Scientists have established a bundle of processes that go wrong in the skin for people who have eczema (also called atopic dermatitis), and it may help us to figure out how to combat this chronic condition.
Back in 2006, researchers found a strong bond between people who did not miss a particular skin protein, and the risk of developing eczema. And in 2017, scientists relied on those results to show exactly what was going wrong, and their results could bring us even closer to an eczema cure.
Eczema is a common skin condition that affects up to 20 percent of children and 3 percent of adults worldwide. Although there is no shortage of creams and lotions that help reduce the chronic symptoms of eczema, we have not yet found a cure that can cure it forever.
For the past decade, scientists have known that eczema is associated with a genetic deficiency of filaggrin (filament-aggregating protein) in the skin. This protein helps to shape the individual skin cells, and plays an important role in the barrier function of our skin.
If a person has a genetic mutation that prevents the proper delivery of filaggrin, they may develop skin conditions, such as eczema or ichthyosis vulgaris, where skin cells do not germinate, and instead accumulate in a pattern resembling fish scales.
But until recently, researchers were unsure how eczema actually develops when filaggrin is lacking.
The breakthrough came in 2016, when scientists from Newcastle University in the UK in conjunction with GSK Boots pursued a series of proteins and molecular pathways that lead to this unsatisfactory skin problem.
“We have shown for the first time that loss of the filaggrin protein alone is sufficient to alter important proteins and pathways involved in triggering eczema,” explained lead researcher Nick Reynolds of Newcastle University at the time.
To detect these mechanisms, the team used a lab-created three-dimensional live skin equivalent (LSE) model. They altered the top layer of this lab-made ‘skin’ to become filaggrin-deficient, just like in people who have the genetic mutation.
They found that this deficiency could only trigger a host of molecular changes in important regulatory mechanisms in the skin. This affects issues such as cell structure, barrier function, and even how cells arise and respond to stress.
“Notably, we first identified 17 proteins that were significantly differentiated after completion [filaggrin removal] in LSE cultures, ”the team wrote in their 2017 paper.
The researchers then checked their initial findings by analyzing proteins in real people’s skin samples, and compared the results between participants with eczema and healthy subjects.
They found that several of the proteins they discovered were similarly altered in only those with eczema – just as the lab-based model had shown.
While this is simply the next piece of the puzzle in terms of a deeper understanding of conditions such as eczema, it is a truly promising step.
Once scientists are sure what is happening in the skin if you have the defective filaggrin gene, they can start looking for medications that can prevent this.
“This kind of research allows scientists to develop treatments that focus on the actual root cause of the disease, instead of just managing its symptoms,” Nina Goad of the British Association of Dermatologists said in a press release.
If you suffer from random attacks of dermatitis, this is a very exciting prospect.
The study was published in the Journal of Allergy and Clinical Immunology.
A version of this article was first published in May 2017.
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