What is new in the pathophysiology of acne, an overview.

Acne is a chronic inflammatory disease of the pilosebaceous unit. Its pathophysiology includes hyperseborrhoea, abnormal follicular keratinization and Propionibacterium acnes proliferation in the pilosebaceous unit. Recent research has shed some new light on the involvement of the sebaceous gland, as well as on the pro-inflammatory activity of the cutaneous microbiome. During puberty, alteration of the sebaceous lipid profile, called dysseborrhoea, stress, irritation, cosmetics and potential dietary factors lead to inflammation and formation of different types of acne lesions. Dysbiosis, the process leading to a disturbed skin barrier and disequilibrium of the cutaneous microbiome, resulting in the proliferation of P. acnes strains, is another important process that triggers acne. P. acnes activates the innate immunity via the expression of protease activated receptors (PARs), tumour necrosis factor (TNF) α and toll-like receptors (TLRs), and the production of interferon (INF) γ, interleukins (IL-8, IL12, IL-1), TNF, and matrix metalloproteinases (MMPs) by keratinocytes, resulting in the hyperkeratinization of the pilosebaceous unit. Rebalancing the natural microbiome of the skin by restoring the natural skin barrier, limiting the proliferation of P. acnes on the skin by using topical antibacterials which do not cause resistance and regulating quantity and quality of sebum will be the main acne treatment challenges in the future. The aim of this article to provide an update on the involvement of the sebaceous gland, the innate immunity and the cutaneous microbiome, how all of these factors promote acne and to illustrate their links with current and future treatments.