Effects of calmodulin antagonists on human adenoidal mast cells

Bent, S A S van der; Braam, U.; Schmutzler, W.

doi:10.1007/bf01969015

Cited by 3 publications

(1 citation statement)

References 7 publications

(9 reference statements)

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“…Calmodulin plays an important role in calcium fluxes leading to MC degranulation. Calmodulin antagonists can reduce histamine release from MCs and inhibit animal models of MC-dependent anaphylaxis [155,156]. Nicotinamide is able to inhibit IgEstimulated MC histamine release [157] and also inhibits neutrophil and eosinophil activation and degranulation [158].…”

Section: Other Mast Cell Inhibitorsmentioning

confidence: 99%

Drug therapy for ocular allergy

Hingorani

1998

Expert Opinion on Investigational Drugs

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The spectrum of ocular allergy ranges from mild, non-sight threatening disease, such as hay fever, to disorders such as atopic keratoconjunctivitis (AKC) which cause permanent ocular surface changes and reduced vision. The ideal treatment is with topical preparations. Launched topical preparations include anti-histamines and mast cell (MC) stabilisers, which are safe, but only moderately potent, steroids, which are very potent, but carry very serious side-effects, and cyclosporin A, which is not widely available and difficult to tolerate. There are a number of anti-histamines, MC stabilisers (and combinations thereof) and steroids in development which are of potential interest. Other possibilities for therapeutic intervention include inhibition of tryptase, cyclooxygenase (COX), leukotrienes (LTs), bradykinins (BKs), platelet activating factor (PAF) and immunoglobulin E (IgE). Therapies based on cytokine antagonism and agonism, T-cell inhibition and adhesion molecule antagonism might be expected to provide safe, but potent new modes of treatment. The increasing interest in research into the pathogenesis of ocular allergic inflammation may lead to more relevant approaches, such as eosinophil inhibition. Success will be highly dependent on the ability to produce suitable topical ophthalmic preparations.

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Section: Other Mast Cell Inhibitorsmentioning

confidence: 99%

Drug therapy for ocular allergy

Hingorani

1998

Expert Opinion on Investigational Drugs

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The influence of H1-, H2- and H3-receptors on the spontaneous and ConA induced histamine release from human adenoidal mast cells

et al. 1991

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The effects of the H3-agonist R-alpha-methylhistamine (R-alpha-MeHA) and the H3-antagonist thioperamide on the spontaneous and concanavalin A (ConA) induced histamine release from human mast cells were tested and compared with the effect of some H1- and H2-receptor active substances. R-alpha-MeHA (10(-9)-10(-7) M) exerted no effect on histamine release whereas thioperamide increased the spontaneous release at 10(-6)-10(-4) M but inhibited the ConA induced release in a narrow concentration range (10(-6)-10(-5) M). This enhancement might be taken as an indication of the existence of H3-receptor dependent autoregulation although presently other mechanism cannot be excluded.

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