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Cutibacterium acnes (formerly Propionibacterium acnes) is a Gram-positive, anaerobic bacterium that resides within the pilosebaceous units of human skin and is a primary driver of acne vulgaris [1]. The membrane and cytoplasmic enzymes of C. acnes represent a broad group of bacterial proteins essential for survival, including those involved in cell wall synthesis, protein translation, and the breakdown of sebum into pro-inflammatory free fatty acids [2]. Therapeutic intervention often involves the use of benzoyl peroxide, which acts as a potent oxidizing agent that non-specifically targets these bacterial enzymes and proteins, leading to bacterial death [3]. Additionally, various antibiotics such as clindamycin and tetracyclines target specific cytoplasmic components, like the 50S and 30S ribosomal subunits, to inhibit protein synthesis [4]. While effective, the use of broad-spectrum agents against these enzymes has led to significant concerns regarding antibiotic resistance and the disruption of the commensal skin microbiome [5].
Oxidation of bacterial proteins, inhibition of the 30S or 50S ribosomal subunits, and inhibition of DNA gyrase or metabolic pathways.
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