Inhibition of IgE-Mediated Histamine Release from Human Basophils and Mast Cells by Fenoterol

Marone, Gianni; Ambrosio, G.; Bonaduce, Domenico; Genovese, Arturo; Triggiani, Massimo; Condorelli, M

doi:10.1159/000233573

Cited by 42 publications

(12 citation statements)

References 9 publications

(15 reference statements)

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“…Bronchodilating drugs, isoproterenol, salbutamol and theophylline, and glucocorticoids, hydrocortisone, prednisolone and dexamethasone, inhibited the ACA significantly. Although these drugs are reported to in hibit antigen-induced mediator release from mast cells (32)(33)(34), they also inhibit vascular permeability in crease non-specifically (35,36). These drugs inhibit PCA and skin reactions caused by chemical mediators significantly in rats and mice (22,37).…”

Section: Discussionmentioning

confidence: 99%

Active Cutaneous Anaphylaxis (ACA) in the Mouse Ear

Inagaki

Miura

Nagai

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-Active cutaneous anaphylaxis (ACA) was studied in the ear of female BALB/c mice. Mice were immunized with ovalbumin in the presence of aluminium hydroxide gel or complete Freund's adjuvant (CFA). Two weeks after the immunization, ACA was elicited in the mouse ear by injecting 10,ul of antigen solution intradermally into the ear lobe. ACA was assessed by the amount of extravasated dye, which was given intravenously just after the antigen injection. Antiallergic drugs (tra nilast, ketotifen and azelastine), antihistamines (chlorpheniramine, diphenhydramine and mequitazine), fl-stimulants (isoproterenol and salbutamol), theophylline and glucocorticoids (hydrocortisone, predni solone and dexamethasone) inhibited the reaction significantly. These drugs inhibited both ACA in mice immunized with alum-precipitated antigen and ACA in mice injected with CFA-emulsified antigen similarly. ACA in the mouse ear might be a useful tool for studying drugs for allergy.Keywords: Active cutaneous anaphylaxis, Ear (mouse), Antiallergic drug, IgE antibody, IgG1 antibody Passive cutaneous anaphylaxis (PCA) (1, 2) is a use ful experimental model for studying drugs for allergy (3 6). The rat has been the most useful species for this purpose and the reaction is assessed by measuring the amount of extravasated dye (7,8). On the other hand, the mouse is the most established experimental animal and there are many strains of mice with unique im munological characteristics (9-12).Furthermore, Feinberg (13) reported the suitability of mouse ear for induction of PCA, and Prouvost-Danon and Binaghi (14) demonstrated that mouse ear had higher reactivity for PCA than mouse dorsal skin. According to these re ports, we established a method for PCA in the mouse ear by assessing the amount of extravasated dye (15) and characterized it pharmacologically and immunologi cally (16-23). However, although passive sensitization provides a simple model that is suitable for analyzing the mechanisms involved in both allergic reactions and drug action, active sensitization is also important for studying allergic diseases, because allergic diseases are caused by active sensitization. In the present study, therefore, we applied the technique of mouse ear PCA to active cutaneous anaphylaxis (ACA) elicited in female BALB/c mice, and examined the effect of drugs which are used for allergic diseases on the ACA. MATERIALS AND METHODS MiceFemale BALB/c mice were used for ACA and male ddY mice were used for titration of serum antibodies. Both mice were purchased from Japan SLC, Inc. (Hamamatsu, Japan). Antigen and adjuvantsOvalbumin (OA, 5 times crystalized) was purchased from Seikagaku Kogyo Co., Ltd. (Tokyo, Japan). As adjuvants, aluminium hydroxide gel (alum) and com plete Freund's adjuvant (CFA) were used. Alum was prepared according to the method of Levine and Vaz (24), and CFA was obtained from Nacalai Tesque, Inc. (Kyoto, Japan). ACATen-weeks-old female BALB/c mice were immunized with OA in the presence of an adjuvant. To induce IgE antibody mainly, 1,ug...

