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Interleukin-33 modulates the expression of human β-defensin 2 in human primary keratinocytes and may influence the susceptibility to bacterial superinfection in acute atopic dermatitis

Authors

  • A. Alase,

    1. Leeds Institute of Molecular Medicine, Division of Rheumatic and Musculoskeletal Disease, LMBRU, University of Leeds, Leeds, U.K.
    2. Centre for Skin Sciences, School of Life Sciences, University of Bradford, Bradford, U.K.
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  • J. Seltmann,

    1. Division of Immunodermatology and Allergy Research, Department of Dermatology, Hannover Medical School, Hannover, Germany
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  • T. Werfel,

    1. Division of Immunodermatology and Allergy Research, Department of Dermatology, Hannover Medical School, Hannover, Germany
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  • M. Wittmann

    1. Leeds Institute of Molecular Medicine, Division of Rheumatic and Musculoskeletal Disease, LMBRU, University of Leeds, Leeds, U.K.
    2. Centre for Skin Sciences, School of Life Sciences, University of Bradford, Bradford, U.K.
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  • Funding sources
    This work was supported by Higher Education Funding Council of England, The Royal Society (joint grant) and DFG grant GRK1441.

  • Conflicts of interest
    None declared.

  • A.A. and J.S. contributed equally to this work.

Adewonuola Alase.
E-mail: a.a.alase@leeds.ac.uk

Summary

Background  Interleukin (IL)-33 is a member of the IL-1 family and has been implicated in Th2-driven allergic diseases such as atopic dermatitis (AD) and asthma. The principal Th2 cytokine IL-4, found highly expressed in acute allergic eczema, is known to downregulate human β-defensin 2 (hBD2) expression in human keratinocytes and this is associated with superinfection in patients with AD.

Objectives  To investigate the effect of IL-33 on the expression of hBD2 in human keratinocytes.

Methods  hBD2 production by stimulated keratinocytes was measured by enzyme-linked immunosorbent assay.

Results  Our results showed that serum is a very potent inducer of hBD2 and 2·5% human serum was much more potent in inducing hBD2 than 20 ng mL−1 of tumour necrosis factor-α. Interestingly, serum from patients with AD showed an impaired ability to induce hBD2 in normal keratinocytes. IL-33 significantly downregulated serum-induced hBD2. The downregulatory capacity of IL-33 was found to be 1·5- to 2-fold weaker compared with IL-4.

Conclusions  Our data suggest that IL-33 can significantly contribute to the decreased expression of hBD2 in acute eczematous reaction clinically characterized by spongiosis and oozing – thus indicative for contact of the epidermis with serum components.

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