It has been previously demonstrated in nasal challenge studies that there is an increased sensitivity to allergen following an initial allergen challenge. A similar feature has been demonstrated following natural allergen exposure in patients with seasonal allergic rhinitis. To further explore the characteristics of this "priming" phenomenon and its relationship to other expressions of their allergic airway disease, 28 hay fever patients with strictly seasonal disease were studied. Skin tests with the relevant pollen allergen and histamine were performed and the size of the immediate and late phase allergic reaction was determined. An initial nasal allergen challenge was followed by a rechallenge of the nose with allergen 24 h later using a lavage technique. Determinations of TAME-esterase activity, as a biochemical marker of the allergic reaction, were made in the returned lavage fluid. The number of sneezes was counted and nasal symptoms were also assessed using a scoring technique. 19 of 28 patients (67%), displayed an increased responsiveness at rechallenge with similar findings in terms of symptom scores and TAME-esterase measurements. The increase was statistically significant for the symptoms of nasal blockage, which increased from 0.7 +/- 0.1 (mean +/- SEM) to 1.1 +/- 0.2 (P less than 0.05), and nasal secretion which rose from 1.1 +/- 0.2 to 1.7 +/- 0.2 (P less than 0.01). A composite nasal symptom score which also took account of the number of sneezes, increased from 2.9 +/- 0.4 to 4.0 +/- 0.3 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
The effect of glucocorticosteroid (GCS) treatment on ovalbumine-induced IgE-mediated immediate and late allergic response was studied in sensitized guinea pigs. The results show that the GCS budesonide (BUD) inhibits the allergen-induced IgE-mediated immediate and late bronchial obstruction. The effect on the early reaction is correlated to the inhibition of leukotrienes and histamine release. The importance of mediator release inhibition for the antianaphylactic effect of GCS is discussed. In examining the effect on the late reaction, it was found that BUD had to be present during the early reaction but did not inhibit the early reaction. Furthermore, the effect on the late reaction was correlated to the inhibition of vascular leakage but not to the infiltration of inflammatory cells as examined in bronchoalveolar lavage. The results indicate that some triggering factors important for the development of the late reaction are released during the early reaction. Inhibition of the release of that factor or the activation of inflammatory cells by that factor might be the mechanism behind the antiinflammatory activities of GCS.
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