Abstract
It has been suggested that the IgE-dependent late-phase reaction to allergen exposure, with the features of an inflammatory cellular infiltration and airway hyperreactivity, is a link between anaphylaxis and continuous allergic airway disease. Our main knowledge of the cellular response to allergen in sensitized individuals has been derived from allergen-challenge models. To explore the dynamics of the cellular response during the actual disease, patients with a strictly seasonal allergic rhinitis were studied during natural allergen exposure. Ten patients suffering from an isolated birch-pollen allergy were followed from a symptom free state before, during, and to the height of the birch-pollen season. Repeated parallel cell samplings from the nasal mucosa were performed with cytologic imprints on plastic strips, nasal lavages with the recovery of the cells in the lavage fluid with cytocentrifugation on object slides for cytologic study, and scrapings from the nasal surface with a curette for histologic and ultrastructural evaluation. The histamine content was determined in lavage fluid and cell pellets. The tosyl-α-tosyl- l-arginine methyl esterase activity of the nasal lavage fluid was also determined as a biochemical marker of the allergic inflammatory reaction. The birch-pollen season was moderate in terms of pollen counts, and this resulted in mild to moderate nasal symptoms that ran parallel to the birch pollen counts. The total number of cells recovered in the lavage fluid was 1.2 ± 0.4 (SEM) × 10 6 before and 3.2 ± 2.0 per 10 6 cells (not significant) during pollen exposure. Most cells were neutrophils and mononuclear cells. The proportion of eosinophils increased from 2.5 ± 1.0% to 19.2 ± 7.4% ( p < 0.01) of the total cell number, and both the percentage and total number of eosinophils closely followed the nasal symptoms and pollen counts. The resulting total number of eosinophils thereby increased 20 fold from 35 ± 23 per 10 3 to 661 ± 585 × 10 3 cells ( p < 0.05). The histamine content of the cell pellet, indicating the presence of basophil mediator cells, increased from 0 (below the detection limit of the assay) to 1.4 ± 0.3 ng ( p < 0.05) during the pollen season with a time course after that of the eosinophils. The number of mast cells found on the imprints also increased during the pollen season but did not start to appear until after 4 to 5 days of pollen exposure. The tosyl-α- l-arginine methyl esterase in the lavage fluid, as a marker of allergic activity, increased from 1.3 ± 0.1 to 2.3 ± 0.4 counts per minute × 10 3 ( p < 0.01). These results reemphasize the role of the eosinophil in the pathogenesis of continuous allergic mucosal disease and suggest that it may have an effector function, in addition to a protector role in allergic airway disease.
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