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The release of IL‐31 and IL‐13 after nasal allergen challenge and their relation to nasal symptoms
Author(s) -
Baumann Ralf,
Rabaszowski Matthaeus,
Stenin Igor,
GaertnerAkerboom Maria,
Scheckenbach Kathrin,
Wiltfang Jens,
Schipper Joerg,
Wagenmann Martin
Publication year - 2012
Publication title -
clinical and translational allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.979
H-Index - 37
ISSN - 2045-7022
DOI - 10.1186/2045-7022-2-13
Subject(s) - medicine , provocation test , rhinorrhea , allergen , allergy , immunology , nasal provocation test , nasal lavage , pathology , alternative medicine
Background IL‐31, a recently discovered member of the gp130/IL‐6 cytokine family, is mainly expressed by human mast cells and T helper type 2 cells. IL‐31 is a key trigger of atopic dermatitis. Recent studies also suggest a role of IL‐31 in the pathogenesis of other allergic diseases including allergic rhinitis. In the present study we studied the release of IL‐31 and IL‐13 in allergen‐challenged allergic rhinitis patients. Methods Seven seasonal allergic volunteers underwent unilateral nasal provocation with allergen (and a control challenge) with the disc method out of the allergy season. Nasal symptom scores (rhinorrhea, itching, sneezing, obstruction) and bilateral nasal secretions were quantified before and after allergen provocation. IL‐13 and IL‐31 in nasal secretions and serum were measured by electrochemiluminescent immunoassay or ELISA, respectively. Results Nasal allergen challenge induced the typical clinical symptoms and physiological changes. IL‐31 and IL‐13 in nasal secretions increased in four and five, respectively, volunteers at 5 h after allergen but not after control challenge. We observed correlation trends between nasal IL‐31 concentrations and IL‐13 concentrations (r = 0.9, p = 0.002), and IL‐31 contents and symptom scores (r = 0.9, p = 0.013) 5 h after allergen provocation. No IL‐31 could be detected contralaterally or systemically in the sera. Conclusions The observed local upregulation of IL‐31 mainly during the late phase reaction after nasal allergen challenge suggests a role of IL‐31 in allergic rhinitis. In which way IL‐31 modulates the inflammatory reaction and type 2 responses in allergic rhinitis remains to be investigated.

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