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Major differences between human atopic dermatitis and murine models, as determined by using global transcriptomic

David A Ewald1, Shinji Noda2, Margeaux Oliva3

  • 1Laboratory for Investigative Dermatology, Rockefeller University, New York, NY; Exploratory Biology, LEO Pharma A/S, Ballerup, Denmark; Regulatory Genomics, Integrative Systems Biology, Center for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, Kgs. Lyngby, Denmark.

The Journal of Allergy and Clinical Immunology
|October 6, 2016
PubMed
Summary
This summary is machine-generated.

The IL-23-injected murine model best simulates human atopic dermatitis (AD) transcriptomic profiles, reflecting key immune responses. However, no single model fully replicates all AD aspects, necessitating careful selection based on research focus.

Keywords:
Atopic dermatitisIL-2NC/NgaT(H)1T(H)17T(H)2contact dermatitisfilaggrinmouse modelovalbuminoxazolonepsoriasis

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Area of Science:

  • Immunology
  • Dermatology
  • Genomics

Background:

  • Atopic dermatitis (AD) involves complex immune and barrier dysfunctions.
  • Murine models are crucial for preclinical AD treatment evaluation.
  • Transcriptomic profiles of existing AD models and their comparison to human AD are not fully understood.

Purpose of the Study:

  • To evaluate transcriptomic profiles of six common murine models of AD.
  • To compare these profiles with the human AD transcriptomic fingerprint.

Main Methods:

  • Transcriptomic profiling using microarrays and qRT-PCR on biopsy specimens from six murine models (NC/Nga, flaky tail, Flg-mutated, ovalbumin-challenged, oxazolone-challenged, IL-23-injected).
  • Analysis of gene expression data from human AD, psoriasis, and contact dermatitis cohorts.
  • Application of fold change (≥2) and false discovery rate (≤0.05) criteria for gene array analysis.

Main Results:

  • The IL-23-injected, NC/Nga, and oxazolone-challenged models showed the highest homology (37%, 18%, 17%) to the human AD transcriptome.
  • IL-23-injected and NC/Nga mice exhibited robust TH1, TH2, and TH17 activation, similar to human AD.
  • Other models displayed distinct immune profiles: TH1-centered (oxazolone), TH17-polarized (flaky tail), or barrier defect without inflammation (Flg-mutated).

Conclusions:

  • No single murine model completely recapitulates the human AD profile.
  • Each model represents different aspects of immune or barrier dysfunction in AD.
  • The IL-23-injected model demonstrates the best simulation of human AD among the tested models, though model selection should align with translational goals.