As mentioned above, P. acnes also plays an active role in the process of inflammation. P. acnes is a gram-positive, anaerobic, and microaerobic bacterium found in the sebaceous follicle. Adolescents with acne have higher concentrations of P. acnes compared to nonacne controls. However, there is no correlation between the raw number of P. acnes organisms present in a sebaceous follicle and the severity of the acne (27).
The cell wall of P. acnes contains a carbohydrate antigen that stimulates antibody development. Those patients with the most severe acne have the highest titers of antibodies (28). The anti-P. acnes antibody enhances the inflammatory response by activating the complement cascade and thus initiating pro-inflammatory events (29). P. acnes also facilitates inflammation by eliciting a delayed type hypersensitivity response (30) and by producing lipases, proteases, hyaluronidases, and chemotactic factors (31). Additionally, P. acnes has been shown to stimulate an upregulation of cytokines by binding to toll-like receptor 2 (TLR-2) on monocytes and polymorphonuclear cells surrounding the sebaceous follicle (32). After binding TLR-2, pro-inflammatory cytokines such as IL-1, IL-8, IL-12, and TNF-alpha are released (33,34).
The four elements of acne pathogenesis—follicular keratinocyte hyperproliferation, seborrhea, inflammation, and P. acnes—are intertwined steps in the formation of acne. Various acne treatments target different elements in acne pathogenesis. Understanding the mechanisms of action of the multitude of therapeutic options in treating acne will help assure better therapeutic results.