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Antigen-induced mediator release in primates.

R H Gundel1, P Kinkade, C A Torcellini

  • 1Department of Pharmacology, Boehringer Ingelheim Pharmaceuticals, Inc., Ridgefield, Connecticut 06877.

The American Review of Respiratory Disease
|July 1, 1991
PubMed
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Allergic airway responses in primates involve significant increases in leukotriene C4 (LTC4), prostaglandin D2 (PGD2), and histamine. Iodoxamide tromethamine effectively blocked mediator release, highlighting its therapeutic potential.

Area of Science:

  • Pulmonary immunology
  • Allergic airway inflammation
  • Respiratory pharmacology

Background:

  • Allergic asthma involves the release of bronchoactive mediators.
  • Understanding these mediators is crucial for developing effective treatments.

Purpose of the Study:

  • To investigate the release of specific bronchoactive mediators in allergic primates during antigen-induced airway responses.
  • To assess the effects of anti-inflammatory drugs on mediator release.

Main Methods:

  • Cynomolgus monkeys with naturally occurring Ascaris suum sensitivity were studied.
  • Antigen inhalation was used to induce an acute allergic response.
  • Bronchoalveolar lavage (BAL) was performed to collect airway samples.
  • Quantification of leukotriene C4 (LTC4), prostaglandin D2 (PGD2), and histamine was performed using RP-HPLC, radioimmunoassay, and fluorometric assay.

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Main Results:

  • Antigen inhalation caused significant increases in BAL LTC4 (40-fold), PGD2 (10-fold), and histamine (20-fold).
  • Dexamethasone inhibited LTC4 and PGD2 release but had a weaker effect on histamine.
  • Indomethacin strongly inhibited PGD2 release but had variable effects on LTC4 and no effect on histamine.
  • Iodoxamide tromethamine significantly blocked the release of all three mediators, while mepyramine (H1 antagonist) had no effect.

Conclusions:

  • Acute allergic airway responses in primates are characterized by substantial release of LTC4, PGD2, and histamine.
  • Iodoxamide tromethamine demonstrates potent inhibition of these key allergic mediators.
  • These findings support the role of these mediators in allergic airway inflammation and suggest potential therapeutic targets.