Funding sources This work was supported by Higher Education Funding Council of England, The Royal Society (joint grant) and DFG grant GRK1441.
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
Article first published online: 27 SEP 2012
© 2012 The Authors. BJD © 2012 British Association of Dermatologists 2012
British Journal of Dermatology
Volume 167, Issue 6, pages 1386–1389, December 2012
How to Cite
Alase, A., Seltmann, J., Werfel, T. and Wittmann, M. (2012), 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. British Journal of Dermatology, 167: 1386–1389. doi: 10.1111/j.1365-2133.2012.11140.x
Conflicts of interest None declared.
A.A. and J.S. contributed equally to this work.
- Issue published online: 26 NOV 2012
- Article first published online: 27 SEP 2012
- Accepted manuscript online: 14 JUL 2012 10:10AM EST
- Accepted for publication 30 June 2012
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.