Dysregulation of the epithelial barrier by environmental and other exogenous factors

The “epithelial barrier hypothesis” proposes that the exposure to various epithelial barrier–damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense ag...

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Veröffentlicht in:Contact dermatitis Jg. 85; H. 6; S. 615 - 626
Hauptverfasser: Mitamura, Yasutaka, Ogulur, Ismail, Pat, Yagiz, Rinaldi, Arturo O., Ardicli, Ozge, Cevhertas, Lacin, Brüggen, Marie‐Charlotte, Traidl‐Hoffmann, Claudia, Akdis, Mubeccel, Akdis, Cezmi A.
Format: Journal Article
Sprache:Englisch
Veröffentlicht: Oxford, UK Blackwell Publishing Ltd 01.12.2021
Wiley Subscription Services, Inc
Schlagworte:
Adaptive Immunity
Allergens
Allergens - adverse effects
Allergic diseases
allergy
Asthma
atopic dermatitis
Atopy
barrier dysfunction
Dermatitis, Atopic - etiology
Dermatitis, Atopic - genetics
Dermatitis, Atopic - immunology
Dermatitis, Atopic - physiopathology
Eczema
Electrical impedance
Environmental Exposure
Environmental factors
Epigenesis, Genetic
Epigenetics
epithelium
Epithelium - anatomy & histology
Epithelium - physiopathology
Humans
Immune response
Immunity, Innate
Microbiomes
Microbiota - physiology
Permeability
Review
Reviews
rhinitis
sinusitis
Spectroscopy
type 2 immunity
Urbanization
sinusitis
allergy
atopic dermatitis
asthma
epithelium
rhinitis
barrier dysfunction
type 2 immunity
ISSN:0105-1873, 1600-0536, 1600-0536
Online-Zugang:Volltext
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Abstract The “epithelial barrier hypothesis” proposes that the exposure to various epithelial barrier–damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense against environmental factors. Recent reports have shown that industrial products disrupt the epithelial barriers. Innate and adaptive immune responses play an important role in epithelial barrier damage. In addition, recent studies suggest that epithelial barrier dysfunction plays an essential role in the pathogenesis of the atopic march by allergen sensitization through the transcutaneous route. It is evident that external factors interact with the immune system, triggering a cascade of complex reactions that damage the epithelial barrier. Epigenetic and microbiome changes modulate the integrity of the epithelial barrier. Robust and simple measurements of the skin barrier dysfunction at the point‐of‐care are of significant value as a biomarker, as recently reported using electrical impedance spectroscopy to directly measure barrier defects. Understanding epithelial barrier dysfunction and its mechanism is key to developing novel strategies for the prevention and treatment of allergic diseases. The aim of this review is to summarize recent studies on the pathophysiological mechanisms triggered by environmental factors that contribute to the dysregulation of epithelial barrier function.
AbstractList The “epithelial barrier hypothesis” proposes that the exposure to various epithelial barrier–damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense against environmental factors. Recent reports have shown that industrial products disrupt the epithelial barriers. Innate and adaptive immune responses play an important role in epithelial barrier damage. In addition, recent studies suggest that epithelial barrier dysfunction plays an essential role in the pathogenesis of the atopic march by allergen sensitization through the transcutaneous route. It is evident that external factors interact with the immune system, triggering a cascade of complex reactions that damage the epithelial barrier. Epigenetic and microbiome changes modulate the integrity of the epithelial barrier. Robust and simple measurements of the skin barrier dysfunction at the point‐of‐care are of significant value as a biomarker, as recently reported using electrical impedance spectroscopy to directly measure barrier defects. Understanding epithelial barrier dysfunction and its mechanism is key to developing novel strategies for the prevention and treatment of allergic diseases. The aim of this review is to summarize recent studies on the pathophysiological mechanisms triggered by environmental factors that contribute to the dysregulation of epithelial barrier function.
The "epithelial barrier hypothesis" proposes that the exposure to various epithelial barrier-damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense against environmental factors. Recent reports have shown that industrial products disrupt the epithelial barriers. Innate and adaptive immune responses play an important role in epithelial barrier damage. In addition, recent studies suggest that epithelial barrier dysfunction plays an essential role in the pathogenesis of the atopic march by allergen sensitization through the transcutaneous route. It is evident that external factors interact with the immune system, triggering a cascade of complex reactions that damage the epithelial barrier. Epigenetic and microbiome changes modulate the integrity of the epithelial barrier. Robust and simple measurements of the skin barrier dysfunction at the point-of-care are of significant value as a biomarker, as recently reported using electrical impedance spectroscopy to directly measure barrier defects. Understanding epithelial barrier dysfunction and its mechanism is key to developing novel strategies for the prevention and treatment of allergic diseases. The aim of this review is to summarize recent studies on the pathophysiological mechanisms triggered by environmental factors that contribute to the dysregulation of epithelial barrier function.The "epithelial barrier hypothesis" proposes that the exposure to various epithelial barrier-damaging agents linked to industrialization and urbanization underlies the increase in allergic diseases. The epithelial barrier constitutes the first line of physical, chemical, and immunological defense against environmental factors. Recent reports have shown that industrial products disrupt the epithelial barriers. Innate and adaptive immune responses play an important role in epithelial barrier damage. In addition, recent studies suggest that epithelial barrier dysfunction plays an essential role in the pathogenesis of the atopic march by allergen sensitization through the transcutaneous route. It is evident that external factors interact with the immune system, triggering a cascade of complex reactions that damage the epithelial barrier. Epigenetic and microbiome changes modulate the integrity of the epithelial barrier. Robust and simple measurements of the skin barrier dysfunction at the point-of-care are of significant value as a biomarker, as recently reported using electrical impedance spectroscopy to directly measure barrier defects. Understanding epithelial barrier dysfunction and its mechanism is key to developing novel strategies for the prevention and treatment of allergic diseases. The aim of this review is to summarize recent studies on the pathophysiological mechanisms triggered by environmental factors that contribute to the dysregulation of epithelial barrier function.
