Impaired Tight Junctions in Atopic Dermatitis Skin and in a Skin-Equivalent Model Treated with Interleukin-17

Autor: Megumi Tobiishi, Yoshiki Tokura, Yukiko Ota, Takuo Yuki, Ayumi Kusaka-Kikushima
Rok vydání: 2016
Předmět:
0301 basic medicine
Keratinocytes
Pathology
Physiology
Stratum granulosum
Cell Membranes
lcsh:Medicine
Filaggrin Proteins
Pathology and Laboratory Medicine
Epithelium
0302 clinical medicine
Animal Cells
Immune Physiology
Claudin-1
Medicine and Health Sciences
lcsh:Science
Barrier function
Cells
Cultured

Skin
Innate Immune System
Multidisciplinary
Tight junction
integumentary system
Interleukin-17
Interleukin
Atopic dermatitis
medicine.anatomical_structure
030220 oncology & carcinogenesis
Physical Sciences
Amino Acid Analysis
Cytokines
Anatomy
Integumentary System
Junctional Complexes
Cellular Structures and Organelles
Cellular Types
Filaggrin
Research Article
medicine.medical_specialty
Cell Physiology
Immunology
Materials Science
Material Properties
Biology
Research and Analysis Methods
Permeability
Dermatitis
Atopic

Tight Junctions
03 medical and health sciences
Signs and Symptoms
Diagnostic Medicine
medicine
Skin equivalent
Humans
Molecular Biology Techniques
Molecular Biology
Molecular Biology Assays and Analysis Techniques
Tight Junction Proteins
Epidermis (botany)
Tumor Necrosis Factor-alpha
Interleukins
lcsh:R
Biology and Life Sciences
Membrane Proteins
Epithelial Cells
Cell Biology
Molecular Development
medicine.disease
030104 developmental biology
Biological Tissue
Immune System
Zonula Occludens-1 Protein
Lesions
lcsh:Q
Interleukin-4
Epidermis
Developmental Biology
Zdroj: PLoS ONE
PLoS ONE, Vol 11, Iss 9, p e0161759 (2016)
ISSN: 1932-6203
Popis: Tight junction (TJ) dysfunction in the stratum granulosum leads to aberrant barrier function of the stratum corneum (SC) in the epidermis. However, it is unclear whether TJs are perturbed in atopic dermatitis (AD), a representative aberrant SC-related skin disease, and whether some factors related to AD pathogenesis induce TJ dysfunction. To address these issues, we investigated the alterations of TJs in AD skin and the effects of Th2 and Th17 cytokines on TJs in a skin-equivalent model. The levels of TJ proteins were determined in the epidermis of nonlesional and lesional skin sites of AD. Western blot and immunohistochemical analyses revealed that the levels of zonula occludens 1 were decreased in the nonlesional sites of AD, and the levels of zonula occludens 1 and claudin-1 were decreased in the lesional sites relative to the levels in skin from healthy subjects. Next, we examined the effects of interleukin (IL)-4, tumor necrosis factor-α, IL-17, and IL-22 on the TJ barrier in a skin-equivalent model. Only IL-17 impaired the TJ barrier. Furthermore, we observed a defect in filaggrin monomer degradation in the IL-17-treated skin model. Thus, TJs are dysfunctional in AD, at least partly, due to the effect of IL-17, which may result in an aberrant SC barrier.
Databáze: OpenAIRE