Scientists have pinpointed a bunch of processes that go wrong in the skin for people who have eczema (also known as atopic dermatitis), and it could help us finally figure out how to combat this chronic condition.
Back in 2006, researchers found a strong link between people lacking in a certain skin protein, and the risk of developing eczema. Last year, scientists built on those results to show exactly what goes wrong, and their results could even take us closer to an eczema cure.
Eczema is a common skin condition affecting up to 20 percent of children and 3 percent of adults worldwide. While there’s no shortage of creams and lotions that help alleviate the chronic symptoms of eczema, we still haven’t found a cure that can clear it up for good.
For the past decade, scientists have known that eczema is associated with a genetic lack of filaggrin (filament aggregating protein) in the skin. This protein helps shape individual skin cells, and plays an important role in our skin’s barrier function.
If a person has a genetic mutation that prevents proper filaggrin supply, they can develop skin conditions such as eczema or ichthyosis vulgaris, where skin cells don’t shed, and instead pile up in a pattern that looks like fish scales.
But until recently, researchers weren’t sure how eczema actually develops when filaggrin is lacking.
The breakthrough came in 2016, when scientists from Newcastle University in the UK in collaboration with GSK Stiefel tracked down a series of proteins and molecular pathways that lead to this insufferable skin problem.
“We have shown for the first time that loss of the filaggrin protein alone is sufficient to alter key proteins and pathways involved in triggering eczema,” lead researcher Nick Reynolds from Newcastle University explained at the time.
To track down these mechanisms, the team used a lab-created three-dimensional living 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 alone could trigger a host of molecular changes in important regulatory mechanisms in the skin. This affected things like cell structure, barrier function, and even how cells got inflamed and responded to stress.
“Notably, for the first time, we have identified 17 proteins that are significantly differentially expressed after [filaggrin removal] in LSE cultures,” the team wrote in their paper.
The researchers then verified their initial findings by analysing proteins in skin samples from actual humans, comparing the results between participants with eczema and healthy subjects.
They found that several of the proteins they detected were similarly altered in only those with eczema – just like the lab-based model had demonstrated.
While this is just the next piece of the puzzle in terms of a deeper understanding of conditions like eczema, it’s a really promising step.
Once scientists know for sure what goes on in the skin if you have the faulty filaggrin gene, they can start looking for drugs that can stop that from happening.
“This type of research allows scientists to develop treatments that target the actual root cause of the disease, rather than just managing its symptoms,” Nina Goad from the British Association of Dermatologists said in a press statement.
If you suffer from random bouts of dermatitis, that’s a really 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.