Full-thickness human skin equivalent models of atopic dermatitis

Research output: Chapter in Book/Report/Conference proceedingChapter

16 Scopus citations

Abstract

Atopic dermatitis is a chronic inflammatory skin disease caused by complex multifactorial etiology. In the recent years, there have been significant advances in tissue engineering and the generation of in vitro skin models representative of healthy and diseased states. This chapter describes the methodology for the fabrication of in vitro human skin equivalent (HSE) from human keratinocytes and fibroblasts using a fibrin-based dermal matrix and serum-free culture conditions. Modification of the culture conditions with the supplementation of Th2 cytokines such as interleukin-4 induces the development of atopic dermatitis-like skin model. The chapter also describes the histological and immunohistochemical tools for characterization of the HSE model. The reconstruction of tissue-engineered HSE models that recapitulate the essential features of atopic dermatitis provides powerful tools for deeper understanding of the underlying pathological mechanisms on epidermal level, identification and testing of novel treatment options, and safety and toxicological evaluation in a pathophysiologically relevant system.

Original languageEnglish (US)
Title of host publicationMethods in Molecular Biology
PublisherHumana Press Inc.
Pages367-383
Number of pages17
Volume1879
DOIs
StatePublished - 2019

Publication series

NameMethods in molecular biology (Clifton, N.J.)
PublisherHumana Press
ISSN (Print)1064-3745

Bibliographical note

Publisher Copyright:
© Springer Science+Business Media New York 2018.

Keywords

  • 3D tissue constructs
  • Atopic dermatitis
  • Fibrin
  • Full-thickness
  • Human skin equivalent
  • Organoids
  • Organotypic culture
  • Tissue engineering
  • Fibroblasts/cytology
  • Humans
  • Cells, Cultured
  • Keratinocytes/cytology
  • Fibrin/metabolism
  • Dermatitis, Atopic/pathology
  • Models, Biological
  • Skin, Artificial
  • Skin/cytology
  • Cytokines/metabolism
  • Tissue Engineering

PubMed: MeSH publication types

  • Research Support, Non-U.S. Gov't
  • Journal Article

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