Alexandra Farhangui

Introduction. Staphylococcus epidermidis is a common skin bacterium that has been shown to both promote wound healing and increase ceramide levels on the skin.^{1, 2} Ceramides are lipids derived from sphingomyelin and have been shown to be protective against skin water loss.³ Additionally, the absence of ceramide has been implicated in plaque psoriasis development, and studies have shown that psoriatic tissue contains decreased levels of both ceramide and S. epidermidis.^{3, 4} This connection raises a compelling question: Can we leverage the healing potential of S. epidermidis via ceramide production to heal skin from diseases like psoriasis? Methods. To analyze ceramide production, the skin of hairless mice was compromised using mechanical and chemical irritants, treated with a bacterial solution, and measured for water loss and ceremide content.¹ Identification of bacterial genes involved in ceramide production used bacterial gene knockout assays and were confirmed with plasmid rescue experiments.¹ In addition, confocal microscopy was used to measure the concentration of CD8⁺ T-Cells and the rate of wound healing after exposure to S. epidermidis,^{5, 4} and knockout mutations of serine palmitoyltransferase were made in mice to understand the function of ceramide.³ Lastly, ceramide application to the skin was analyzed with Fourier transform infrared spectroscopy and small angle X-ray diffraction to assess changes in stratum corneum lipid organization.⁶ Results. S. epidermidis was found to produce ceramide on the skin using the bacterial enzyme, sphingomyelinase. Surprisingly, S. epidermidis was found to recruit CD8⁺ T-Cells and promote wound healing though a non-classical MHCI pathway.¹ Psoriatic tissue analyses revealed a reduction in ceramide content and S. epidermidis colonies.^{5, 4}, while mice with knockouts for serine palmitoyltransferase were unable to produce ceramide and developed psoriatic lesions.³ Lastly, studies interrogating ceramide as a treatment revealed ceramide application increased orthorhombic organization in lipids, facilitating repair, denser lipid packing, and decreased water loss.⁶ Conclusions. These studies demonstrate that the skin commensal S. epidermidis produces ceramide and increases the rate of wound healing through immune cell recruitment. Plaque psoriasis has been associated with low levels of ceramide, as well as low levels of S. epidermidis, and it has been manifested in vivo by inhibiting ceramide production by the skin. These findings present an exciting opportunity to use Staphylococcus epidermis as a treatment for plaque psoriasis and other skin diseases by leveraging our microbiome and the commensal relationship between S. epidermidis and ourselves.

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