Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 128, Issue 1, Pages 116-124Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2011.03.043
Keywords
IL-25; IL-25 receptor; asthma; skin late-phase response; allergen challenge
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Funding
- Dana Foundation
- Asthma UK
- Department of Health via the National Institute for Health Research (NIHR)
- NHS Foundation Trust
- King's College London
- King's College Hospital NHS Foundation Trust
- Medical Research Council [G1000758B, G1000758] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0508-10212] Funding Source: researchfish
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Background: IL-25 is thought to participate in allergic inflammation by propagating T(H)2-type responses. Objective: To address the hypothesis that allergen provocation increases expression of IL-25 and its receptor IL-25R in the asthmatic bronchial mucosa and skin dermis of atopic subjects. Methods: Sequential single and double immunostaining was used to evaluate the numbers and phenotypes of IL-25 and IL-25R immunoreactive cells in bronchial biopsies from mild atopic subjects with asthma (n = 10) before and 24 hours after allergen inhalation challenge and skin biopsies from atopic subjects (n = 10) up to 72 hours after allergen subepidermal injection. Results: IL-25 immunoreactivity was expressed by a majority of epidermal cells in both organs at baseline and was not further augmented by challenge. IL-25R immunoreactive cells were rare in the epidermis before or after challenge. Allergen challenge was associated with significantly (P < .01) increased expression of IL-25 and IL-25R immunoreactivity in the submucosa of both organs. IL-25 immunoreactivity colocalized with eosinophils, mast cells, and endothelial cells, whereas IL-25R immunoreactivity colocalized with eosinophils, mast cells, endothelial cells, and T lymphocytes. In both organs, correlations were observed between increases in IL-25 expression and the magnitudes of the late-phase allergen-induced clinical responses. Conclusion: Allergen provocation induces functionally relevant, increased expression of IL-25 and its receptor in the asthmatic bronchial mucosa and dermis of sensitized atopic subjects. In addition to T cells, eosinophils, mast cells, and endothelial cells are potential sources and targets of IL-25 in the course of allergic inflammation. (J Allergy Clin Immunol 2011; 128: 116-24.)
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