Identifying key components and therapeutic targets of the immune system in hidradenitis suppurativa with an emphasis on neutrophils

Hidradenitis suppurativa (HS) is a chronic, inflammatory, recurrent, and debilitating skin disease of the hair follicle unit that typically develops after puberty. The disorder is characterized by comedones, painful inflammatory nodules, abscesses, dermal tunnels, and scarring, with a predilection for intertriginous areas of the body (axillae, inguinal, and anogenital regions). Recruitment of neutrophils to HS lesion sites may play an essential role in the development of the painful inflammatory nodules and abscesses that characterize the disease. This is a review of the major mediators involved in the recruitment of neutrophils to sites of active inflammation including bacterial components (endotoxins, exotoxins, capsule fragments, etc.), the complement pathway anaphylatoxins C3a and C5a, tumor necrosis factor-alpha (TNF- α), interleukin 17 (IL-17), interleukin 8 (CXCL8/IL-8), interleukin 36 (IL-36), interleukin 1 (IL-1), lipocalin-2, leukotriene B4 (LTB4), platelet-activating factor, kallikrein, matrix metalloproteinases (MMPs), and myeloperoxidase inhibitors. Pharmacologic manipulation of the various pathways involved in the process of neutrophil recruitment and activation could allow for successful control and stabilization of HS lesions and the remission of active, severe flares.