The latest study provides an understanding of teenage acne. Acne among teenagers doesn’t always result in a pathological state. Instead, it may a natural and temporary inflammatory condition.
Physiological changes in skin and teenage acne
This condition occurs due to the exposure of maturing facial skin to new microbes and an increase in sebum production. Whereas, sebum is an oily substance secreted by sebaceous glands in the skin. All these findings were published in the journal “Trends in Immunology” on September 26, 2019.
The study’s novel framework suggests that the development of new therapies should emphasize on promoting some specific mechanisms. That are capable of restoring homeostasis between facial skin and its chemical and microbial milieu.
The first author of the study Andrea Szegedi of the University of Debrecen in Hungary says that the key message is that, one shouldn’t consider teenage acne as an accidentally occurring disease escorted by pathological processes. Rather, acne is an unavoidable inflammation caused by physiological changes in the skin during adolescence.
Among many inflammatory skin diseases, acne vulgaris is distinctive due to its specific localization on the skin regions rich in sebaceous glands. Moreover, it is also unique due to its high prevalence in teenagers, occurrence within a narrow range related to puberty, and frequent resolution.
For instance, spontaneous remission of acne occurs in up to 50% of affected patients. By contrast, other inflammatory skin diseases, like rosacea and psoriasis, have chronic intermittent courses. Szegedi and her colleagues have proposed a new concept that may explain why acne has strong regional and age specificity, resolution, and prevalent occurrence.
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Acne – an inflammatory response
Based on dermatological and immunological data, the research team has given a further hypothesis. And suggested that sudden changes in the composition of microbiota within sebaceous-gland-rich skin and enhanced sebum production during teenage may result in an inflammatory response.
That replaces the former homeostatic host-microbiota crosstalk, consequently leading to the manifestation of acne. This new hypothesis challenges conventional thinking. And also involves recent scientific data and explains special clinical characteristics of acne.
The authors cite evidence in mice presenting that even short-term exposure to new commensal microbes on the skin can result in the robust accumulation of T lymphocytes (WBCs). That will lead to the production of pro-inflammatory cytokines like interferon-gamma and interleukin 17.
The authors have also highlighted mRNA data showing that acne lesions have more pro-inflammatory cytokines as compared to healthy skin. Besides this, bacteria associated with acne can induce both inflammatory and homeostatic states.
For instance, C. acnes strains associated with acne can activate T-cells that produce interferon-gamma and interleukin 17. Whereas, its strains associated with healthy skin can promote protective immune responses. The authors suggest that increased sebum production in teenagers seems as essential for the otherwise commensal C. acnes to cause inflammation.
And the genome-wide association data in teenagers with acne is also consistent with their hypothesis. While this data implies that polymorphism in the genes playing a role in tolerance initiation and inflammatory genes has an association with disease manifestation.
According to the authors’ statement, future research should target identifying the process behind the spontaneous resolution of acne. Szegedi and her colleagues believe that this research will be highly helpful for the development of new treatments for acne.