ArticlePloS one2011
Propionibacterium acnes CAMP factor and host acid sphingomyelinase contribute to bacterial virulence: potential targets for inflammatory acne treatment.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 113 citations in OpenAlex.
- The Bacterial Landscape of Facial Skin: From Homeostasis to Skin Conditions.Dermatology and therapy · 2026Review
- Surgical relevance of a pedicled omental flap for the treatment of a recurrent giant mycotic left ventricular pseudoaneurysm: a case report and review of the literature.Journal of medical case reports · 2026Review
- Targeting macrophage polarization: mechanisms and potential of mesenchymal stromal/stem cells therapy in acne treatment- a narrative review.Frontiers in immunology · 2026Review
- Cutibacterium Adaptation to Life on Humans Provides a Potential C acnes Infection Biomarker.The Journal of investigative dermatology · 2026Article
- Is There a Place for Biologics in Acne?American journal of clinical dermatology · 2025Review
- Microbiota-Host Interactions: Exploring Their Dynamics and Contributions to Human Diseases.MicrobiologyOpen · 2025Review
- Insights into microbial dysbiosis andMicrobial genomics · 2025Article
- Microbiome and Postbiotics in Skin Health.Biomedicines · 2025Review
- Evaluation of anti-acne activity of human whole saliva against acne vulgaris: An in vitro study.Journal of cosmetic dermatology · 2025Article
- Macrophages in acne vulgaris: mediating phagocytosis, inflammation, scar formation, and therapeutic implications.Frontiers in immunology · 2024Review
- Functional divergence of a bacterial enzyme promotes healthy or acneic skin.Nature communications · 2023Article
- Evolving approaches to profiling the microbiome in skin disease.Frontiers in immunology · 2023Review
- Skin dysbiosis and Cutibacterium acnes biofilm in inflammatory acne lesions of adolescents.Scientific reports · 2022Article
- The role of serum C-reactive protein in the diagnosis of periprosthetic shoulder infection.Archives of orthopaedic and trauma surgery · 2022Article
- Characterization of aInternational journal of molecular sciences · 2022Article
- The defense response of Caenorhabditis elegans to Cutibacterium acnes SK137 via the TIR-1-p38 MAPK signaling pathway.Bioscience, biotechnology, and biochemistry · 2022Article
- UVB-Induced Microvesicle Particle Release and Its Effects on the Cutaneous Microenvironment.Frontiers in immunology · 2022Review
- Group B Streptococcus CAMP Factor Does Not Contribute to Interactions with the Vaginal Epithelium and Is Dispensable for Vaginal Colonization in Mice.Microbiology spectrum · 2021Article
- Porphyrins produced by acneiciScience · 2021Article
- Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIn the progression of acne vulgaris, the disruption of follicular epithelia by an over-growth of Propionibacterium acnes (P. acnes) permits the bacteria to spread and become in contact with various skin and immune cells. METHODOLOGY/PRINCIPAL
findingsWe have demonstrated in the present study that the Christie, Atkins, Munch-Peterson (CAMP) factor of P. acnes is a secretory protein with co-hemolytic activity with sphingomyelinase that can confer cytotoxicity to HaCaT keratinocytes and RAW264.7 macrophages. The CAMP factor from bacteria and acid sphingomyelinase (ASMase) from the host cells were simultaneously present in the culture supernatant only when the cells were co-cultured with P. acnes. Either anti-CAMP factor serum or desipramine, a selective ASMase inhibitor, significantly abrogated the P. acnes-induced cell death of HaCaT and RAW264.7 cells. Intradermal injection of ICR mouse ears with live P. acnes induced considerable ear inflammation, macrophage infiltration, and an increase in cellular soluble ASMase. Suppression of ASMase by systemic treatment with desipramine significantly reduced inflammatory reaction induced by intradermal injection with P. acnes, suggesting the contribution of host ASMase in P. acnes-induced inflammatory reaction in vivo. Vaccination of mice with CAMP factor elicited a protective immunity against P. acnes-induced ear inflammation, indicating the involvement of CAMP factor in P. acnes-induced inflammation. Most notably, suppression of both bacterial CAMP factor and host ASMase using vaccination and specific antibody injection, respectively, cooperatively alleviated P. acnes-induced inflammation. CONCLUSIONS/SIGNIFICANCE: These findings envision a novel infectious mechanism by which P. acnes CAMP factor may hijack host ASMase to amplify bacterial virulence to degrade and invade host cells. This work has identified both CAMP factor and ASMase as potential molecular targets for the development of drugs and vaccines against acne vulgaris.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.