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Published on: September 7, 2013
eDNA-Mediated Cutaneous Protection Against UVB Damage Conferred by Staphylococcal Epidermal Colonization
Sapir Ron-Doitch1,2, Marina Frušić-Zlotkin2, Yoram Soroka2
1Biofilm Research Laboratory, Faculty of Dental Medicine, Institute of Dental Sciences, Hebrew University-Hadassah, Jerusalem 91120, Israel.
Skin bacteria Staphylococcus epidermidis and Staphylococcus aureus form biofilms on human skin. These biofilms protect skin from UV damage by activating natural antioxidant defenses.
Area of Science:
- Microbiology
- Dermatology
- Biochemistry
Background:
- The human skin hosts diverse microorganisms, including Staphylococcus epidermidis and Staphylococcus aureus.
- These bacteria can form biofilms, enhancing adhesion and stability on the skin surface.
- Skin is exposed to oxidative stress, like UV radiation, necessitating antioxidant defense mechanisms such as the Nrf2-Keap1 pathway.
Purpose of the Study:
- To investigate the morphology and matrix composition of S. aureus and S. epidermidis biofilms on healthy human skin.
- To determine if these skin bacteria provide protection against UV-induced oxidative stress.
Main Methods:
- Exploration of bacterial morphology and extracellular matrix (ECM) composition on ex vivo human skin.
- Assessment of the protective effects of bacterial cultures and their isolated extracellular DNA (eDNA) against UVB-induced apoptosis.
Main Results:
- S. aureus and S. epidermidis exhibit biofilm-like morphology when adhering to healthy human skin.
- The bacterial ECM comprises extracellular polysaccharides (EPS) and extracellular DNA (eDNA).
- Both bacterial cultures and isolated S. aureus biofilm eDNA demonstrated protective effects against UVB-induced apoptosis.
Conclusions:
- Skin staphylococci form biofilms on human skin with a matrix of EPS and eDNA.
- These bacteria and their biofilm eDNA offer cutaneous protection against UVB-induced apoptosis.
- Skin microbiota play a role in maintaining cutaneous redox balance by activating the skin's antioxidant defense mechanisms.
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