Cutibacterium Acnes and Acne Vulgaris: Pathogenesis, Antimicrobial Resistance, and Therapeutic Strategies

Acne vulgaris is a common chronic inflammatory skin disorder affecting pilosebaceous units, characterized by non-inflammatory (comedones) and inflammatory (papules, pustules, nodules) lesions, with a global prevalence of approximately 240 million individuals in 2021. This review focuses on the role of Cutibacterium acnes (C. acnes) in acne pathogenesis, its antimicrobial resistance, and therapeutic strategies. C. acnes, a gram-positive anaerobic bacterium resident in sebaceous follicles, contributes to acne through mechanisms including excessive sebum production, follicular hyperkeratinization, and induction of inflammation via toll-like receptors and complement pathways. Key therapeutic agents (clindamycin, tretinoin, benzoyl peroxide, and azelaic acid) are discussed in terms of their chemical properties and mechanisms, targeting bacterial growth, follicular function, and inflammation. A critical challenge is the rising antimicrobial resistance of C. acnes, with over 50% of strains resistant to erythromycin and clindamycin globally, and rates exceeding 90% in some regions. Strategic combination therapies, such as antibiotics with BPO or triple combinations (e.g., clindamycin/BPO/adapalene), have shown efficacy in reducing resistance and enhancing lesion clearance, highlighting their importance in managing resistant strains. This review underscores the need for targeted approaches to address C. acnes pathogenesis and resistance, improving acne management and patient outcomes.