Cutibacterium acnes and follicular keratin (C. acnes / Keratin)

Cutibacterium acnes and follicular keratin represent a composite therapeutic target in the treatment of acne vulgaris, involving both a microbial pathogen and a host structural component. Cutibacterium acnes (formerly Propionibacterium acnes) is a Gram-positive anaerobic bacterium that colonizes the pilosebaceous unit, where it promotes inflammation by activating toll-like receptors and releasing chemotactic factors [1]. Follicular keratin refers to the keratinocytes lining the hair follicle; in acne, abnormal hyperkeratinization leads to the formation of a keratin plug, or microcomedo, which traps sebum and bacteria [2]. Therapeutic intervention typically involves a dual approach: reducing the bacterial load and normalizing the keratinization process. Antibiotics and benzoyl peroxide are used to decrease C. acnes populations, while topical retinoids like tretinoin target follicular keratinocytes to prevent the formation of comedones [3]. This target complex is central to the pathogenesis of inflammatory and non-inflammatory acne lesions. Managing this target requires balancing antimicrobial efficacy with the regulation of host cell proliferation and differentiation [4]. Sources: [1] Dessinioti, C., & Katsambas, A. D. (2010). "The role of Propionibacterium acnes in acne pathogenesis: facts and controversies." Clinics in Dermatology. [2] Zouboulis, C. C. (2004). "The human sebaceous gland: a model of keratinocyte and sebocyte biology." Investigative Dermatology. [3] Williams, H. C., et al. (2012). "Acne vulgaris." The Lancet. [4] Leyden, J. J. (1995). "New understandings of the pathogenesis of acne." Journal of the American Academy of Dermatology.

Other names

Propionibacterium acnesP. acnesSkin microbiomeFollicular hyperkeratosisPilosebaceous unit microorganismsFollicular keratinocytes

Antimicrobial activity via oxidative stress or protein synthesis inhibition in C. acnes, combined with comedolytic activity through the modulation of follicular keratinocyte proliferation and desquamation.