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Section: Discussionmentioning

confidence: 99%

Active Cutaneous Anaphylaxis (ACA) in the Mouse Ear

Inagaki

Miura

Nagai

et al. 1992

Japanese Journal of Pharmacology

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“…Human heart mast cells are present mainly in the right atrium and in the sino-atrial and atrio-ventricular nodes [3]. H is released in man by immunological and nonimmunological mechanisms [4,5], all of which can lead to an increased plasma level of H and cardiac dysfunction. In the guinea-pig H has a positive inotropic effect [3], increases cardiac output, has a negative dromotropic effect and induces ventricular arrhythmias [6].…”

Section: Introductionmentioning

confidence: 99%

Non-invasive assessment of electrophysiological effects of histamine infusion in mam

et al. 1985

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The electrophysiological changes induced by sequential infusion of histamine (H) (0.4 and 1.0 mcg/kg/min for 10 min each) were investigated by conventional ECG and High Resolution ECG (H.R.ECG). The latter permits external non-invasive recording of the potentials generated in the cardiac conduction system. H was infused i.v. in 5 normal volunteers with a mean age of 30 years. H infusions were begun with 0.4 mcg/kg/min and continued for 10 min. After a 60 min recovery period a second 10 min infusion (1 mcg/kg/min) was administered. In man H produced a dose-dependent increase in heart rate, a significant depression of the ST-T complex, and a depression in STJ point. The QRS complex duration was unmodified. H.R.ECG showed significant changes in the morphology and voltage of the atrial activity. The electrophysiological effects disappeared within a few minutes after discontinuing the infusions of H.

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“…p2-Agonists have been found to be potent inhibitors of histamine release, but differences exist among the cell types studied (22)(23)(24)(25)(26). These in vitro effects have been confirmed during bronchial allergen challenge (27), exercise challenge (28), or skin tests with allergens (for review, see Bousquet & Michel [29]).…”

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Ex vivo pharmacologic modulation of basophil histamine release in asthmatic patients

Lebel

Arnoux

Chanez

et al. 1996

Allergy

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Histamine is one of a range of mediators which play an important role in asthma, and the “releasability” of basophils has been shown to be upregulated in this disease. In vitro, β2‐agonists and to a lesser extent corticosteroids have been shown to reduce histamine release. The ex vivo effects of salmeterol and inhaled corticosteroids on histamine release were studied in 78 asthmatic patients with variable disease severity and 20 control subjects. Spontaneous and anti‐IgE‐induced histamine release was measured in all subjects. Fifteen patients were not receiving any form of treatment, 42 were treated with inhaled corticosteroids, and 21 received inhaled corticosteroids and salmeterol. Seven patients treated with inhaled corticosteroids and seven patients treated with inhaled corticosteroids and salmeterol were tested twice to assess the effect of salmeterol on histamine release. Nine patients treated with inhaled corticosteroids were tested before and after 1 month of salmeterol treatment to determine the possible inhibition by salmeterol. Patients who were treated with inhaled corticosteroids and salmeterol showed significantly lower levels of spontaneous histamine release (median: 2.5%) than untreated (5.2%) and inhaled corticosteroids‐treated asthmatics (3.4%). No tachyphylaxis to salmeterol was observed when patients were tested twice at a 3‐month interval. This study suggests that salmeterol may have an additive anti‐inflammatory effect with inhaled corticosteroids, although this hypothesis must be tested by further studies involving cells obtained by bronchoalveolar lavage and studies with bronchial biopsies.

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Inhibition of IgE-Mediated Histamine Release from Human Basophils and Mast Cells by Fenoterol

Cited by 42 publications

References 9 publications

Active Cutaneous Anaphylaxis (ACA) in the Mouse Ear

Active Cutaneous Anaphylaxis (ACA) in the Mouse Ear

Non-invasive assessment of electrophysiological effects of histamine infusion in mam

Ex vivo pharmacologic modulation of basophil histamine release in asthmatic patients

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