Author Ardicli, Ozge
Akdis, Mubeccel
Akdis, Cezmi A.
Mitamura, Yasutaka
Ogulur, Ismail
Traidl‐Hoffmann, Claudia
Pat, Yagiz
Rinaldi, Arturo O.
Cevhertas, Lacin
Brüggen, Marie‐Charlotte
AuthorAffiliation 6 Christine Kühne‐Center for Allergy Research and Education Davos Switzerland
1 Swiss Institute of Allergy and Asthma Research (SIAF) University of Zurich Davos
4 Department of Microbiology, Faculty of Veterinary Medicine Bursa Uludag University Bursa Turkey
2 Division of Pediatric Allergy and Immunology School of Medicine, Marmara University Istanbul Turkey
7 Department of Dermatology University Hospital Zurich Zurich Switzerland
8 Faculty of Medicine University of Zurich Zurich Switzerland
3 Department of Medical Microbiology, Faculty of Medicine Aydin Menderes University Aydin Turkey
5 Department of Medical Immunology Institute of Health Sciences, Bursa Uludag University Bursa Turkey
9 Department of Environmental Medicine, Faculty of Medicine University of Augsburg Augsburg Germany
AuthorAffiliation_xml – name: 7 Department of Dermatology University Hospital Zurich Zurich Switzerland
– name: 4 Department of Microbiology, Faculty of Veterinary Medicine Bursa Uludag University Bursa Turkey
– name: 8 Faculty of Medicine University of Zurich Zurich Switzerland
– name: 9 Department of Environmental Medicine, Faculty of Medicine University of Augsburg Augsburg Germany
– name: 2 Division of Pediatric Allergy and Immunology School of Medicine, Marmara University Istanbul Turkey
– name: 1 Swiss Institute of Allergy and Asthma Research (SIAF) University of Zurich Davos
– name: 3 Department of Medical Microbiology, Faculty of Medicine Aydin Menderes University Aydin Turkey
– name: 5 Department of Medical Immunology Institute of Health Sciences, Bursa Uludag University Bursa Turkey
– name: 6 Christine Kühne‐Center for Allergy Research and Education Davos Switzerland
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  surname: Mitamura
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  surname: Pat
  fullname: Pat, Yagiz
  organization: Aydin Menderes University
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  surname: Rinaldi
  fullname: Rinaldi, Arturo O.
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  surname: Cevhertas
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  surname: Brüggen
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  organization: University of Zurich
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  surname: Traidl‐Hoffmann
  fullname: Traidl‐Hoffmann, Claudia
  organization: University of Augsburg
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  surname: Akdis
  fullname: Akdis, Mubeccel
  organization: University of Zurich
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  givenname: Cezmi A.
  surname: Akdis
  fullname: Akdis, Cezmi A.
  email: akdisac@siaf.uzh.ch
  organization: Christine Kühne‐Center for Allergy Research and Education
BackLink https://www.ncbi.nlm.nih.gov/pubmed/34420214$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2021 The Authors. published by John Wiley & Sons Ltd.
2021 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.
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Issue 6
Keywords sinusitis
allergy
atopic dermatitis
asthma
epithelium
rhinitis
barrier dysfunction
type 2 immunity
Language English
License Attribution-NonCommercial-NoDerivs
2021 The Authors. Contact Dermatitis published by John Wiley & Sons Ltd.
This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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Notes Yasutaka Mitamura and Ismail Ogulur Contributed equally to this work.
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ORCID 0000-0001-8282-7762
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OpenAccessLink https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcod.13959
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PublicationTitle Contact dermatitis
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Snippet The “epithelial barrier hypothesis” proposes that the exposure to various epithelial barrier–damaging agents linked to industrialization and urbanization...
The "epithelial barrier hypothesis" proposes that the exposure to various epithelial barrier-damaging agents linked to industrialization and urbanization...
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StartPage 615
SubjectTerms Adaptive Immunity
Allergens
Allergens - adverse effects
Allergic diseases
allergy
Asthma
atopic dermatitis
Atopy
barrier dysfunction
Dermatitis, Atopic - etiology
Dermatitis, Atopic - genetics
Dermatitis, Atopic - immunology
Dermatitis, Atopic - physiopathology
Eczema
Electrical impedance
Environmental Exposure
Environmental factors
Epigenesis, Genetic
Epigenetics
epithelium
Epithelium - anatomy & histology
Epithelium - physiopathology
Humans
Immune response
Immunity, Innate
Microbiomes
Microbiota - physiology
Permeability
Review
Reviews
rhinitis
sinusitis
Spectroscopy
type 2 immunity
Urbanization
Title Dysregulation of the epithelial barrier by environmental and other exogenous factors
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fcod.13959
https://www.ncbi.nlm.nih.gov/pubmed/34420214
https://www.proquest.com/docview/2597683327
https://www.proquest.com/docview/2563697869
https://pubmed.ncbi.nlm.nih.gov/PMC9293165
Volume 85
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