Clinical Allergy: Rhinitis and Asthma
Regulation of Proinflammatory Cytokines in Seasonal Allergic RhinitisBachert C. · van Kempen M. · van Cauwenberge P.
ENT Department, University Hospital Ghent, Belgium
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Background: Mediators and cytokines have been demonstrated to be released due to nasal allergen exposure in sensitized subjects, but little is known about the release of cytokines and their antagonists under natural conditions. Methods: Mediators – histamine, eosinophilic cationic protein (ECP), leukotrienes (LT) C4/ D4/E4 – and cytokines – interleukin (IL)–1β, IL–8, IL–1 receptor antagonist (ra) – were measured in nasal secretions throughout the grass pollen season (6 visits) and for 6 weeks thereafter (3 visits) in patients with seasonal allergic rhinitis (n = 13) and compared to controls (n = 12). A second study was performed comparing nasal secretions of 13 subjects allergic to house dust mite to 8 controls. Results: Compared to controls, leukotrienes and ECP were significantly elevated at nearly all time points in and postseason in the allergic group. Whereas IL–1β was significantly elevated throughout the study period, IL–1ra was significantly decreased from visit 1 to 3. IL–8 showed no increase compared to controls. Data from subjects with perennial allergic rhinitis supported these findings and additionally demonstrated decreased concentrations of IL–8 and myeloperoxidase in secretions compared to controls. Conclusion: Allergic rhinitis represents a persistent inflammation in terms of an activation of eosinophils and constant upregulation of the proinflammatory cytokine IL–1β in the pollen season and thereafter. We additionally could demonstrate a dysfunction of the anti–inflammatory capacity, i.e. IL–1ra, a naturally occurring antagonist. Persistent inflammation may furthermore lead to the dysregulation of local cellular immunity by reducing the number and activity of neutrophils on the mucosal surface.
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