- In a new study, researchers investigated how bacteria may affect eczema pathology.
- They reported that S. aureus bacteria mutate in eczema patches, enabling them to spread more quickly.
- Experts say the findings may have implications for helping to treat eczema.
The condition affects about
While there is no cure for eczema, medications do exist to manage its symptoms. These include as topical corticosteroids and emollients and sometimes topical immunosuppressants.
Eczema is thought to arise from a mix of environmental and genetic factors. Irritants found in soaps and surface cleaners, for example, can trigger the immune system, which then causes inflammation that may present as an eczema flare-up.
People with eczema may have reduced filaggrin production due to variants in the gene the encodes for this protein. Filaggrin plays an important role in strengthening the skin.
Bacteria can enter breaks in the skin of people with eczema, where they can grow and multiply. The immune system may try to control this colonization by increasing inflammation, leading to more skin damage and itchiness.
Understanding more about how bacteria spread into the skin of people with eczema and how it increases inflammation could aid the development of new drugs to treat the condition.
Recently, researchers investigated how the bacteria Staphylococcus aureus adapts to the skin of people with eczema. They reported that the bacteria develop mutations, which mean they no longer have a cellular capsule and can thus grow faster on the skin.
Medical News Today spoke with Dr. Alain Michon, the medical director of Project Skin MD Ottawa in Canada who was not involved in the study, about the findings.
“Targeted treatment of S.Aureus bacteria strains with capD mutations could be valuable not only to help treat acute episodes of eczema but also to prevent flare-ups and keep eczema under control,” Michon said.
The more of the bacteria they have, the more severe their eczema tends to be.
S. aureus is thought to contribute to eczema pathology by secreting toxins and recruiting immune cells, something that further damages the skin barrier.
The researchers conducted this longitudinal study on 23 children in Mexico between 5 and 15 years old with moderate to severe eczema.
All the participants were being treated with standard care, including topical steroids, emollient moisturizers, and bleach baths.
The researchers took samples of skin microbes from the children once a month for three months and then again at nine months. Samples were taken from common eczema-affected sites such as the backs of knees and inside of elbows. They also took samples from forearms, which are usually not affected by the bacteria, and the nostrils.
The researchers then cultured S. aureus cells from each site, yielding almost 1,500 unique colonies. This enabled them to observe how the bacertail cells evolved in greater detail.
Ultimately, they found that most participants had a single lineage of S. aureus over the study period, meaning that new strains did not come in over time from the environment or other people. They noted, however, that each lineage mutated a lot during the study.
In particular, the researchers noted that many mutations occurred that reduced or eliminated function of a gene known as capD, which encodes for an enzyme necessary for synthesizing polysaccharide — a capsule-like coating that protects S. aureus from immune cells.
Over the course of the study, the researchers found that capD mutations took over the entire S. aureus microbiome population in a third of the participants.
In one child, the researchers had initially detected four different mutations of capD. However, by the end of the study, one of the variants became dominant and spread to the entire microbiome.
From further experiments, the researchers said they found that mutations in capD allowed the bacteria to grow faster than those with a regular capD gene.
Lastly, the researchers analyzed almost 300 publically available genomes of bacteria isolated from people with and without eczema.
They found that those with eczema were more likely to have S. aureus variants that could not produce capsular polysaccharides than those without eczema.
Medical News Today spoke with Dr. J. Wes Ulm, a bioinformatic scientific resource analyst and biomedical data specialist at the National Institutes of Health who was not involved in the study, about how mutations that make S. aureus more detectable by the immune system increase the spread of the bacteria – and eczema – on the skin.
Ulm noted that from a certain perspective, it may seem like a disadvantage for S. aureus to become more easily detectable by the immune system. He continued to explain, however, that loss or reduction in capD expression could increase the bacteria’s ability to grow and spread as energy that would otherwise be spent in making a productive capsule can be channeled directly into growth.
Furthermore, lacking a capsule would allow the bacterium to latch onto the skin surface more easily, increasing its efficiency in spreading throughout the skin.
“When the capD-deficient strain becomes more predominant on the [skin’s] microbiome, its lack of capD makes it more easily detected and targetable by the immune system there,” Ulm said. “And this, in turn, can enhance the immune response and magnify the inflammatory reaction giving rise to the characteristic rash and symptoms of eczema.”
Michon said that the study’s small sample size limits how far these findings may apply to other populations.
He added that some participants’ microbiomes may have been altered in those who took antibiotics prior to and during the study, which may have affected the results.
Cameron K. Rokhsar, FAAD FAACS, a dermatologist and fellowship-trained cosmetic and laser surgeon in Manhattan and Long Island in New York who was not involved in the study, also noted other limitations.
“The limitation of these findings is that bacterial overgrowth is only part of the whole mystery,” Rokhsar told Medical News Today. “The real issue with atopic dermatitis is the dysfunctional barrier particular to these patients. Putting patients on antibiotics help atopic dermatitis flares but does not cure eczema.”