Acne may be a natural, transient inflammatory state when skin is exposed to microbes


Teenage acne may be a natural, transient inflammatory state occurring when the maturing facial skin is exposed to new microbes and enhanced production of sebum, according to researchers at the University of Debrecen in Hungary. Details of the study were published online ahead of print in the journal Trends in Immunology (Sept. 26, 2019). Based on immunological and dermatological data, the study’s authors say changes in the makeup of the microbiota composition within sebaceous-gland-rich skin during adolescence, accompanied by increased sebum production, may result in an inflammatory response that replaces the previous homeostatic host-microbiota crosstalk, which leads to the manifestation of acne. The researchers cite evidence in mice which shows that even a short-term encounter with new commensal microbes on the skin can initiate the robust accumulation of T lymphocyte white blood cells producing pro-inflammatory cytokines, including interleukin 17 and interferon gamma. They also highlight messenger RNA data showing that acne lesions contain more pro-inflammatory cytokines characteristic of host-microbiota interactions than healthy skin. Additionally, acne-associated bacteria can induce both homeostatic and inflammatory states. For example, Cutibacterium acnes strains associated with acne are capable of activating T cells that produce interleukin 17 and interferon gamma, whereas other C. acnes strains associated with healthy skin promote protective immune responses. The study’s authors suggest that high sebum production in teenagers seems to be essential for the otherwise commensal C. acnes community to initiate inflammation. For example, human macrophages treated with different sebum components secrete significantly elevated concentrations of pro-inflammatory cytokines such as interleukin-1 and tumour necrosis factor alpha in the presence of C. acnes. In line with their hypothesis, genome-wide association data in adolescents with severe acne suggest that polymorphisms in inflammatory genes, and genes playing a role in the initiation of tolerance, are associated with disease manifestation. The researchers suggest future studies should focus on identifying how acne spontaneously resolves, for example, through reduced sebum production, compositional changes in C. acnes strains, the regulation of the skin immune system, or improved skin barrier integrity.

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