Peeling skin syndrome is a family of congenital skin disorders. The ichthyosis leads to the shedding of dry, thick, and scaly layers of the epidermis. The patients’ life quality gets affected by excessive itching, skin inflammation, and redness. The disease occurs because of nonsense mutations due to the complete deletion of the CDSN gene encoding. This therapeutic study aims to correct protein deficiencies.

CDSN gene encodes an epidermal protein called corneodesmosin. Its deficiency gets compensated using protein replacement therapy. The treatment also improves intercellular cohesion between stratum granulosum (SG) and stratum corneum (SC). The human CDSN gets recombinantly expressed in E Coli. It gets transported to the outer keratinocyte membrane using a liposome-based carrier system. The study factored in the size, stability, and toxicity of the carrier cationic lipopeptides. The researchers investigated the epidermal and primary keratinocyte interactions.

The liposomes get accumulated at the membranes of keratinocytes. The CDSN-deficient epidermal areas of SG got replenished. Histological exam and penetration assay revealed an improvement in epidermal integrity. The liposomal encapsulated CDSN treatment was effective in the treatment of peeling skin syndrome.

It is the first pre-clinical in vitro experiment of protein replacement. It can guide future therapies involving specific epidermal areas.