Staphylococcus epidermidis-Skin friend or foe?

Abstract

Our skin is our first line of defense against environmental and pathogenic challenges. It is densely populated by a flora of bacteria, fungi, and viruses that normally interact with each other and with our immune system to promote skin health and homeostasis. Staphylococcus epidermidis is one of the most abundant bacterial colonizers of healthy human skin. While the field has historically assumed that all S. epidermidis isolates behave similarly, emerging evidence suggests that colonization by specific strains of S. epidermidis can either help or hurt the skin barrier depending on the context. In this short review, we discuss what is currently understood about S. epidermidis strain-level diversity and evaluate costs and benefits of S. epidermidis skin colonization. We challenge the current dogma that "all S. epidermidis strains behave equally" and posit that behavior is in fact highly context and strain dependent. Finally, in light of current proposals to use skin commensals as nonantibiotic treatments for acute or chronic skin diseases, we conclude that more work is urgently needed to fully understand the pathogenic and protective roles of commensals before we use them therapeutically.

Fig 1. The ubiquitous skin commensal S. epidermidis positively and negatively impacts barrier homeostasis and integrity.

(A) S. epidermidis phenol soluble modulins PSMγ and PSMδ can synergize with keratinocyte-derived AMPs to kill opportunistic skin pathogens like MRSA and Streptococcus pyogenes. S. epidermidis also makes anti-MRSA quorum sensing inhibitor peptides and a variety of small antimicrobials known as lantibiotics to mediate skin colonization resistance. (B) S. epidermidis lipoteichoic acid and some lipopeptides can dampen the inflammatory response to skin injury, accelerating wound healing. Early skin colonization with S. epidermidis is crucial for development of immune cell subsets including effector T cells and MAIT cells, and long-term S. epidermidis skin colonization may help the cutaneous immune system distinguish between commensal and pathogenic bacteria. (C) Certain S. epidermidis strains can “bloom” and exacerbate AD or NS skin lesions through production of the EcpA protease. Inflammatory S. epidermidis biofilms that occlude sweat glands have also been shown to exacerbate some AD lesions. AD, atopic dermatitis; AMPs, antimicrobial peptides; MAIT cells, mucosal-associated invariant T cells; MRSA, methicillin-resistant Staphylococcus aureus; NS, Netherton syndrome; PSM, phenol soluble modulins; QS, quorum sensing.