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Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses

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 S... Full description

Journal Title: Journal of allergy and clinical immunology 2011, Vol.128 (1), p.116-124
Main Author: Corrigan, Chris J., MD, PhD
Other Authors: Wang, Wei, MD , Meng, Qiu, MD , Fang, Cailong, MD, PhD , Eid, Ghada, MD , Caballero, M. Rosario, MD , Lv, Ze, MSc , An, Yunqing, MD , Wang, Yui-Hsi, PhD , Liu, Yong-Jun, MD, PhD , Kay, A. Barry, MD, PhD , Lee, Tak H., MD, DSc , Ying, Sun, MD, PhD
Format: Electronic Article Electronic Article
Language: English
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Quelle: Alma/SFX Local Collection
Publisher: New York, NY: Mosby, Inc
ID: ISSN: 0091-6749
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title: Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
format: Article
creator:
  • Corrigan, Chris J., MD, PhD
  • Wang, Wei, MD
  • Meng, Qiu, MD
  • Fang, Cailong, MD, PhD
  • Eid, Ghada, MD
  • Caballero, M. Rosario, MD
  • Lv, Ze, MSc
  • An, Yunqing, MD
  • Wang, Yui-Hsi, PhD
  • Liu, Yong-Jun, MD, PhD
  • Kay, A. Barry, MD, PhD
  • Lee, Tak H., MD, DSc
  • Ying, Sun, MD, PhD
subjects:
  • Abridged Index Medicus
  • Adult
  • allergen challenge
  • Allergens - immunology
  • Allergies
  • Allergy and Immunology
  • Asthma
  • Asthma - immunology
  • Asthma - metabolism
  • Biological and medical sciences
  • Biomedical engineering
  • Biopsy
  • Bronchi - immunology
  • Bronchi - metabolism
  • Cancer
  • Chronic obstructive pulmonary disease, asthma
  • Cytokines
  • Endothelium
  • Female
  • Fiber optics
  • Fundamental and applied biological sciences. Psychology
  • Fundamental immunology
  • Humans
  • Hypersensitivity, Immediate - immunology
  • Hypersensitivity, Immediate - metabolism
  • IL-25
  • IL-25 receptor
  • Immunohistochemistry
  • Immunopathology
  • Interleukin-17 - biosynthesis
  • Interleukin-17 - immunology
  • Male
  • Medical colleges
  • Medical sciences
  • Oncology, Experimental
  • Patients
  • Phosphatases
  • Pneumology
  • Pollen
  • Receptors, Interleukin - biosynthesis
  • Receptors, Interleukin - immunology
  • Receptors, Interleukin-17 - biosynthesis
  • Respiratory Mucosa - immunology
  • Respiratory Mucosa - metabolism
  • Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
  • Skin - immunology
  • Skin - metabolism
  • skin late-phase response
  • Smooth muscle
  • Young Adult
ispartof: Journal of allergy and clinical immunology, 2011, Vol.128 (1), p.116-124
description: 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.
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0091-6749
fulltext: fulltext
issn:
  • 0091-6749
  • 1097-6825
url: Link


