Understanding more about how eczema develops could lead to better treatment options. Scientists have found out the second layer of skin contributes to the itchy skin condition, building on what was previously known.
Researcher Lisa Beck, M.D., lead study author and associate professor in the Department of Dermatology at the University of Rochester Medical Center explains, "Our findings challenge the belief that the top layer of the skin or stratum corneum is the sole barrier structure: It suggests that both the stratum corneum and tight junctions need to be defective to jumpstart the disease."
Eczema is the most common skin condition that affects humans, also known as ectopic dermatitis. When the skin layers are destroyed by inflammation, allergens like mold, dust mites, pollen and pet dander penetrate and cause problems with the immune system.
Current treatment for eczema is topical and oral corticosteroids and creams that treat the symptoms of itching, scaling and leaking skin lesions. Because options are limited, researchers are anxious to find ways to stop eczema.
The new study, published in the Journal of Allergy and Clinical Immunology, finds a second skin layer barrier with cell-to-cell connections known as tight junctions also play a role in eczema development.
The discovery came about when the scientists examined skin layers, using resistance and permeability tests on individuals with healthy skin and those with eczema. They found the tight junctions (TJs) that prevent water and particles from passing through the skin were strong and tight in healthy subjects, but those with eczema had loose, easily permeated tight junctions.
The research team was then able to locate a specific protein in the tight junction - protein, claudin-1 - that was reduced in eczema patients and found to be lower in individuals with psoriasis.
Anna De Benedetto, M.D., postdoctoral-fellow at the Medical Center and first author of the new study says, "Our hypothesis is that reduced claudin-1 may enhance the reactivity to environmental antigens and lead to greater allergen sensitization and susceptibility in people with eczema." She says there may be a gene defect that makes claudin-1 less plentiful in those susceptible to atopic dermatitis, a term that encompasses a variety of allergic skin disorders.
The University of Rochester researchers plan further studies. In the meantime, they have applied for patent protection on drug compounds that can increase claudin-1 for treatment of eczema that affects close to 15 million Americans who suffer decreased quality of life from itching.
The new study finds a new focus on tight junctions that are cell to cell skin barriers located in a different skin layer than previously known to be involved in developing eczema. The findings could mean better treatment of the skin disorder, pending further studies and verification of the current research findings.
The Journal of Allergy and Clinical Immunology: doi: 10.1016/j.jaci.2010.10.018