The Role of the Skin Microbiome in Acne: Challenges and Future Therapeutic Opportunities

Abstract

Acne vulgaris is a widespread dermatological condition that significantly affects the quality of life of adolescents and adults. Traditionally, acne pathogenesis has been linked to factors such as excess sebum production, follicular hyperkeratinization, and the presence of Cutibacterium acnes (C. acnes). However, recent studies have highlighted the role of the skin microbiome, shifting focus from individual pathogens to microbial community dynamics. This review critically evaluates existing research on the skin microbiome and its relationship to acne, focusing on microbial diversity, C. acnes strain variability, and emerging therapies targeting the microbiome. While certain studies associate C. acnes with acne severity, others show this bacterium's presence in healthy skin, suggesting that strain-specific differences and overall microbial balance play crucial roles. Emerging therapeutic approaches, such as probiotics and bacteriophage therapy, aim to restore microbial equilibrium or selectively target pathogenic strains without disturbing the broader microbiome. However, the lack of standardized methodologies, limited longitudinal studies, and the narrow focus on bacterial communities are major limitations in current research. Future research should explore the broader skin microbiome, including fungi and viruses, use consistent methodologies, and focus on longitudinal studies to better understand microbial fluctuations over time. Addressing these gaps will enable the development of more effective microbiome-based treatments for acne. In conclusion, while microbiome-targeted therapies hold promise, further investigation is needed to validate their efficacy and safety, paving the way for innovative, personalized acne management strategies.

Keywords: C. acnes; acne vulgaris; microbiome-targeted therapies; probiotics; skin microbiome.

Figure 1

C. acnes plays multiple roles in acne development, including enhancing local inflammation and modulating immune responses. It stimulates sebocytes to release pro-inflammatory cytokines (TNFα, IL-6, IL-8, and IL-12) through TLR2 activation and induces IL-1β secretion via the NLRP3 inflammasome. C. acnes also drives Th17/Th1 responses, promoting IL-17A and IFNγ production. Additionally, C. acnes affects skin physiology by modulating keratinocyte differentiation lipid production and promoting reactive adipogenesis in dermal fibroblasts, contributing to acne pathogenesis.