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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.

Alase, Adewonuola A.
; 
Seltmann, J.
; 
Werfel, T.
; 
Wittmann, Miriam
Publication Date
2012-12
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Keywords
Interleukin (IL)-33, IL-1 family, Cytokines, Pathogenesis, Atopic diseases, Atopic dermatitis (AD), Allergic asthma
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Abstract
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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http://hdl.handle.net/10454/7432
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Alase A, Seltmann J, Werfel T, Wittmann M. IL-33 Modulates the Expression of Human Beta Defensin 2 in Human Primary Keratinocytes and may influence the susceptibility to bacterial superinfection in acute atopic dermatitis. Br J Dermatol. 2012 Jul 14. doi: 10.1111/j.1365-2133.2012.11140.x.
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https://doi.org/10.1111/j.1365-2133.2012.11140.x
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