Acne vaccine targeting Cutibacterium acnes secretory lipase suppresses the bacteria-induced pro-inflammatory interleukin-6 and macrophage inflammatory protein-2 production.

BACKGROUND

Limited attention paid to acne vulgaris has hindered progress in studying its pathological mechanisms and developing new treatments. While direct evidence confirming Cutibacterium acnes (C. acnes) as the initial trigger of acne vulgaris is scarce, the bacterium clearly drives inflammation within acne lesions.

MATERIALS AND

METHODS

Mass spectrometric analysis demonstrated that C. acnes lipase digested triglycerides into various fatty acids, which increased sebum production in sebocytes. The secretory lipase was selected as an immunogenic antigen to generate antibodies in mice. Serum from mice vaccinated with C. acnes lipase was used to assess antibody titers via test strips. Pro-inflammatory interleukin-6 (IL-6) and macrophage inflammatory protein-2 (MIP-2) expression were measured by enzyme-linked immunosorbent assay. Passive immunization with neutralization antibodies to lipase was conducted by administering anti-lipase serum co-cultured with C. acnes.

RESULTS

Palmitic acid, a lipase-derived fatty acid, was identified as a major pro-inflammatory stimulus in sebocytes, confirming the central role of lipase in acne inflammation. Mice vaccinated with C. acnes lipase showed protection against C. acnes-induced inflammation in an ear model. Therefore, neutralization antibodies to lipase significantly reduced C. acnes-induced production of pro-inflammatory IL-6 and MIP-2.

CONCLUSIONS

The C. acnes secretory lipase is a key virulence factor contributing to acne inflammation. Vaccination with C. acnes lipase significantly reduced bacterial colonization and the production of pro-inflammatory IL-6 and MIP-2. These findings support the potential of C. acnes lipase-targeted vaccines as a novel, antigen-specific strategy for both the treatment and prevention of acne vulgaris.