Abstract
The early response to antigen precedes the onset of a chronic inflammatory response that includes the late reaction, defined as the recurrence of symptoms and mediator release hours later. We hypothesized that during the late-phase nasal response to antigen provocation, released histamine originates from basophils, on the basis of the pattern of mediator release. ~ We subsequently showed the presence of basophils in the late reaction 2 but could not exclude mast cells as a source of histamine release. With the development of assays to measure tryptase, a sensitive and specific marker of mast cell degranulation, and 9c~,1113 PGF2, the major metabolite of prostaglandin (PG) D2, it became possible to exclude the mast cell as the source of histamine release. METHODS Study design Twe]ve volunteers who were free of symptoms but had a history of ragweed- or grass-induced allergic rhinitis, a positive intradermal skin test result, and a positive early response to nasal challenge were selected. The Internal Review Board of the Johns Hopkins Medical Institutions gave approval for the study, and each patient gave informed consent. Nasal challenges During the laboratory visit, the subjects underwent a nasal challenge with a relevant antigen extract5 The recovered fluid from the lavage was processed immediately for prostanoids, and the remainder was stored on ice until the completion of the experiment. After centrifuging, the supernatants obtained were processed for the
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