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Long-Term and Clinically Relevant Full-Thickness Human Skin Equivalent for Psoriasis.

Smriti Singh1, Yvonne Marquardt2, Rahul Rimal1

  • 1DWI-Leibniz Institute for Interactive Materials, Forkenbeckstrasse 50, Aachen 52074, Germany.

ACS Applied Bio Materials
|January 12, 2022
PubMed
Summary

A novel, stable 3D human skin equivalent (HSE) model was developed for psoriasis research. This advanced HSE model successfully mimics psoriatic disease phenotypes and allows for testing therapeutic interventions like anti-IL-17A antibodies.

Keywords:
IL-17Ahuman skin equivalentspsoriasisscaffold freesecukinumab

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Area of Science:

  • Biotechnology
  • Dermatology
  • Inflammation Research

Background:

  • Psoriasis is a chronic, immune-mediated skin disease with no cure.
  • Current preclinical models like animal testing and simple cell cultures have limitations in fully recapitulating psoriasis.
  • Existing 3D skin equivalents lack the long-term stability needed for complex disease modeling and drug testing.

Purpose of the Study:

  • To develop a stable, scaffold-free, full-thickness human skin equivalent (HSE) model.
  • To establish a psoriasis-like phenotype in the HSE model using recombinant human interleukin 17A (rhIL-17A).
  • To evaluate the efficacy of the anti-IL-17A antibody secukinumab in treating the induced psoriatic phenotype in the HSE model.

Main Methods:

  • Fabrication of HSEs using a cell coating technique with layer-by-layer assembly for enhanced stability (up to 49 days).
  • Induction of a psoriatic phenotype by stimulating HSEs with rhIL-17A.
  • Treatment of rhIL-17A-stimulated HSEs with the anti-IL-17A antibody secukinumab.
  • Analysis of gene expression changes using microarray and RT-PCR, followed by gene ontology analysis.

Main Results:

  • rhIL-17A stimulation led to downregulation of keratinocyte differentiation markers and upregulation of pro-inflammatory cytokines and chemokines in HSEs.
  • Treatment with secukinumab effectively reversed the rhIL-17A-induced gene expression changes.
  • Gene ontology analysis confirmed the pro-inflammatory and chemotactic effects of rhIL-17A and the therapeutic impact of secukinumab.

Conclusions:

  • The developed scaffold-free HSE model offers long-term stability and accurately replicates key molecular aspects of psoriasis.
  • This HSE model serves as a viable alternative to animal testing and ex vivo skin explants for studying psoriasis pathogenesis.
  • The model demonstrates the molecular efficacy of anti-IL-17A therapy, paving the way for advanced preclinical drug evaluation.