Failed Wound Healing Promotes Psoriasis

Main Category: Eczema / Psoriasis
Also Included In: Immune System / Vaccines
Article Date: 23 Apr 2006 - 15:00 PDT

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Inflammatory skin disorders result in many changes to the skin surface, one of which is an impairment of the epidermal barrier that protects the body from an often hostile environment. Now, in a study appearing online in April, in advance of print publication in the May issue of the Journal of Clinical Investigation, Julia Segre and colleagues from the National Human Genome Research Institute in Bethesda, Maryland report that the converse is also true: that damage to the skin surface actually promotes development of the chronic inflammatory condition psoriasis, and that the protein connexin 26 is involved in this process.

The authors examined newborn, juvenile, and adult mice lacking the protein Klf4, which have a severe defect in epidermal barrier formation. They found that connexin 26 (Cx26) - a protein that helps form channels between neighboring cells for the distribution of nutrients and signaling molecules - was overexpressed in these mice. Persistent Cx26 expression kept wounded skin in a state of hyper-proliferation, which prevented wound healing and triggered an ongoing inflammatory reaction. The authors concluded that Cx26 expression must be downregulated in utero in order for the epidermal barrier to form before birth, and similarly downregulated after wound healing to allow the skin to repair itself. The study suggests that the most effective treatments for inflammatory skin disorders might be those that suppress the immune response and enhance the maturation of new skins cells in order to restore the skin surface to normal after injury.

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TITLE: Connexin 26 regulates epidermal barrier and wound remodeling and promotes psoriasiform response

AUTHOR CONTACT:
Julia A. Segre
National Human Genome Research Institute, Bethesda, Maryland, USA.

View the PDF of this article at: https://www.the-jci.org/article.php?id=27186

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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