Severe skin inflammation and filaggrin mutation similarly alter the skin barrier in patients with atopic dermatitis

Authors

  • G. Mócsai,

    1. Department of Dermatology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    2. Department of Dermatological Allergology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • K. Gáspár,

    1. Department of Dermatology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    2. Department of Dermatological Allergology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • G. Nagy,

    1. Department of Dermatology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    2. Department of Dermatological Allergology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • B. Irinyi,

    1. Department of Dermatology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    2. Department of Dermatological Allergology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • A. Kapitány,

    1. Department of Dermatology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    2. Department of Dermatological Allergology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • T. Bíró,

    1. Department of Physiology, DE-MTA ‘Lendület’ Cellular Physiology Research Group, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • E. Gyimesi,

    1. 3rd Department of Internal Medicine, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • B. Tóth,

    1. Department of Infectious and Pediatric Immunology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • L. Maródi,

    1. Department of Infectious and Pediatric Immunology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author
  • A. Szegedi

    Corresponding author
    1. Department of Dermatology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    2. Department of Dermatological Allergology, Medical and Health Science Center, University of Debrecen, Debrecen, Hungary
    Search for more papers by this author

  • Funding sources This work was supported by Hungarian Research Grants (OTKA K81381, TÁMOP-4·2·2.A-11/1/KONV-2012-0023-‘VÉD-ELEM’, OTKA K101761 and LP003/2011).
  • Conflicts of interest None declared.

Summary

Background

Filaggrin (FLG) deficiency is a well-known predisposing factor for the development of atopic dermatitis (AD). Decreased FLG expression can be the result of haploinsufficiency or severe inflammation, which can cause acquired FLG alterations. FLG mutations are related to several clinical and laboratory parameters of AD; however, some recent data seem to contradict these associations.

Objectives

Our aim was to determine which clinical and biochemical parameters are connected to FLG haploinsufficiency and which ones are also associated with acquired FLG alterations due to severe skin symptoms in patients with AD.

Methods

We introduced a novel classification of patients with AD, based on FLG mutations and SCORAD (SCORing Atopic Dermatitis). Based on these parameters, we created three groups of patients with AD: mild-to-moderate wild-type (A), severe wild-type (B) and severe mutant (C). In all groups, we assessed laboratory and clinical parameters and performed immunohistochemical analyses.

Results

Groups B and C contained patients with equally severe symptoms based on the SCORAD. The two severe groups did not differ significantly with respect to barrier-specific parameters, whereas group A had significantly better results for the barrier function measurements. However, significant differences were detected between groups B and C with respect to the allergic sensitization-specific parameters.

Conclusions

These findings suggest that skin barrier function correlates with the severity of skin inflammation and can be equally impaired in patients with FLG mutant- and wild-type AD with severe symptoms. Nevertheless, our results also suggest that patients with FLG mutant-type AD may have a higher risk of allergic sensitization compared with patients with the wild-type.

Ancillary