title: Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses.
abstract: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: King's College London, MRC and Asthma UK Centre in Allergic Mechanisms of Asthma, Division of Asthma, Allergy and Lung Biology, London, United Kingdom.
authors.forename: Chris J
authors.initials: CJ
authors.lastname: Corrigan
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Qiu
authors.initials: Q
authors.lastname: Meng
authors.forename: Cailong
authors.initials: C
authors.lastname: Fang
authors.forename: Ghada
authors.initials: G
authors.lastname: Eid
authors.forename: M Rosario
authors.initials: MR
authors.lastname: Caballero
authors.forename: Ze
authors.initials: Z
authors.lastname: Lv
authors.forename: Yunqing
authors.initials: Y
authors.lastname: An
authors.forename: Yui-Hsi
authors.initials: YH
authors.lastname: Wang
authors.forename: Yong-Jun
authors.initials: YJ
authors.lastname: Liu
authors.forename: A Barry
authors.initials: AB
authors.lastname: Kay
authors.forename: Tak H
authors.initials: TH
authors.lastname: Lee
authors.forename: Sun
authors.initials: S
authors.lastname: Ying
mesh_terms: D000328:Adult; D000485:Allergens / Q000276:immunology; D001249:Asthma / Q000276:immunology* / Q000378:metabolism; D001980:Bronchi / Q000276:immunology / Q000378:metabolism; D005260:Female; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000276:immunology* / Q000378:metabolism; D007150:Immunohistochemistry; D020381:Interleukin-17 / Q000096:biosynthesis* / Q000276:immunology; D008297:Male; D018123:Receptors, Interleukin / Q000096:biosynthesis* / Q000276:immunology; D053722:Receptors, Interleukin-17 / Q000096:biosynthesis*; D020545:Respiratory Mucosa / Q000276:immunology* / Q000378:metabolism; D012867:Skin / Q000276:immunology* / Q000378:metabolism; D055815:Young Adult
chemical_list: D000485:Allergens; C560912:IL-25 receptor protein, human; C486701:IL25 protein, human; D020381:Interleukin-17; D018123:Receptors, Interleukin; D053722:Receptors, Interleukin-17