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Human beta-defensin 2 may be key to protecting barrier function in eczema

Triggering production of a protective molecule in the skin may help maintain skin barrier function in patients with atopic dermatitis (AD), according to findings published online ahead of print in The Journal of Investigative Dermatology (Oct. 1, 2016).

The investigators, from the University of Edinburgh’s MRC Centre for Inflammation Research, found that human skin cells could be instructed to produce human beta-defensin 2 (hBD2). According to the paper, hBD2 is known to kill bacteria, but the authors found it also acts to prevent damage to the skin barrier caused by Staphylococcus aureus.

Using immortalized and primary keratinocytes, they observed that S. aureus protease SspA/V8 was the main secreted factor impairing barrier integrity, whether from laboratory strains of the bacteria or strains collected from patients with AD. This damage was inhibited by an interleukin (IL)-1-beta mediated mechanism, and induction of keratinocytes expression hBD2 was the mechanism behind this protective effect.

“Eczema is a disease of our times and is incredibly common. It is very exciting to think there could be a way of recruiting the body’s natural defence systems to help us tackle a condition that has such a huge impact on people,” Dr. Richard Weller, study author and senior lecturer in dermatology at the University of Edinburgh, said in a press release.

The authors note that while endogenous production of hBD2 is usually sufficient to protect the skin barrier from the V8-mediated damage, the keratinocytes of patients with AD do not usually produce enough hBD2. However, when hBD2 was applied to lab-grown keratinocytes, it helped the skin to remain intact, with the cells strengthening protection against the bacterial damage ‘like reinforcing mortar between the bricks in a wall’, according to the release.

“This is a great chance to work with something that the body makes naturally to develop new therapies for atopic eczema, which affects so many people’s lives,” said senior author Dr Donald J. Davidson, MRC research fellow in the University of Edinburgh’s MRC Centre for Inflammation Research.

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