The Anti-Inflammatory Activities of Propionibacterium acnes CAMP Factor-Targeted Acne Vaccines

Journal : Journal of investigative dermatology Date of publication : Nov 2018 original article Location of study : Department of Dermatology, School of Medicine, University of California, San Diego, California, USA;


Incidence: acne : more than 85% of teenagers and over 40 million people in the United States Bacteria : estimated density of 102 to 105 cm2 and >60% of commensal Here, they used a vaccination approach to test whether P. acnes Christie-Atkins-Munch-Petersen (CAMP) factor, a secretory virulence factor is a main source of inflammation in acne vulgaris.

4 actions of CAMP factor

  1. P. acnes CAMP factor is able to bind to immunoglobulin G and M classes and acts as a pore-forming toxin
  2. CAMP factor combined with sphingomyelinase exerts the co-hemolytic activity that can confer cytotoxicity to both keratinocytes and macrophages
  3. induce cell death of sebocytes in sebaceous glands and trigger inflammation
  4. stimulating the cells to produce proinflammatory cytokines, including IL-8, IL-1b, IL-12, and tumor necrosis factor-a, leading to the inflammation in acne vulgaris

What is done ?

Previous : vaccination using surface sialidase or heat-killed P. Acnes as an antigen significantly suppressed P. acnes-induced inflammation

Now : specific secretory virulence factor as a vaccine because it has been reported that specific inhibition of secretory virulence factors presents less selective pressure for the development of resistant bacteria and they are immunogenic


1. Changes in anaerobic environment

Quantitative proteomic analysis using non gel based isotopecoded protein label method 23/243 proteins showed up/down variations CAMP shown 1.5 times increase in anaerobic environment

2. Necessity of CAMP factor for causing inflammation

Wild type bac vs mutant CAMP containing bac in mice ears • Compared with injection with wild-type P. acnes, injection of mice with mutant camp caused less swelling , redness and secretion of MIP-2 b)mouse ear injected with mutant camp resulted in significantly less P. acnes growth than those injected with wild-type P. Acnes

3. Antibodies to CAMP

3 situations were assessed healthy(1:400 antibody titre),acne patients(1:800) and mice with very high titre.all 3 were incubated overnight with p.acne . Cell death was significantly inhibited (>24%) only when the anti-CAMP factor mouse sera with titers greater than 1:62,500 were used, suggesting that the low titers of antibodies to CAMP factor produced in humans are not sufficient to reduce the cytotoxicity of P. acnes.

4. vaccination with recombinant CAMP factor

Recombinat CAMP 2 doses 2week apart followed by ELISA for antibodies after 5 weeks showed titreof 1:800000 And with adjuvant aluminium -4 fold increase Similarly,on testing on mice ear,vaccinated mice showed lesser erythema,thickness,colonization and MIP2 production Vaccination with P. acnes CAMP factor elicited protective immunity against P. acnes

5. CAMP factor in acne lesions]

Human acne explants via punch biopsy. mRNA quantification by PCR and CAMP(protein) with ELISA was done.Both were substantially higher in lesional skin. IHC using Mab was done to see the distribution of CAMP.

6. CAMB factor Mab in ex vivoacne models

Proinflammatory cytokines were quantified and 8/11 esimated showed significant elevation. The ex vivo explants derived from acne lesional and nonlesional skin were incubated with the mAb to CAMP factor for 24 hours. Incubation of ex vivoexplants with the mAb to hepatitis B surface antigen served as a control.

mAb to CAMP factor exhibited the neutralizing capability to attenuate the production of both IL-8 and IL-1b in ex vivo explants obtained from acne lesional skinsDS

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