Abstract
The human skin microbiome consists of various microbes including an array of bacteria that help to guard against foreign microbes and educate the surrounding immune cells. Many skin inflammatory disorders have been related to states of chronic inflammation, immune system dysregulation and microbiome shifts at disease sites. One example is atopic dermatitis in which chronic inflammation and microbiome shifts during disease flare-ups temporarily decrease microbial diversity at the lesion area by an increase in Staphylococcus colonization. Staphylococcal biofilms are also prominent at lesion sites and both Staphylococcus aureus and Staphylococcus epidermidis cause infection at wound sites and a main culprit of nosocomial infections. Fluoxetine is a selective serotonin reuptake inhibitor commonly prescribed as an oral antidepressant medication but has been shown to have antimicrobial as well as anti-inflammatory properties. Since these Staphylococcus species have been shown to have increasing multi-drug resistance, by using a novel non-antibiotic method, dysbiosis of the skin microbiome can be rectified and maintained to reduce disease severity and flares. We tested fluoxetine on growth and biofilm formation of S. aureus and S. epidermidis in laboratory conditions at four different concentrations of fluoxetine. At a starting bacterial amount of 106 colony forming units, fluoxetine decreased S. aureus growth and biofilm formation while not affecting S. epidermidis. However, at a higher starting bacterial amount of 108 CFU only biofilm formation of S. epidermidis was increased with fluoxetine treatment. We discovered fluoxetine treatment to modulate growth and biofilm formation of S. aureus and S. epidermidis. Future work could lead to fluoxetine as a skin microbiome modulating therapeutic in skin disorders such as atopic dermatitis.