also the activation induced morphometric changes in mast cells.

3T3 Cells↗
PubMed1999

[Antileukotriene drugs: a new treatment for asthma].

Asthma incidence and prevalence have significantly increased during the last 25 years, making this pathology to be one of the most diffused in the industrialized world. It affects 5% of the adult population and the 10-15% of the children. The aethipathogenesis of asthma clearly involves a number of mediators, among which leukotrienes play an important role inducing bronchoconstriction, oedema and mucus hypersecretion. Thus, compounds inhibiting either the action or formation of these mediators are potentially interesting as antiasthma drugs. Two strategies for modulating the actions of the leukotrienes are currently undergoing clinical evaluation: cysteinyl leukotriene receptor antagonism and 5-lipoxygenase (5-LO) inhibition. These two classes of agents are here reviewed and their clinical utility as antiasthma drugs is evaluated.

Animals↗
PubMed1996

Inhaled PGE2 prevents aspirin-induced bronchoconstriction and urinary LTE4 excretion in aspirin-sensitive asthma.

Bronchial overproduction of leukotrienes and inhibition of prostaglandin synthesis are involved in the pathogenesis of aspirin-induced asthma. We investigated whether inhaled prostaglandin E2 (PGE2) attenuates the response to bronchial challenge with lysine acetylsalicylate (LASA) and the associated increase in urinary leukotriene E4 (u-LTE4) in seven aspirin-sensitive subjects with asthma. Each subject performed two challenges with a single dose of LASA that caused a decrease in FEV1 of 20% or more in a preliminary test, immediately after inhaling 100 micrograms PGE2 in 4 ml saline or placebo, according to a randomized double-blind protocol. FEV1 was recorded at 30-min intervals for 4 h. u-LTE4 was measured by combined high-performance liquid chromatography enzyme immunoassay at 2-h intervals. After placebo, LASA caused an obstructive reaction in all patients, with a maximum decrease in FEV1 of 35 +/- 5% with respect to baseline. u-LTE4 rose from 911 +/- 261 picograms (pg)/mg creatinine at baseline to a maximum value of 2249 +/- 748 after challenge. Inhaled PGE2 provided almost complete protection in all patients. Baseline u-LTE4 was 883 +/- 243 pg/mg creatinine and did not change significantly during the test, reaching a maximum value of 864 +/- 290 (p < 0.05 versus placebo). These results confirm that PGE2 is highly effective in preventing aspirin-induced asthma and suggest that this effect is mediated by inhibition of sulfidopeptide leukotriene production.

Administration, Inhalation↗
PubMed1994

An improved assay for urinary LTE4.

An improved method for the measurement of urinary LTE4 is described, based on the combined use of solid phase extraction (SPE)-HPLC-enzyme-immunoassay (EIA). This allows the use of homologous radioactive tracer in easily measurable amount for HPLC retention time evaluation and recovery estimation. Recovery linearly correlated with the total amount of LTE4 present in the extracted sample, indicating the existence of a carrier effect. Identification of immunoreactivity in HPLC fractions as LTE4 was based on parallel dilution assay and confirmed by the observable isotopic separation between tritium labeled LTE4 and immunoreactive LTE4. Critical selection of urine sample size, on the basis of creatinine content, together with efficient purification by SPE, resulted in total absence of aspecific immunoreactivity in fractions surrounding those associated with LTE4. Urinary LTE4 was measured in normal subjects and in cirrhotic patients, where an increased LTE4 excretion has been reported. The method described fulfils the criteria of specificity, sensitivity and accuracy necessary for a potential successful use in the study of sulfidopeptide leukotrienes formation in normal and pathological conditions.

Adult↗