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RESEARCH PAPER
Acne vaccine targeting Cutibacterium acnes secretory lipase suppresses the bacteria-induced pro-inflammatory interleukin-6 and macrophage inflammatory protein-2 production
1
Research Center for Vaccine and Drugs, National Research and Innovation Agency (BRIN), Bogor, West Java, Indonesia
2
Department of Biology, Faculty of Military Mathematics and Natural Sciences, Universitas Pertahanan, Bogor, West Java, Indonesia
3
Department of Biomedical Sciences and Engineering, National Central University, Zhongli, Taoyuan, Taiwan
4
Department of Pharmacy, Universitas Katolik Widya Mandala Surabaya, Surabaya, East Java, Indonesia
5
Department of Fundamental of Science, School of Nursing, Mongolian National University of Medical Sciences, Ulaanbaatar, Mongolia
6
Department of Life Sciences, National Central University, Zhongli, Taoyuan, Taiwan
7
Immunology Research Center, National Health Research Institutes, Zhunan, Miaoli, Taiwan
8
Research Center for Veterinary Science, National Research and Innovation Agency (BRIN), Bogor, West Java, Indonesia
9
Research Center of Polymer Technology, National Research and Innovation Agency (BRIN), South Tangerang, Banten, Indonesia
Submission date: 2025-10-17
Final revision date: 2026-04-20
Acceptance date: 2026-05-06
Publication date: 2026-06-27
Corresponding author
BioTechnologia 2026;107(2):163-180
KEYWORDS
TOPICS
ABSTRACT
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.
Material 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.
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.
Material 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.
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