Highlights from the 2013 International Investigative Dermatology (IID) Meeting in Edinburgh: Introduction

Edinburgh Castle

Every 4 years, the Eurorpean, North American and Japanese dermatologic research societies host a joint meeting. Last week the 2013 International Investigative Dermatology meeting took place in Edinburgh, Scotland. Over the next several days we will summarize some of the highlights of research on the skin barrier that was presented there, alternating posts of research from the Elias group with work coming from other laboratories around the world.

Highlights of  research from the Elias laboratory will include these reports.  1) How mutations in a gene (filaggrin) that cause dry skin (ichthyosis vulgaris), while also predisposing to eczema (atopic dermatitis), evolved in order to allow more vitamin D to be formed in the skin. 2) How the pigment-generating cells (melanocytes) in darkly-pigmentated skin improve skin function, producing superior skin barrier and antimicrobial defenses. 3) Why psychological stress is not always bad for you.  4)  Why acne may be another disorder of the skin barrier – here the problem lies in the barrier of the sebaceous-rich hair follicle. 5) Some formulations and cosmetic ingredients that improve permeability barrier function also enhance the skin’s antimicrobial defense.

A host of reports and several lectures presented new research of relevance to the skin barrier and its disorders coming from work out of many laboratories around the world.  Here are several that we will be reviewing for our followers in the coming days. 1) Beck and colleagues from the University of Rochester reported promising results of an early-stage clinical trial using a systemic drug, dupilumab, a monoclonal antibody against IL-4, in the treatment of adults with severe atopic dermatitis. 2) A Japanese group presented work, using an animal model of atopic dermatitis, that illuminates why patients with atopic dermatitis cannot tolerate bathing with most soaps. 3) Several reports and talks addressed the topic of the skin microbiome and how its alterations favor the growth of pathogenic bacteria, such as S. aureus and S. pyogenes, in atopic dermatitis.  4) In a lecture, Dr. Antony Young of King’s College London described a study demonstrating that even when sunscreens are used optimally to prevent sun burns, ample vitamin D continues to be generated.

The following are our reviews of some highlights from the 2013 IID meeting:

1.   A very common genetic mutation among Northern Europeans that today underlies a propensity to develop dry skin as well as eczema (or atopic dermatitis) originally evolved in order to augment vitamin D production in the skin.  To read our report, click here.

2. Dupilumab, a new ‘biologic’ treatment designed to counteract the inflammation in atopic dermatits shows promising results in an early stage clinical trial.  To read our report, click here.

3. Melanin acidifies the stratum corneum, explaining why darkly pigmented skin exhibits a superior barrier.  To read our report, click here.

4.  Contrary to conventional wisdom, stress may not be all bad for you:  there may be some benefits to inflammatory diseases from psychological stress.  To read our report, click here.

5. The skin microbiome is much more complex than previously recognized.  Many new species of resident bacteria have been identified using the DNA based technology.  But pathogenic strains of Staphylococci remain the culprits for persons with atopic dermatis.  To read our report, click here.

6. Skin products that hasten repair of a damaged permeability barrier also improve the antimicrobial defenses of the skin.  To read our report, click here.

7. The first step in acne may be a defective permeability barrier.  This holds promise for new modalities of prevention and treatment.  To read our report, click here.

8. Sunscreens can be used properly to prevent sunburns yet still allow for adequate vitamin D production.  To read our report, click here.

More reviews coming soon.


Copyright © 2013 Elias and Williams

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