Mediator release during nasal provocation: A model to investigate the pathophysiology of rhinitis

Alkis Togias, Robert M. Naclerio, David Proud, Claus Baumgarten, Stephen Peters, Peter S. Creticos, Jane Warner, Anne Kagey-sobotka, N. Franklin Adkinson, Philip S. Norman, Lawrence M. Lichtenstein

Research output: Contribution to journalArticlepeer-review

Abstract

The pathogenesis of rhinitis was investigated using a model of nasal provocation with different types of stimuli. Allergic subjects had an immediate response to antigenic challenge with symptoms of rhinitis highly correlated with increments in the concentrations of histamine, prostaglandin D2, kinins and kininogens, leukotrienes, and toluene sulfonyl arginine methyl ester esterase activity in their nasal secretions. This reaction was abated by a tricyclic antihistamine also capable of inhibiting mediator release from human mast cells in vitro and, in some subjects, by disodium cromoglycate. In a number of patients, symptoms reappeared three to 12 hours after nasal provocation. This late reaction also involves release of all of the aforementioned mediators except for prostaglandin D2, and preliminary data suggest that it can be inhibited by oral or topical steroids. Cold; dry air can induce rhinitis with mast cell mediator release from selected subjects. The pathogenesis of this reaction is unclear, but there are indications that osmolarity changes are responsible for mast cell activation. Thus, mast cells can be induced to release mediators and cause nasal symptoms by both immunologic and physical mechanisms, which may account for the pathophysiology of several types of rhinitis.

Original languageEnglish (US)
Pages (from-to)26-33
Number of pages8
JournalThe American journal of medicine
Volume79
Issue number6 SUPPL. 1
DOIs
StatePublished - Dec 20 1985

ASJC Scopus subject areas

  • Medicine(all)

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