The skin barrier is the body's defense against infections and environmental insults.
Antimicrobial peptides (AMPs) expressed in human skin, including defensins and cathelicidin,
play an important role in host defense against pathogens by killing microbes, but
may also affect inflammation, angiogenesis, and wound healing [
[1]
]. Aberg et al. reported that the epidermal permeability barrier was abnormal in CRAMP (murine homolog
of human cathelicidin LL-37) knock out mice, suggesting that AMPs may affect epidermal
permeability [
[2]
]. As tight junctions (TJs) are a key component of the permeability barrier [
3
,
4
], we hypothesized that AMPs regulate the permeability barrier by affecting TJs. Thus,
we investigated whether human beta defensin-1 (hBD-1) – an AMP expressed ubiquitously
in the epidermis that is known to affect keratinocyte function – regulates the development
of TJs and the formation of the epidermal permeability barrier.To read this article in full you will need to make a payment
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References
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- Perturbation of lamellar granule secretion by sodium caprate implicates epidermal tight junctions in lamellar granule function.J Dermatol Sci. 2010; 59: 107-114
- Tight junction regulates epidermal calcium ion gradient and differentiation.Biochem Biophys Res Commun. 2011; 406: 506-511
- Mechanical and metabolic injury to the skin barrier leads to increased expression of murine β-defensin-1, -3, and -14.J Invest Dermatol. 2011; 131: 443-452
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Article info
Publication history
Published online: May 28, 2013
Received:
December 13,
2012
Identification
Copyright
© 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
