Recent advances in understanding Propionibacterium acnes ( Cutibacterium acnes) in acne

Abstract

The skin commensal Propionibacterium acnes, recently renamed Cutibacterium acnes, along with the other major pathophysiological factors of increased seborrhea, hyperkeratinization of the pilosebaceous unit, and inflammation, has long been implicated in the pathogenesis of acne. Recent advances have contributed to our understanding of the role of P. acnes in acne. Although there are no quantitative differences in P. acnes of the skin of patients with acne compared with controls, the P. acnes phylogenic groups display distinct genetic and phenotypic characteristics, P. acnes biofilms are more frequent in acne, and different phylotypes may induce distinct immune responses in acne. P. acnes plays a further important role in the homeostasis of the skin's microbiome, interacting with other cutaneous commensal or pathogenic microorganisms such as Staphylococcus epidermidis, Streptococcus pyogenes, and Pseudomonas species. In the era of increasing antimicrobial resistance, the selection of acne treatment targeting P. acnes and the prevention of antibiotic resistance play a key role in improving outcomes in acne patients and public health.

Keywords: Priopionibacterium acnes; acne; antimicrobial resistance; biofilm; phylotypes.

Figure 1.. Propionibacterium acnes: loss of diversity, selection of phylotypes, and its different target activities in acne.

P. acnes induces the production of AMP, TLRs, cytokines, PARs, MMP, IL-1a, CAMP, hyaluronate lyase, and porphyrins, resulting in the formation of inflammatory acne lesions. It modulates the differentiation of keratinocytes by inducing keratin 10, filaggrin, and desmocollin 1 expression. It stimulates the sebaceous glands and sebum synthesis via the CRH/CRH receptor pathway. AMP, antimicrobial peptide; CAMP, Christie–Atkins–Munch-Peterson; CRH, corticotropin-releasing hormone; EV, extracellular vesicle; IFNγ, interferon-gamma; IL, interleukin; MMP, matrix metalloproteinase; PAR, protease-activated receptor; TLR, Toll-like receptor.

Figure 2.. Treatment algorithm for predominant comedonal facial acne.

*Dose of treatments adjusted according to adverse events (for example, irritation). BPO, benzyl peroxide. From Gollnick et al. . Reprinted with permission from John Wiley & Sons.

Figure 3.. Treatment algorithm for predominant papulopustular facial acne.

*Dose of treatments adjusted according to adverse events (for example, irritation). ^†Second generation. ^‡Clindamycin 1%/tretinoin 0.025% (not with oral antibiotic), adapalene 0.1%/BPO 2.5%, clindamycin 1%/BPO 5% (not with oral antibiotic). ^§Female patients only; contraceptive pill containing a progestin with anti-androgenic activity preferred. BPO, benzyl peroxide. From Gollnick et al. . Reprinted with permission from John Wiley & Sons.