Gallo: beta-defensins coordinate Skin Barrier Injuries

Written by on March 24, 2011 in research, What Causes Rosacea? with 0 Comments

This short abstract from Dr. Richard Gallo is an introduction to an article further on in the journal edition from Dr. Ahrens et al.

Gallo’s interest is piqued by the possibility of a coordinated defense effort from the permeability and antimicrobial barriers of the skin.

Ahrens was able to show that certain Antimicrobial peptides (AMPs), called beta-defensins were upregulated (i.e. they became more prevalent and sensitive) in response to an insult to the skin for eg. a tape strip being removed.

This looks to be another small step in understanding the immune system and thus potentially help in skin disorders. Dr. Gallo has been active in researching related AMPs, namely Cathelicidin.

The coordinated response of the physical and antimicrobial peptide barriers of the skin, Borkowski AW, Gallo RL., J Invest Dermatol. 2011 Feb;131(2):285-7.

Division of Dermatology, Department of Medicine, University of California at San Diego and VA San Diego Health Care System, San Diego, California, USA.

Antimicrobial peptides (AMPs) are an essential and multifunctional element for immune defense of the skin during infection and injury. In this issue, Ahrens et al. characterize the response of β-defensins, a class of AMPs, following acute and chronic challenges to the permeability barrier of the skin. Their findings suggest that the antimicrobial and permeability barriers of the skin are closely linked.

Comment on:

Mechanical and metabolic injury to the skin barrier leads to increased expression of murine β-defensin-1, -3, and -14 (J  Invest Dermatol. 2011 Feb;131(2):443-52.)

Ahrens K, Schunck M, Podda GF, Meingassner J, Stuetz A, Schröder JM, Harder J, Proksch E., Department of Dermatology, University of Kiel, Kiel, Germany.

Protection of the skin against microbiological infection is provided by the permeability barrier and by antimicrobial proteins. We asked whether the expression of murine β-defensins (mBDs)-1, -3, and -14-orthologs of human β-defensins hBD-1, -2, and -3, respectively–is stimulated by mechanically/physicochemically (tape stripping or acetone treatment) or metabolically (essential fatty acid-deficient (EFAD) diet) induced skin barrier dysfunction.

Both methods led to a moderate induction of mBD-1 and mBD-14 and a pronounced induction of mBD-3 mRNA. Protein expression of the mBDs was increased as shown by immunohistology and by western blotting. Artificial barrier repair by occlusion significantly reduced the increased expression of mBD-14 after mechanical injury and of all three mBDs in EFAD mice, supporting an interrelationship between permeability and the antimicrobial barrier. mBD-3 expression was stimulated in vitro by tumor necrosis factor-α (TNF-α), and a neutralizing anti-TNF-α antibody significantly reduced increased mBD-3 expression after barrier injury in mouse skin, indicating that induction of mBD-3 expression is mediated by cytokines. The expression of mBD-14 was stimulated by transforming growth factor-α and not by TNF-α.

In summary, we demonstrated upregulation of mBD1, -3, and -14 after mechanically and metabolically induced skin barrier disruption, which may be an attempt to increase defense in the case of permeability barrier dysfunction.

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