Abstract
Staphylococcus aureus (S. aureus) is one of the well-known agents causing atopic dermatitis (AD) in susceptible individuals, and Staphylococcus epidermidis (S. epidermidis) produces class I thermostable bacteriocins that can selectively kill S. aureus, suggesting protective roles against AD. There is a large need for developing precise therapies only to target S. aureus and not to harm the beneficial microbiome. On the agar well diffusion assay, live planktonic S. epidermidis showed clear zones of inhibition of S. aureus growth, but heat-killed cells and cell-free supernatants did not show this. These results would lead us to hypothesize that cytoplasmic bacteriocin from S. epidermidis will be a promising agent to inhibit S. aureus growth. Therefore, we have extracted a novel thermolabile cytoplasmic bacteriocin from S. epidermidis using trichloroactic acid (TCA)/acetone precipitation method after cell lysis with a SDS-containing buffer. These bacteriocin selectively exhibited antimicrobial activity against S. aureus and methicillin-resistance Staphylococcus aureus (MRSA), presenting no active actions against S. epidermidis, E. coli, and Salmonella Typhimurium. The extracted cytoplasmic bacteriocin compounds revealed several diffuse bands of approximately 40–70 kDa by SDS-PAGE. These findings suggest that these cytoplasmic bacteriocin compounds would be a great potential means for S. aureus growth inhibition and topical AD treatment.
Highlights
Atopic dermatitis (AD) is a chronic inflammatory skin disease that manifests as dry skin and eczematous dermatitis with prominent itch [1]
Dysbiosis contributes to the pathogenesis of AD by both detrimental effects from S
We found that live planktonic S. aureus or methicillin-resistant S. aureus (MRSA) induced human mast cell degranulation, but no effect had been found in heat-killed bacteria [8]
Summary
Atopic dermatitis (AD) is a chronic inflammatory skin disease that manifests as dry skin and eczematous dermatitis with prominent itch [1]. Pathogenesis of AD is quite obviously associated with the skin microbiome. The correlation of Staphylococcus aureus (S. aureus) with AD during active disease exacerbation has been well documented [2,3,4,5]. AD is a long-standing inflammatory skin disease typified by epidermal barrier dysfunction that can affect the bacterial community of the skin. A S. aureus cell wall product, lipoteichoic acid (LTA), is shown to cause skin barrier damage by inhibiting the expression of epidermal barrier proteins filaggrin and loricrin. Dysbiosis contributes to the pathogenesis of AD by both detrimental effects from S
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