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This target group encompasses the essential metabolic and replicative machinery of Cutibacterium acnes (formerly Propionibacterium acnes) and other commensal skin bacteria. Key components include DNA gyrase and topoisomerase IV, which manage DNA supercoiling during replication; DNA-directed RNA polymerase, responsible for transcription; and the 30S and 50S ribosomal subunits, which facilitate protein translation (Walsh, 2003; Wilson, 2014). In the context of acne vulgaris, C. acnes proliferates within the pilosebaceous unit, where these biosynthetic processes allow the bacteria to produce lipases, proteases, and hyaluronidases that damage host tissue and trigger inflammation (Dréno et al., 2018). Antibiotics such as tetracyclines (e.g., doxycycline, sarecycline) and macrolides (e.g., erythromycin) target the 30S and 50S subunits respectively, effectively halting bacterial growth and reducing the inflammatory load. Fluoroquinolones like nadifloxacin target the DNA-related enzymes to prevent bacterial division. Because this entry refers to a wide array of distinct enzymes across various species of the skin flora rather than a single molecular entity, it is classified as a broad therapeutic category rather than a specific canonical target.
Inhibition of DNA replication via DNA gyrase and topoisomerase IV, inhibition of transcription via DNA-directed RNA polymerase, and inhibition of translation via binding to the 30S or 50S ribosomal subunits.
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