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S. aureus: the bacterial culprit that drives atopic dermatitis (National Eczema Association)

S. aureus: the bacterial culprit that drives atopic dermatitis (National Eczema Association)

The relationship between atopic dermatitis and Staphylococcus aureus is longstanding and complex. A Dutch company is investing in a new technology that targets staph to help reduce disease severity.

Approximately 1,000 species of bacteria live on the surface of the skin, but available data suggests one plays an outsized role in atopic dermatitis (AD): Staphylococcus aureus (staph).

A Polish research team recently published a review article in the February 2019 issue of Advances in Dermatology and Allergology that evaluated the findings of a large number of studies on the complex relationship between staph and AD.

When cultured during an eczema flare, staph overgrowth is seen in the inflamed skin of 90% of eczema patients.

What has been unclear is whether the bacterium actually causes an AD flare or simply takes advantage of the favorable environment — the dry, cracked skin that is the hallmark of eczema — to set up shop and cause trouble.

The researchers lean toward the former view based on evidence gathered during their review of the literature.

First, staph tends to crowd out the friendly bacterial species, called commensals, that provide the balance and diversity necessary to a healthy microbiome. The researchers see staph as a likely suspect in causing the unstable skin microbiome that is characteristic of AD.

Second, staph creates all kinds of problematic byproducts that interfere with the immune system’s ability to mount a normal response — another hallmark of AD.

Among these by-products is biofilm, a slimy matrix in which bacteria can hide, thrive and evade attack by immune cells that would normally be able to clear the infection. The chronic skin damage seen in AD offers a perfect setting for biofilm formation, the researchers said.

Staph also secretes enzymes that help allergens penetrate the skin and superantigens that provoke an unusually large inflammatory response.

Despite the potential for staph to exert these negative effects, the co-authors warned against antibiotics as a routine treatment for AD, primarily because of concerns around antibiotic resistance, but also because of the chronic nature of AD.

Keeping an AD patient on antibiotics over long periods of time is inappropriate and ultimately harmful, they wrote.

With the shortage of effective antimicrobial treatments and the rise of resistant strains of staph — among other virulent species — the search is on for alternatives to antibiotics. Enter endolysin technology.

While antibiotics work by interfering with essential bacterial structures and processes or thwarting their ability to reproduce, the endolysin approach relies on viruses to do the job.

Endolysins are enzymes produced by viruses, called bacteriophages, that infect bacteria. These viruses latch on to the bacterium’s cell wall and inject their DNA inside it. That’s how the viruses reproduce.

To help new bacteriophages emerge, the endolytic enzyme breaks the bacterial cell wall open and kills the bacterium in the process.

A Dutch company (Micreos) has been investing in this new technology, recently launching its over-the-counter topical eczema product, Gladskin.

The product’s key ingredient is Staphefekt, the company’s version of an endolytic enzyme, which specifically targets staph. Gladskin also aims to restore the balance of the skin microbiome and ease the symptoms of eczema across the spectrum of disease severity.

Because of its unique mechanism of action, bacterial resistance should not be a problem, the manufacturer said, and researchers in the fields of immunology and microbiology agree with that claim.

Time will tell if the new technology takes hold and ultimately replaces traditional antibiotics. For now, it’s a trend that’s worth watching.

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