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Modulation by nedocromil sodium of immunologic and nonimmunologic activation of monocytes, macrophages, and platelets

M Joseph1, A Tsicopoulos, A B Tonnel

  • 1Centre d'Immunologie et de Biologie Parasitaire, CJF INSERM 90-06, Institut Pasteur, Lille, France.

The Journal of Allergy and Clinical Immunology
|July 1, 1993
PubMed

Insights

Nedocromil sodium effectively inhibits IgE-mediated responses in human immune cells like monocytes and platelets. This drug reduces cytotoxic mediator generation and lysosomal enzyme release, showing therapeutic potential.

Area of Science:

  • Immunology
  • Pharmacology

Background:

  • Immunoglobulin E (IgE)-mediated responses are central to allergic inflammation.
  • Mast cells, basophils, macrophages, and platelets are key effector cells in IgE-dependent reactions.
  • Nedocromil sodium is an anti-allergic drug with mast cell stabilizing properties.

Purpose of the Study:

  • To investigate the effects of nedocromil sodium on IgE-dependent stimulation of human monocytes, alveolar macrophages, and blood platelets.
  • To assess the drug's impact on cytotoxic mediator generation, free radical production, and lysosomal enzyme release.
  • To evaluate nedocromil sodium's efficacy in IgE-activated rat peritoneal macrophages and platelets, and in aspirin-sensitive asthma patients' platelets.

Main Methods:

  • In vitro studies using human monocytes, alveolar macrophages, and blood platelets.
  • Assessment of IgE-mediated cytotoxic mediator generation, including schistosome larvae killing and chemiluminescence for free radical production.
  • Measurement of lysosomal enzyme release and synthesis in alveolar macrophages.
  • In vitro and ex vivo testing on IgE-activated rat peritoneal macrophages and platelets, and aspirin-sensitive asthma patients' platelets.

Main Results:

  • Nedocromil sodium significantly inhibited IgE-mediated cytotoxic mediator generation in human monocytes and platelets.
  • The drug demonstrated strong inhibition of schistosome larvae killing and reduced free radical production.
  • Significant inhibition of lysosomal enzyme release and synthesis was observed in alveolar macrophages, with optimal effects at 10(-9) to 10(-7) mol/L.
  • Similar inhibitory effects were noted in IgE-activated rat peritoneal macrophages and platelets.
  • Nedocromil sodium inhibited abnormal platelet responses in aspirin-sensitive asthma patients.

Conclusions:

  • Nedocromil sodium effectively suppresses IgE-dependent cellular activation and mediator release in various human immune cells.
  • The drug exhibits potential as a therapeutic agent for conditions involving IgE-mediated inflammation and hypersensitivity.
  • Nedocromil sodium's inhibitory effects extend to platelet responses relevant in aspirin-sensitive asthma.

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