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An acne vaccine to make patients happy CAMPers?

DII small banner By Warren R. Heymann, MD
Nov. 12, 2018

acne-polycystic-ovary-syndrome.jpgWhen walking back to my office after receiving my flu shot, I thought about how wonderful it be to have a preventive therapy for common dermatologic disorders such as acne. That may not be so far-fetched.

Acne vulgaris (referred to as acne in this commentary) is predominantly an inflammatory disorder of the pilosebaceous unit. The pathogenesis is multifactorial, involving four interrelated mechanisms: increased sebum production, hyperkeratinization of the follicular infundibulum, inflammation, and Cutibacterium acnes (formerly Proprionibacterium acnes). Dermatologists are experts in how to treat acne. Andrea Zaenglein recently published an outstanding review of acne management in the Clinical Practice section of the New England Journal of Medicine. If you have not given much thought lately about how you treat acne, relying on the “same old, same old,” make sure you read this manuscript. (1)
The cutaneous microbiome is mostly constituted by bacteria belonging to the three main genera of Corynebacteria, Propionibacteria and Staphylococci. Interplay between these microbes is essential for skin homeostasis. Dréno et al state: “Contrary to what was previously thought, acne vulgaris is not the result of a greater proliferation of all C. acnes strains, as patients with acne do not harbour more C. acnes in follicles than normal individuals. Instead, acne might be triggered by the selection of a subset of C. acnes strains, including the acne‐associated phylotype IA1, probably enhanced by a hyperseborrheic environment. Besides, biofilm formation and differences in virulence and inflammatory potential of C. acnes strains might enhance their pathogenicity.” (2) It has been suggested that the biofilm may act as glue, contributing to the binding of corneocytes, resulting in microcomedone formation. (3) Ultimately, it is dysbiosis combined with the intrinsic properties of C. acnes that might be conducive to the activation of innate immunity, resulting in cutaneous inflammation. (2)

The CAMP (Christie-Atkins-Munch-Peterson) factor is produced by multiple bacteria, including streptococci and Bartonella species. CAMP factor causes degradation of host cells by enzymatic and/or pore formation via targeting host cell membranes. This action can then stimulate production of pro-inflammatory cytokines, including IL-1 beta, IL-8, IL-12, and TNF-alpha, via toll-like receptor 2. (4)

There are 5 CAMP factors; CAMP factor 2 appears to be most important in C. acnes. Wang et al collected acne lesions from patients to establish an ex vivo acne model for validation of the efficacy of CAMP factor antibodies in the neutralization of the acne inflammatory response. The C. acnes CAMP factor and two proinflammatory cytokines (IL-8 and IL-1 beta) were expressed at higher levels in acne lesions than those in nonlesional skin. Incubation of ex vivo acne explants with monoclonal antibodies to CAMP factor markedly attenuated the amounts of IL-8 and IL-1 beta. This ex vivo acne model confirmed that C. acnes CAMP factor is an essential source of inflammation in acne vulgaris. The authors also demonstrated that vaccination of mice with CAMP factor considerably reduced the growth of C. acnes and production of MIP-2, a murine counterpart of human IL-8. (5)

Future studies with CAMP factor 2-targeted vaccines will be necessary to determine if acne inflammation can be abrogated in humans. Should it prove successful, it will be a shot in the arm for many afflicted with acne, making them happy CAMPers, indeed.

Point to remember: A vaccine in mice directed against CAMP factor diminishes acne inflammation in a mouse model — can humans be far behind?

1. Zaenglein A. Acne vulgaris. N Engl J Med 2018; 379: 1343-52.
2. Dréno B, et al. Cutibacterium acnes (Propionibacterium acnes) and acne vulgaris: A brief look at the latest updates. J Eur Acad Dermatol Venereol 2018; 32 (Suppl 2): 5-14.
3. Beylot C, et al. Proprionibacterium acnes: An update on its role in the pathogenesis of acne. J Eur Acad Dermatol Venereol 2014; 28: 271-8.
4. Nakatsuji T, et al. Proprionibacterium acnes CAMP factor and host sphingmyelinase contribute to bacterial virulence: Potential targets for inflammatory acne treatment. PLoS 2011; 6: e14797.
5. Wang Y, et al. The anti-inflammatory activities of Propionibacterium acnes CAMP factor-targeted acne vaccines. J Invest Dermatol 2018; 138: 2355-2364.

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