PATHOGENETIC MECHANISM OF ACNE-COUPLED INFLAMMATION

Abstract

Acne (Ac) represents a widespread dermatosis most commonly found in adolescents and adults covering 6-85% total cases. It has been traditionally believed that Propionibacterium acnes (P. acnes) colonizes ducts of the sebaceous hair follicles (SHFs), activates innate immune response and triggers transition of non-inflammatory erosions (comedones) into inflammatory lesions such as papules, pustules and nodules. Moreover, it was also shown that inflammatory reaction develops at late Ac stage and its severe course. Today, it has been evidenced that Ac-coupled inflammation develops at all stages of dermatosis, perhaps in a subclinical manner, even prior to emergence of comedones.It is commonly accepted that acne targets SHFs displaying location-related marked morphological, microbiological and metabolic diversity. For instance, SHFs is profoundly affected by altered hormone and immunological properties as well as environmental cues.Comparative studies examining efficacy nd medicated therapy with anti-inflammatgory potential evidence about early inflammatory reaction related to acne.The data obtained confirm that P. acnes elicits inflammatory reaction in acne that additionally maintains P. acnes proliferation. It was found that P. acnes initiates TLR2-mediated innate immune reaction both at early and late stages of developing dermatosis. Such reaction results in upregulated immune genes including those encoding cytokines and chemokines recruiting immune cells.Today, owing to clinical, immunological, histology and immunohistochemistry data there has been accumulated evidence confirming significance of ongoing inflammation as a pathophysiological basis for emerging acne.Upon that, pathophysiological mechanisms triggering inflammatory reaction in acne are complex and poorly investigated, thereby underlying a need to conduct further studies.