In the The Journal of Clinical Investigation, researchers from the National Human Genome Research Institute, the National Eye Institute, and the National Institute of Child Health and Human Development, all part of the National Institutes of Health (NIH), report that excessive production of a specific protein disrupts the protective properties of the skin barrier.
Once the skin barrier is compromised, immune-system-stimulating chemicals – allergens – can enter the body and cause an inflammatory reaction that, in turn, stimulates skin cells to grow rapidly, further diminishing the protective function of the skin.
The compromised barrier, in turn, becomes more porous to allergens that then stimulate more inflammation in a cycle that eventually produces common skin conditions such as psoriasis and eczema.
It may, however, be possible to break the cycle by creating a temporary, artificial barrier on the skin that blocks incoming allergens. The solution could be as simple as developing a lotion that effectively blocks allergens from getting through damaged skin.
Keeping allergens out of the skin would keep the immune system from over-stimulating cell growth, giving the skin time to re-create a normal barrier. Current therapies for these skin conditions principally focus on suppressing the immune system, but the medicines used can produce undesired side-effects.
Several recent studies have suggested that defects in the skin barrier may be as important to eczema and psoriasis as the hyperactive response of the immune system. In addition, doctors have observed that individuals with eczema are also likely to develop hay fever and asthma, suggesting a common mechanism for both disorders. The other risk factor for these conditions is having a relative with the disorder, suggesting a genetic connection.
To test whether a defective skin barrier can actually produce these diseases, a team of NIH researchers focused on a specific gene called connexin 26, which makes a protein that forms connections between skin cells that create the normal barrier.
To determine connexin 26’s role in psoriasis, NIH researchers created a line of transgenic mice that over-produce connexin 26. The resulting mice develop psoriatic-type skin sores, just like humans with psoriasis.
The discovery broadens the basic understanding of the causes of skin disorders such as psoriasis and eczema, and may well contribute to the basic understanding of asthma and hay fever, conditions that arise when allergens penetrate the tissue barrier in the lungs and nose, respectively.
The genetic studies suggest that researchers now need to focus on both turning down the immune response, as well as restoring a normal skin barrier to keep the outside world out of the body.