Identification and biological basis of immunomodulation of skin inflammation by S. epidermidis

Grantee: Peter Arkwright, Senior Lecturer, The University of Manchester, United Kingdom

Amount: DKK 4,369,423

Atopic eczema is the most common skin disease in many Western countries. Although considered an allergic disease, skin infections with S. aureus are an important cause of eczema flares. In the skin of patients suffering from eczema S. aureus predominate over “good bacteria” such as S. epidermidis (S. epi).

We work on human eczema at the University of Manchester, UK and our collaborators at TUAT University, Tokyo, Japan study a unique NC strain of mouse prone to getting eczema very similar to that seen in humans.

Together over the last 3 years, we have discovered a single factor produced by S. aureus that causes eczema in both humans and mice. We have also found that S. epi prevents the eczematous inflammation by S. aureus.

We now want to work out the exact nature of the factor produced by S. epi that prevents eczema in our system.

Using the methods, we employed in our previous collaborative study, we plan to isolate and identify the factor produced by S. epi based on its size and structure using separation columns and mass spectrometry.

We will then manipulate the genome of S. epi to confirm its identity. Finally, we will determine how the factor blocks S. aureus-driven eczema by studying how it affects S. aureus growth, as well as binding and interaction with skin cells.

Identifying this S. epi-derived factor could lead to the development of new medicines for the treatment of eczema.