Funding sources The study was supported by the Lundbeck Foundation.
Clinical and Laboratory Investigations
Human β-defensin-2 as a marker for disease severity and skin barrier properties in atopic dermatitis
Version of Record online: 30 AUG 2013
© 2013 British Association of Dermatologists
British Journal of Dermatology
Volume 169, Issue 3, pages 587–593, September 2013
How to Cite
Clausen, M.-L., Jungersted, J.M., Andersen, P.S., Slotved, H.-C., Krogfelt, K.A. and Agner, T. (2013), Human β-defensin-2 as a marker for disease severity and skin barrier properties in atopic dermatitis. British Journal of Dermatology, 169: 587–593. doi: 10.1111/bjd.12419
Conflicts of interest None declared.
- Issue online: 30 AUG 2013
- Version of Record online: 30 AUG 2013
- Accepted manuscript online: 6 MAY 2013 10:31AM EST
- Manuscript Accepted: 30 APR 2013
- Lundbeck Foundation
Skin infections related to disrupted antimicrobial defence are a common problem in atopic dermatitis (AD). Altered levels of antimicrobial peptides, including human β-defensin (hBD)-2, have been reported in AD skin, and a link to impaired barrier function has been suggested.
To study hBD-2 in relation to skin barrier function in patients with AD and controls, and to study hBD-2 in relation to disease severity.
Twenty-five patients with AD and 11 controls were enrolled. hBD-2 peptide concentration was determined in stratum corneum samples collected by a minimally invasive tape-stripping method. Disease severity was assessed by SCORing Atopic Dermatitis (SCORAD), and skin barrier function was evaluated by measurement of transepidermal water loss (TEWL) and skin pH. Patients with AD were characterized according to filaggrin mutations.
hBD-2 concentrations in the stratum corneum were found to differ between lesional and nonlesional AD skin and controls, with the highest values in lesional skin (P < 0·001). SCORAD and TEWL were significantly increased in participants with measureable hBD-2 (P < 0·018 and P < 0·007, respectively). Significant correlations between hBD-2 in lesional skin, and TEWL and SCORAD were observed (R = 0·55 and R = 0·44, respectively). No correlations with skin pH were found. hBD-2 was not found to relate to filaggrin mutations.
A significant correlation was found between hBD-2, disturbed skin barrier function and disease severity. The minimally invasive skin sample technique enables evaluation of the stratum corneum and its proteins over time and provides the possibility of relating these findings to treatment, infections and physiological variations.