Propionibacterium acnes, better known as Cutibacterium acnes, is a Gram-positive skin bacterial flora that predominates (> 60% of total bacteria) on the facial skin of humans. P. acnes has been associated with acne vulgaris affecting more than 85%.
for acne often do not give a positive result or are difficult to tolerate by the patient. Promising are the methods of treatment aimed at the organism P. acnes, which is involved in the genesis of inflammation in acne. Christie-Atkins-Munch-Petersen secretory factor (CAMP) is synthesized by P. acnes to trigger pro-inflammatory cytokines. Monoclonal antibodies to CAMP significantly reduced the appearance of inflammatory elements on the skin. Read more
about the studyin the article on estet-portal.com. Role of P. acnes factor in the development of acne
Christie-Atkins-Munch-Petersen factor, synthesized by Propionibacterium acnes, acts as a pore-forming toxin that can induce cytolysis and cytokine secretion through activation of inflammation.
Toxin-induced membrane permeability leads to a decrease in cytoplasmic potassium, which causes inflammation through caspase-1. The P. acnes CAMP factor can cause sebocyte cell death in the sebaceous glands.
P. acnes bacteria has been shown to promote the secretion of IL-6 and IL-8 by follicular keratinocytes, IL-1β, tumor necrosis factor-α, IL-8 and IL-12 by monocytic cells, IL-8 by seborocytes, IL-1.beta., IL-12 and IL-23 by peripheral blood mononuclear cells. In addition, the bacteria caused the secretion of IL-17A and IFN-.gamma. from specific CD4+ T cells.
This activation of pro-inflammatory processes is the basis for the development of acne.
Telegram What does acne-prone skin hide
Presence of the CAMP factor Propionibacterium acnes. (a) Biopsy specimens (4 x 4 x 8 mm) of skin from patients with acne vulgaris. The skin sample contains the hair follicle, epidermis, dermis. Hematoxylin and eosin staining showed that the epidermis (b) in the acne skin area was thicker than (c) in healthy skin.
The area of acne-prone skin (AL) had higher CAMP-factor mRNA expression and protein levels than healthy skin (NAL), P<0.05.
High-magnification images of selected areas in (f) healthy skin and (k) acne-prone skin are shown in gj and lo, respectively. The CAMP factor (red spots) was found in the hair follicle and was expressed at higher levels in (h, m) sebaceous glands, (i, n) epidermis and (j, o) dermis of the affected skin.
• The results of publications in 2008 showed that vaccination with neuraminidase or thermally killed P. acnes as antigen significantly suppressed P. acnes inflammation. an enzyme of bacteria that allows the latter to destroy the shell of the cells of the human body and penetrate into them or introduce their own toxin.
• Vaccination of mice with 10 or 20 µg of recombinant CAMP factor in the presence of aluminum as an adjuvant provides suppression of the production of the cytokine MIP-2 (analogous to human IL-8) and colonization of P. acnes in the skin of the ear.
• In 2009, skin biopsy specimens were collected from the backs of acne patients and healthy individuals. Ex vivo explants were incubated with anti-CAMP antibodies for 24 hours. Ex vivo incubation of explants with antibodies to hepatitis B surface antigen served as a control. in ex vivo explants.
• Human sera with anti-CAMP antibody titers of 1:400 and 1:800 did not protect skin cells from death caused by P. acnes under experimental conditions on human skin tissues affected by acne. Cytolysis was significantly inhibited (> 24%) only after using anti-CAMP mouse sera with titers greater than 1:62,500, indicating that the low titers of anti-CAMP factor antibodies produced in humans are not sufficient to reduce the cytotoxicity of P. acnes.P. acnes type IA, IB or II bacteria encode five different CAMP factor genes (CAMP factors 1-5). CAMP 2 is secreted by all human isolated strains of P. acnes.
Further prospects in the fight against acne
The use of antibiotics to treat acne results in the development of resistant bacteria and has no neutralizing effect on P. acnes secretory toxins.
Isotretinoin, a 13-cis-retinoic acid, is widely used for the systemic treatment of acne. However, retinoic acid can cause depression and is teratogenic and embryotoxic.
Vaccination against the CAMP protein is the most promising treatment for patients with acne.
Future research will include:
1. studying whether vaccines with 2-targeted CAMP vaccines can reduce inflammation caused by different subtypes of P. acnes;
2. determining whether antibodies elicited by CAMP factor 2 vaccination are cross-reactive with other CAMP factor homologues;3. Creation of a multivalent vaccine consisting of a mixture of different recombinant homologues of the CAMP factor, since vaccination of mice with CAMP factor 2 does not completely suppress inflammation caused by P. acnes. diseases associated with P. acnes, including prostate cancer, sepsis, toxic shock syndrome, endocarditis, osteomyelitis, and various surgical infections.
You may be interested in an article on our website estet-portal.com in the "Dermatology" section;
Basics
pathogenetic treatment of acne vulgaris
Adapted from Journal of Investigative Dermatology
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