(1) Cytokines involved in hidradenitis suppurativa (HS) pathogenesis include interleukin (IL)-1b, IL-17, IL-10 and to a lesser extent TNF-a, therefore representing potential therapeutic targets.
(2) An overzealous toll-like receptor response to commensal bacteria may be an initiating factor in the the pathogenesis of this disease. In advanced stages, characterised by sinus tract formation and scarring, superinfection with bacterial strains known to induce soft tissue infection may occur, which frequently responds to intensive targeted antibiotic therapy.
(3) Smoking is epidemiologically linked to HS. The mechanism of action of smoking in initiating or propagating HS is theoretically by:
a. Inducing epidermal hyperplasia and keratinization, leading to occlusion of the follicular infundibulum
b. Alteration of the skin immune response
c. Increasing microbial virulence and decreasing skin antimicrobial peptides

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Dermatologic Clinics
Department of Dermatology

Kelly, G, & Prens, E.P. (2016). Inflammatory Mechanisms in Hidradenitis Suppurativa. Dermatologic Clinics (Vol. 34, pp. 51–58). doi:10.1016/j.det.2015.08.004