The skin is inhabited by Bacteria, archaea, fungi and viruses, collectively referred to as the skin microbiota. These commensals serve as first line of defense at the skin surface and play a vital role in both the establishment and maintenance of the skin’s immune system. Among the bacteria, some of skin commensals are members of the coagulase negative staphylococci (CoNS), including S. epidermidis.

Host/commensal cooperation can be disrupted by the invasion of the common dermatopathogen S. aureus. Despite a relatively low rate of skin colonization, in USA S. aureus is responsible for 76% of all skin and soft-tissue infection, leading to 500 000 hospital visit and 10 million outpatient visits per year.

In this recent article, R. Horswill et al highlight the mechanisms used by commensal bacteria to enhance skin immunity to S. aureus opportunistic infection and summarize strategies through which CoNS directly compete with S. aureus to prevent colonization and disease.

The commensal skin microbiota use various strategies to compete with S. aureus.
The commensal skin microbiota use various strategies to compete with S. aureus.

Researchers show that skin commensals S. epidermidis and S. caprae make a small molecule, less studied than other molecules, called Auto Inducing peptide (AIP) that inhibit S. aureus cell-to-cell communication and prevent S. aureus colonization. Furthermore, they show in experiments with Methicillin Resistant S. aureus (MRSA) during intradermal skin infection that S. caprae provided protection against MRSA colonization. Together, these findings settled the central role of AIP signalling in S. aureus skin infection development, and laid the foundation for a new therapeutic paradigm for inhibiting pathogenesis via AIP-interference.

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