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A potential lead for stopping staph in its tracks

Our skin is covered in a web of billions of tiny organisms including bacteria, viruses and fungi. This web is called the skin microbiome and when healthy, helps our bodies function properly inside and out. Researchers have long known that people with atopic dermatitis (AD) have different skin biology than those who do not have […]

A potential lead for stopping staph in its tracks

Our skin is covered in a web of billions of tiny organisms including bacteria, viruses and fungi. This web is called the skin microbiome and when healthy, helps our bodies function properly inside and out.

Researchers have long known that people with atopic dermatitis (AD) have different skin biology than those who do not have AD. These differences include defects in the skin barrier caused by a gene mutation, which allows allergens and bad bacteria to pass more easily into the body.

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People with AD also have more of a type of harmful bacteria on their skin called Staphylococcus aureus or “staph.” And when not kept in check, staph can cause serious infections.

Led by Richard Gallo, M.D., Ph.D., professor and chair of the department of dermatology at University of California, San Diego

S. aureus aggravates skin conditions such as atopic dermatitis. Photo courtesy of NIAID.

S. aureus aggravates skin conditions such as atopic dermatitis. Photo courtesy of NIAID.

School of Medicine, researchers discovered that our skin microbiome produces a natural antibiotic – called antimicrobial peptides or AMPs – that kill off staph. These scientists also found that the skin microbiome in people with atopic dermatitis does not produce enough of these beneficial AMPs, leaving them at higher risk for infection.

In February, Dr. Gallo and his team published promising results from their research on skin microbiome “transplants” for people with atopic dermatitis. This study took bacteria samples from the unaffected areas of the body of people with AD. Dr. Gallo and his team then identified the beneficial AMPs-producing bacteria. Next, they transplanted the bacteria, protected in a moisturizer, to areas of the patients’ skin with active atopic dermatitis.

“For the field, this is a first — we show clear cause and effect,” Dr. Gallo told The Scientist in a Feb. 27 article posted online. “We selected specific strains of the [beneficial] bacteria that are deficient on patients’ skin, expanded them, placed them in lotion, rubbed them on the skin, and decreased the staph colonization of these patients.”

All five of the patients who received the microbiome transplant showed more than a 90 percent reduction in the amount of staph bacteria found on their skin.

Though research is still preliminary, Gallo’s findings are significant for how we understand and treat atopic dermatitis and its related conditions, including skin infections.

We know that when AMPs are added to atopic skin, they not only have a protective effect, but can also reduce colonization of harmful bacteria. However, developing customized lotions with beneficial bacteria for each and every patient may not be practical or affordable.

That’s why Gallo and his team are now working to find bacteria that will work in a broad group of patients to cut down costs.

“These are naturally occurring organisms,” he told The Scientist. “They’re screened for safety, but you can just grow them without complex chemical synthesis. It’s a very natural treatment.”

And while it remains unclear whether the presence of staph on the skin is a symptom or one of the causes of atopic dermatitis, future clinical trials could unveil that, if it is indeed a symptom, treating atopic dermatitis with personalized lotions may someday lead to a cure.

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