Teenage Acne May Be a Natural, Transient Inflammatory State

 

Acne in adolescence does not always lead to a disease; according to a Forum article that was published on September 26 in the journal Trends in Immunology, it may instead be a natural, brief inflammatory state that occurs when mature facial skin is exposed to new microbes and produces more sebum, an oily substance. 

The primary takeaway is that, rather than considering acne as an accidental disease accompanied by pathological processes, we propose that acne is an unavoidable inflammation precipitated by physiological changes of the sebaceous skin during adolescence, says first author Andrea S Z-E G-E D-I of the University of D-E B R-E C-E N in Hungary. The authors argue that their novel framework suggests that the development of new treatments should focus on promoting mechanisms that restore homeostasis between facial skin and its microbial and chemical milieu. 

Acne vulgar is distinct from other inflammatory skin diseases due to its specific location on skin areas with a lot of sebaceous glands that produce sebum, its occurrence within a limited age range associated with puberty, its high prevalence in teenagers, and its frequent resolution. In contrast to other inflammatory skin diseases like psoriasis and rosacea, which have chronic, intermittent courses, acne vulgar, for instance, experiences spontaneous remission in up to 50% of affected patients. 

S Z-E G-E D-I and her colleagues offer a novel idea in the short forum article that could help explain why acne has strong regional and age specificity, frequent occurrence, and resolution.  They hypothesize, based on immunological and dermatological data, that acne may develop as a result of sudden changes in the microbiota composition of sebaceous-gland-rich skin during adolescence, accompanied by increased sebum production. This inflammatory response may replace the previous homeostatic host-microbiota crosstalk, which was what caused acne to form. 

He states, "Conventional thinking is challenged by our hypothesis that acne is a naturally occurring, transient inflammation state rather than a pathological skin disease". Acne's unique clinical characteristics may be explained by this hypothesis, which incorporates recent scientific data

The creators refer to studies in mice showing that even a momentary experience with new microorganisms on the skin can start the strong gathering of T lymphocyte white platelets delivering favorable to provocative cytokines, including interleukin-17 and interferon-gamma.  In addition, they draw attention to messenger RNA data that demonstrate that healthy skin contains fewer pro-inflammatory cytokines than acne lesions do. 

Additionally, acne-causing bacteria can cause both homeostasis and inflammation. A-C N E-S strains that are associated with acne, for instance, have the ability to activate T cells that produce interleukin-17 and interferon gamma, whereas other A-C N-E S strains that are associated with healthy skin promote immune responses that are protective. 

According to the authors, A-C N-E S community cannot initiate inflammation unless teenagers produce a lot of serums. In the presence of C, human macrophages treated with various components of the sebum, for instance, secrete significantly higher concentrations of pro-inflammatory cytokines like interleukin-1 and tumor necrosis factor-alpha

Polymorphisms in inflammatory genes and genes that play a role in the initiation of tolerance, according to genome-wide association data from adolescents with severe acne, are associated with disease manifestation. Nonetheless, one constraint of their structure is that it applies to skin break out in youth as opposed to in adolescence or adulthood