Роль воспаления в патогенезе угревой болезни

Traditionally, it is believed that the pathogenesis of acne is based on the colonization of sebaceous follicle channels by bacteria Propionibacterium acnes. As a result of this, an immune response develops, and papules, pustules and nodules form. Nevertheless, this point of view is subjected to more and more careful analysis, since there is evidence of the presence of an inflammatory component at all stages of the development of acne, including before the formation of comedones. Read more about the role of inflammation in the pathogenesis of acne on estet-portal.com in this article.

The main damaging factors in the pathogenesis of acne

Pathogenetic pathways of inflammatory damage in acne are not yet fully understood. The influence of several factors that initiate an inflammatory skin lesion is assumed. These include infection with Propionibacterium acnes, exposure to inflammatory mediators including cytokines and peptidases, and changes in sebaceous glands secretion.  

Studies have shown that inflammatory skin changes in acne develop before the appearance of comedones.

In unaffected skin biopsies from acne patients, CD3+, CD4+, and T-cells in the dermis have been found to be elevated, as well as macrophage numbers. These changes are similar to those that develop in papules.

Acne:
•  Role of Propionibacterium acnes in the development of inflammation in acne;
•    the effect of inflammatory mediators on the severity of acne;
•    how the activity of the sebaceous glands affects the course of acne.

The role of Propionibacterium acnes in the development of inflammation in acne

The role of Propionibacterium acnes in the etiology of acne has been recognized for over a century. Skin biopsy studies in patients with acne have shown that Propionibacteria is identified in 68% of one-day acne lesions and 79% of three-day lesions. From a clinical point of view, the role of P. acnes in the development of inflammation in acne has been confirmed by a number of studies. They showed that antimicrobials such as tetracycline and minocycline suppress P. acnes in patients with moderately severe acne. This led to a significant reduction in the number of inflammatory lesions.   

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Influence of inflammatory mediators on the severity of acne

P. acnes has been shown to induce the release of pro-inflammatory cytokines and the expression of antimicrobial peptides. Colonization with P. acnes induces monocyte activation followed by the synthesis of IL-12, which is the major pro-inflammatory cytokine. Through its activation, P. acnes can also induce the expression of the β-defensin protein. [beta]-defensins (defensin-1, defensin-2 and defensin-3) are a family of antimicrobial peptides produced in the skin in response to microbial infection. They have basic properties such as:
•    modification of cell migration and maturation;
•    cytokine induction;
•    chemoattraction of immunocompetent cells.

Thus, P. acnes may act as a trigger to induce inflammation. Due to the impact of this microorganism, a whole cascade of inflammatory processes is launched.

How the activity of the sebaceous glands affects the course of acne

Despite the fact that changes in sebum formation do not directly affect the development of acne, the activity of the sebaceous glands can affect the severity of the inflammatory process. Sebaceous lipids may have pro-inflammatory effects, but some lipids, such as oleic or palmitic acid, have antibacterial activity.

Given the antimicrobial activity of lipids, it can be concluded that the sebaceous glands play an important role in the innate immune defense of the skin.

Thus, increased secretion of sebum does not cause acne, however, a violation of the lipid composition of the secretion of the sebaceous glands can initiate the activation of the inflammatory cascade at the beginning of the development of acne.


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