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Study from Kiel shows: dry skin and atopic dermatitis change the skin’s microbiome

06.02.2018

In comparison to healthy individuals, the skin of patients with atopic dermatitis has a clearly modified and less diverse pattern of bacterial colonization. This not only applies to areas with acute or chronic eczema, but also to parts of the skin without inflammation, as discovered by a team from the Cluster of Excellence "Inflammation at Interfaces” during a study. However, there are differences between areas of the body which are accompanied by a different composition of skin lipids. First author Dr Hansjörg Baurecht (University Medical Center Schleswig-Holstein), was surprised by the fact that these locational differences take a backseat when the skin becomes inflamed. “The natural differences in the microbiome’s composition in different parts of the body are then abrogated, and a pattern of bacterial colonization emerges that is typically less diverse, when the skin inflammation becomes chronic.” The results of the study have now been published in the Journal of Allergy and Clinical Immunology.

Our skin is home to countless microorganisms, which together are referred to as the microbiome. At various places on the body, we can find bacterial strains that are typical for that region - and the bacterial composition can sometimes be considerably different, for example between our foreheads and the soles of our feet. This is initially neither good nor bad, but simply determined by the respective environment. The skin’s moisture level, pH value, temperature and lipid content affect the colonization pattern, as do genetic factors and environmental influences. The subtle interaction between skin cells, immune cells and the microbiome ensures that the skin performs its role as a barrier. Changes to the microbiome can affect this.

The best described cause for a general disturbance to the skin’s barrier is a deficiency in filaggrin, a skin protein. This deficiency arises from inherited mutations in around ten percent of the population. Affected individuals suffer from generally dry skin and reduced barrier functions, meaning that the skin is more permeable to external influences. A congenital filaggrin deficiency does not necessarily lead to atopic dermatitis, but it is associated with a significantly higher risk of developing it. One reason for this may be a change to the skin’s microbiome. The study which has just been published supports this assumption: the bacterial colonization in people with a filaggrin deficiency is similar in some ways to that in atopic dermatitis patients. If the disease develops, the microbiome further changes.

Until now, the skin microbiome in atopic dermatitis patients has only been well investigated for typically affected areas like the elbow creases or backs of the knees. The current study shows that typical changes for atopic dermatitis in the skin’s microbiome are most significantly characterized in these areas, but that parts of the skin that are not affected also display typical changes. These include a reduced bacterial diversity and a different composition of staphylococcus strains.

“The bacterial diversity and the proportion of certain staphylococci, successively decreases from healthy to dry and inflamed skin, whereas certain other strains, particularly S. aureus, become increasingly dominant,” emphasized Dr Hansjörg Baurecht, assistant of the Cluster member Professor Stephan Weidinger (working group at the Department of Dermatology, Venerology and Allergology at the University Medical Center Schleswig-Holstein, UKSH). “Most surprising was that, in acute and chronic eczema in atopic dermatitis patients, we were no longer able to find the differences in the microbiome dependent on the body site that are typical for healthy people. Cutaneous inflammation greatly changes the skin’s microbiome, regardless of the body site. We did not expect it to that extent.”

“Our new findings deepen our understanding of the mutual dependency between the skin’s function and bacterial colonization,” emphasized Professor Stephan Weidinger, deputy director of the UKSH Department in Kiel and head of the Department for Inflammatory Skin Diseases. “The skin’s colonization pattern in atopic dermatitis patients is generally altered, and is both manifestation as well as trigger factor for inflammation. It can also be the starting point for real infections.”


The term atopic dermatitis
Atopic dermatitis (atopic eczema) is one of the most common chronic, non-contagious inflammatory skin diseases. It usually manifests in early childhood and often follows a relapsing-remitting course. An estimated 10 to 20 percent of children and 5 to 10 percent of adults are affected. Symptoms are extreme itching, eczema that keeps coming back, and usually a skin that is generally dry. Atopic dermatitis is mainly caused by a genetic predisposition towards extremely sensitive skin and overreactions of the immune system. Atopic dermatitis means that the supply of moisture and lipids to the skin is disturbed and the natural barrier function is reduced. This allows irritating and allergy triggering substances from the environment to enter the skin more easily.


Original publication:
Baurecht, H, Rühlemann, MC, Rodríguez, E, Thielking, F, Harder, I, Erkens, AS, Stölzl, D, Ellinghaus, E, Hotze, M, Lieb, W, Wang, S, Heinsen, FA, Franke, A and Weidinger, S (2018): Epidermal lipid composition, barrier integrity and eczematous inflammation are associated with skin microbiome configuration. Journal of Allergy and Clinical Immunology, https://doi.org/10.1016/j.jaci.2018.01.019


Contact:
Dr Hansjörg Baurecht
Department of Dermatology, Venerology and Allergology at the University Medical Center Schleswig-Holstein (UKSH)
Tel.: +49 (0)431/500 21111
hbaurecht@dermatology.uni-kiel.de

Prof. Dr Stephan Weidinger
Department of Dermatology, Venerology and Allergology at the University Medical Center Schleswig-Holstein (UKSH)
Tel.: +49 (0)431/500 21110
sweidinger@dermatology.uni-kiel.de


Press contact:
Dr. Tebke Böschen
Telefon: +49 (0)431 880-4682, e-mail: tboeschen@uv.uni-kiel.de
Website: www.inflammation-at-interfaces.de
Twitter: I@I @medinflame


The Cluster of Excellence "Inflammation at Interfaces" has been funded since 2007 by the Excellence Initiative of the German Government and the federal states with a total budget of 68 million Euros. It is currently in its second phase of funding. Around 300 cluster members are spread across the four locations: Kiel (Kiel University, University Medical Center Schleswig-Holstein (UKSH)), Lübeck (University of Lübeck, UKSH), Plön (Max Planck Institute for Evolutionary Biology) and Borstel (Research Center Borstel (FZB) – Center for Medicine and Biosciences) and are researching an innovative, systematic approach to the phenomenon of inflammation, which can affect all barrier organs such as the intestines, lungs and skin.

Cluster of Excellence Inflammation at Interfaces
Scientific Office, Management: Dr. habil. Susanne Holstein
Address: Christian-Albrechts-Platz 4, 24118 Kiel, Germany
Phone: +49 431 880-4850, Fax: +49 431 880-4894
e-mail: spetermann@uv.uni-kiel.de
Twitter: I@I @medinflame

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Dr. Tebke Böschen

press and communication

Cluster Office
Kiel University (CAU)
Christian-Albrechts-Platz 4
24118 Kiel
Germany

Phone: +49 (0)431 880 4682
Fax: +49 (0)431 880 4894
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Internet: www.inflammation-at-interfaces.de