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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
Author(s) -
Alase A.,
Seltmann J.,
Werfel T.,
Wittmann M.
Publication year - 2012
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2012.11140.x
Subject(s) - atopic dermatitis , immunology , superinfection , allergy , medicine , interleukin , downregulation and upregulation , interleukin 33 , cytokine , interleukin 8 , biology , virus , biochemistry , gene
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.