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Acne in adolescents does not always lead to a pathological condition; According to a Forum article published Sept. 26 in the journal, it could be a natural and transient inflammatory state, which occurs when the maturing face skin is exposed to new microbes and to the increased production of an oily substance called sebum. Trends in immunology. The authors argue that their new framework suggests that the development of new treatments should be focused on promoting homeostasis restoration mechanisms between facial skin and its microbial and chemical environment.
"The main message to remember is that instead of considering acne as an accidental disease accompanied by pathological processes, we propose that acne is an inevitable inflammation caused by physiological changes in the sebaceous skin during the first year. ", Said the first author, Andrea Szegedi, from the University of Debrecen in Hungary.
Among various inflammatory skin diseases, acne vulgaris is unique because of its specific localization on the sebum-producing sebaceous gland-rich skin regions, its occurrence in a narrow age range associated with puberty, its high prevalence among adolescents and its frequent resolution. For example, up to 50% of patients with spontaneous spontaneous remission of acne vulgaris, unlike other inflammatory skin diseases, such as psoriasis and rosacea, which follow an evolution chronic intermittent.
In the short article of the Forum, Szegedi and his colleagues propose a new concept that could explain why acne is characterized by a strong regional and age specificity, prevalence and resolution. Based on immunological and dermatological data, they hypothesize that sudden changes in the composition of the microbiota composition in the skin rich in sebaceous glands during adolescence, accompanied by an increase in Sebum production, could result in an inflammatory response that replaces the old homeostatic host-microbiota crosstalk, thus leading to the manifestation of acne.
"Our hypothesis, that acne is a transient and naturally developing state of inflammation rather than a pathological skin disease, challenges conventional thinking," said Dr. Szegedi. "This hypothesis incorporates recent scientific data and may explain the particular clinical features of acne."
The authors cite evidence in mice showing that even a short-term encounter with new commensal microbes on the skin can initiate the robust accumulation of T-cell white blood cells producing pro-inflammatory cytokines, including l? 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 ones.
In addition, bacteria associated with acne can induce both homeostatic and inflammatory conditions. For example, acne-associated strains of Cutibacterium acnes are able to activate the T cells that produce interleukin-17 and interferon-gamma, while other strains of C. acnes associated with healthy skin promote protective immune responses.
The authors argue that high sebum production in adolescents appears 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-1β and tumor necrosis factor alpha in the presence of C. acnes.
Consistent with their hypothesis, the genome-wide association data in adolescents with severe acne suggest that polymorphisms of inflammatory genes, and genes playing a role in the initiation of tolerance, are associated with the manifestation of the disease. However, one of the limitations of their framework is that it only applies to acne in adolescence, not in childhood or in childhood. adulthood.
According to the authors, future research should aim to identify the mechanisms of spontaneous resolution of acne, for example by reducing sebum production, altering the composition of C. acnes strains, regulating the immune system of the acne. skin or by improving the integrity of the skin barrier. "We are confident that this research will greatly contribute to the development of new innovative treatments for acne," said Szegedi. "In addition, the mechanisms that initiate, amplify, resolve or perpetuate acne could have common pathways with diseases that develop in other organic systems, and the knowledge gained on a larger scale on this front could help to better understand a variety of pathological conditions. "
Button evidence: A mouse model validates the influence of "good" and "bad" bacteria on acne
Trends in immunology, Szegedi et al .: "Acne: transient arrest in host-microbiotic homeostatic dialogue?" https://www.cell.com/trends/immunology/fulltext/S1471-4906(19)30173-5, DOI: 10.1016 / j.it.2019.08.006
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Teenage acne can be a natural transient inflammatory condition (September 26, 2019)
recovered on September 27, 2019
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