Article
Research has demonstrated that staph aureus is in increased supply on the skin of atopic dermatitis patients coupled with less overall diversity in the number of bacteria on their skin, suggesting therapies that achieve balance in the skin microbiome could help to manage atopic dermatitis.
The skin microbiome and its importance in atopic dermatitis (AD) is being revealed with more and more investigations, and some therapeutic products aimed at minimizing the influence of staph aureus on the skin of patients with AD are now available.
A symposium held at the annual meeting of the Canadian Dermatology Association (CDA) in June focused on the role of the skin microbiome in dermatological diseases. The human microbiome represents a source of genetic diversity, a modifier of disease, and an essential component of immunity and is composed of microbes that live in and on human bodies.1
Molecular technology has permitted investigations to contrast the normal human microbiome with changes in skin which has been affected by various disease states.
“We have all kinds of bacteria on our skin, and the most of them are good bacteria, and they keep part of our immune system intact,” says Charles Lynde M.D., FRCPC, director of the Lynde Institute for Dermatology in Markham, Ontario, Diplomate American Boards Dermatology, and associate professor, department of medicine, University of Toronto.
“There is an emerging concept developing of good bacteria and bad bacteria. Staph aureus is a bad bacterium. If staph aureus is allowed to grow and grow with no competing bacteria on the skin, it continues to colonize the skin and cause problems,” explains Dr. Lynde. “If the microbiome can be made to offer more diversity, patients may have eczema. Atopic dermatitic skin has more staph aureus, and there is less diversity in the numbers of bacteria on their skin.”
An investigation published several years ago put forth that enhancing the bacterial diversity in AD skin could potentially avoid flares.2
Dr. Lynde and co-authors published a paper earlier this year that reviewed the literature on the topic of the connections between the skin microbiome, atopic dermatitis, and the use of emollients.3
They make note of research which observed that bacteria such as actinobacteria, proteobacteria, and cyanobacteria are under-represented in skin that is affected by AD. They also note the fact that Vitreoscilla filiformis biomass has been used in skin care emollients and has been shown to stimulate mRNA expression and antimicrobial peptides in reconstructed epidermis.4
The panel members came to a consensus on several points after reviewing the literature. Some of these points were that the skin microbiome of lesional atopic skin differs from adjacent non-lesional skin in individuals with AD; worsening of AD and dysbiosis of the skin are strongly linked; and the use of specific emollients can enhance microbiome diversity in the skin of atopic individuals.
The Human Microbiome Project was established in 2007 by the National Institutes of Health in the U.S. with a goal of recognizing and describing the microbiome and of developing a database of information.
With the accumulation of knowledge about the skin microbiome, therapeutic targets will begin to be revealed for various dermatological disease states including atopic dermatitis, explains Dr. Lynde.
The commensal organisms which make up the skin microbiome and inhabit the skin are thought to play a role in the modulation of the immune system, thus having an impact on the management of inflammatory skin diseases like atopic dermatitis.
“Staph aureus creates a super antigen that sets up the inflammatory pathway,” says Dr. Lynde. “If you use an emollient that can decrease the number of flares, it offers an alternative to using steroids or calcineurin inhibitors. Considering many parents are steroid-phobic for their children (who have AD), it is good to have alternative choices.”
To respond to the threat of staph aureus and the potential for an imbalance in the skin microbiome of patients who have eczema, over-the-counter products like La Roche Posay’s Lipikar Baume AP, stabilizes the skin microbiome with its patented ingredient called Aqua Posae Filiformis. In addition, the topical therapy is designed to replenish lipids and protect the skin barrier.
“The product is not as strong as a steroid or a calcineurin inhibitor,” notes Dr. Lynde. “This product can be another tool in our armamentarium (for AD). It would be an adjunctive tool more than a primary therapy; however, it could be a primary therapy for mild eczema.”
Moisturizers that contain ceramides are also key in managing AD through the reduction of inflammation, according to Dr. Lynde.
Of note, the gut microbiome is now being studied in terms of its impact on dermatology and respiratory medicine.
“This is why there has been attention paid to probiotics (as a way to) cut down on the prevalence of asthma, food allergies, and eczema,” explains Dr. Lynde. “This (use of probiotics to reduce prevalence of some disease) is still theoretical. It has not been proven.”
William Mohn, PhD, Professor in the Department of Microbiology and Immunology at the University of British Columbia in Vancouver, Columbia, participated in the symposium on the role of the skin microbiome in skin pathologies at the annual CDA meeting and notes that preserving the balance in the microbiome, both the gut and skin, is a component of warding off illness.
You may also like Merger boosts AD offerings
Disclosures: Dr. Mohn reports no relevant disclosures. Dr. Lynde is an investigator/consultant/speaker for La Roche-Posay.
References:
1. Grice EA, Segre JA. The human microbiome: our second genome. Annu Rev Genomics Hum Genet. 2012;13:151-70.
2. Grice EA, Kong HH, Conlan S, et al. Topographical and temporal diversity of the human skin microbiome. Science. 2009;324:1190-2.
3. Lynde CW, Andriessen A, Bertucci V, et al. The Skin Microbiome in Atopic Dermatitis and Its Relationship to Emollients. J Cutan Med Surg. 2016;20(1):21-8.
4. Kong HH, Segre JA. Skin microbiome: looking back to move forward. J Invest Dermatol. 2012;132:933-9.