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titleAllergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
sourceAlma/SFX Local Collection
creatorCorrigan, Chris J., MD, PhD ; Wang, Wei, MD ; Meng, Qiu, MD ; Fang, Cailong, MD, PhD ; Eid, Ghada, MD ; Caballero, M. Rosario, MD ; Lv, Ze, MSc ; An, Yunqing, MD ; Wang, Yui-Hsi, PhD ; Liu, Yong-Jun, MD, PhD ; Kay, A. Barry, MD, PhD ; Lee, Tak H., MD, DSc ; Ying, Sun, MD, PhD
creatorcontribCorrigan, Chris J., MD, PhD ; Wang, Wei, MD ; Meng, Qiu, MD ; Fang, Cailong, MD, PhD ; Eid, Ghada, MD ; Caballero, M. Rosario, MD ; Lv, Ze, MSc ; An, Yunqing, MD ; Wang, Yui-Hsi, PhD ; Liu, Yong-Jun, MD, PhD ; Kay, A. Barry, MD, PhD ; Lee, Tak H., MD, DSc ; Ying, Sun, MD, PhD
descriptionBackground 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.
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3PMID: 21570719
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languageeng
publisherNew York, NY: Mosby, Inc
subjectAbridged Index Medicus ; Adult ; allergen challenge ; Allergens - immunology ; Allergies ; Allergy and Immunology ; Asthma ; Asthma - immunology ; Asthma - metabolism ; Biological and medical sciences ; Biomedical engineering ; Biopsy ; Bronchi - immunology ; Bronchi - metabolism ; Cancer ; Chronic obstructive pulmonary disease, asthma ; Cytokines ; Endothelium ; Female ; Fiber optics ; Fundamental and applied biological sciences. Psychology ; Fundamental immunology ; Humans ; Hypersensitivity, Immediate - immunology ; Hypersensitivity, Immediate - metabolism ; IL-25 ; IL-25 receptor ; Immunohistochemistry ; Immunopathology ; Interleukin-17 - biosynthesis ; Interleukin-17 - immunology ; Male ; Medical colleges ; Medical sciences ; Oncology, Experimental ; Patients ; Phosphatases ; Pneumology ; Pollen ; Receptors, Interleukin - biosynthesis ; Receptors, Interleukin - immunology ; Receptors, Interleukin-17 - biosynthesis ; Respiratory Mucosa - immunology ; Respiratory Mucosa - metabolism ; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis ; Skin - immunology ; Skin - metabolism ; skin late-phase response ; Smooth muscle ; Young Adult
ispartofJournal of allergy and clinical immunology, 2011, Vol.128 (1), p.116-124
rights
0American Academy of Allergy, Asthma & Immunology
12011 American Academy of Allergy, Asthma & Immunology
22015 INIST-CNRS
3Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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0Corrigan, Chris J., MD, PhD
1Wang, Wei, MD
2Meng, Qiu, MD
3Fang, Cailong, MD, PhD
4Eid, Ghada, MD
5Caballero, M. Rosario, MD
6Lv, Ze, MSc
7An, Yunqing, MD
8Wang, Yui-Hsi, PhD
9Liu, Yong-Jun, MD, PhD
10Kay, A. Barry, MD, PhD
11Lee, Tak H., MD, DSc
12Ying, Sun, MD, PhD
title
0Allergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
1Journal of allergy and clinical immunology
addtitleJ Allergy Clin Immunol
descriptionBackground 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.
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3Allergens - immunology
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5Allergy and Immunology
6Asthma
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12Bronchi - immunology
13Bronchi - metabolism
14Cancer
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16Cytokines
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21Fundamental immunology
22Humans
23Hypersensitivity, Immediate - immunology
24Hypersensitivity, Immediate - metabolism
25IL-25
26IL-25 receptor
27Immunohistochemistry
28Immunopathology
29Interleukin-17 - biosynthesis
30Interleukin-17 - immunology
31Male
32Medical colleges
33Medical sciences
34Oncology, Experimental
35Patients
36Phosphatases
37Pneumology
38Pollen
39Receptors, Interleukin - biosynthesis
40Receptors, Interleukin - immunology
41Receptors, Interleukin-17 - biosynthesis
42Respiratory Mucosa - immunology
43Respiratory Mucosa - metabolism
44Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
45Skin - immunology
46Skin - metabolism
47skin late-phase response
48Smooth muscle
49Young Adult
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titleAllergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
authorCorrigan, Chris J., MD, PhD ; Wang, Wei, MD ; Meng, Qiu, MD ; Fang, Cailong, MD, PhD ; Eid, Ghada, MD ; Caballero, M. Rosario, MD ; Lv, Ze, MSc ; An, Yunqing, MD ; Wang, Yui-Hsi, PhD ; Liu, Yong-Jun, MD, PhD ; Kay, A. Barry, MD, PhD ; Lee, Tak H., MD, DSc ; Ying, Sun, MD, PhD
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5Allergy and Immunology
6Asthma
7Asthma - immunology
8Asthma - metabolism
9Biological and medical sciences
10Biomedical engineering
11Biopsy
12Bronchi - immunology
13Bronchi - metabolism
14Cancer
15Chronic obstructive pulmonary disease, asthma
16Cytokines
17Endothelium
18Female
19Fiber optics
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21Fundamental immunology
22Humans
23Hypersensitivity, Immediate - immunology
24Hypersensitivity, Immediate - metabolism
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39Receptors, Interleukin - biosynthesis
40Receptors, Interleukin - immunology
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43Respiratory Mucosa - metabolism
44Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis
45Skin - immunology
46Skin - metabolism
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48Smooth muscle
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atitleAllergen-induced expression of IL-25 and IL-25 receptor in atopic asthmatic airways and late-phase cutaneous responses
jtitleJournal of allergy and clinical immunology
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date2011
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abstractBackground 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.
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