Mast cell mediator release in nonasthmatic subjects after endobronchial adenosine challenge

J Allergy Clin Immunol. 2004 Jul;114(1):34-9. doi: 10.1016/j.jaci.2004.03.006.

Abstract

Background: Adenosine 5'-monophosphate (AMP) has been shown to cause bronchoconstriction in atopic subjects but to have no effect on nonatopic nonasthmatic subjects. Endobronchial AMP challenge has previously been shown to cause mast cell mediator release in asthmatic subjects, but it is unknown whether a similar response occurs in atopic nonasthmatic and nonatopic nonasthmatic control subjects who have no response to inhalation AMP challenge.

Objective: This study examined the change in mast cell-derived products after endobronchial saline challenge and AMP challenge in subjects with and without a positive inhalation response to AMP.

Methods: Inhalation challenge with AMP challenge was performed in normal, atopic nonasthmatic, and atopic asthmatic subjects. Levels of mast cell mediators were measured after endobronchial adenosine challenge and after placebo endobronchial saline challenge.

Results: There were significant increases in histamine, tryptase, protein, and prostaglandin D2 levels (P=.02, P=.02, P=.01, and P=.01, respectively) after AMP challenge compared with after saline challenge in nonatopic nonasthmatic subjects. There was no significant increase in any mediator in either of the other 2 groups.

Conclusion: This study suggests dissociation between mediator release and bronchoconstriction in response to AMP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenosine Monophosphate / pharmacology
  • Adolescent
  • Adult
  • Asthma / immunology*
  • Bronchial Provocation Tests / methods*
  • Bronchoconstriction / drug effects
  • Bronchoconstriction / immunology*
  • Bronchoconstrictor Agents / pharmacology
  • Female
  • Humans
  • Hypersensitivity / immunology
  • Inflammation Mediators / immunology*
  • Male
  • Mast Cells / immunology*

Substances

  • Bronchoconstrictor Agents
  • Inflammation Mediators
  • Adenosine Monophosphate