The presence of bacterial DNA in patients with HS was associated with elevated levels of TNF-α (P < 0.001), IL-1β (P = 0.01) and IL-17 (P < 0.001); however, it was not associated with disease severity or disease location.
Several inflammatory modulators have been implicated in the development of HS, including tumor necrosis factor (TNF)-α as well as interleukin (IL)-1β, IL-10, and IL-17.
The pathogenesis of hidradenitis suppurativa (HS) centers around Th17/Treg dysfunction illustrated by lesional elevation of IL-17A, IL-6, and other inflammatory mediators resulting in a chronic feed-forward inflammatory cascade.
It is unclear whether IL-17 inhibition will parallel TNF-α or IL-1 inhibition in effect, however it is plausible that small molecule targets (Janus kinase1 and phosphodiesterase 4) may provide effective new strategies for treatment of HS.
Spondyloarthritis (SpA), a chronic inflammatory, rheumatic disease, and hidradenitis suppurativa (HS), a chronic, debilitating, inflammatory skin disease, share several clinical and pathophysiological features, such as the association with inflammatory bowel disease and elevated cytokine levels IL-17 and TNF-α.
Several molecules, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), IL-17, IL-12, IL-23, phosphodiesterase 4 (PDE4), lymphocyte function-associated antigen 1 (LFA-1), and complement component 5a (C5a), are modulated by such new biologic agents in HS.
Last, we found that CD27 expression was inversely correlated with T<sub>reg</sub> IL-17 production in skin of patients with psoriasis and hidradenitis suppurativa.
The levels of IL-1<i>β</i>, IL-6, IL-8, IL-10, IL-12p70, IL-17A, sTNF-RII, CRP, and ESR were significantly elevated according to inflammatory activity based on HS-PGA scores (<i>r</i> > 0.25, <i>P</i> < 0.05).
These data suggest that inhibition of pathogenic IL-17 via tumor necrosis factor blockade is associated with improvement in immune dysregulation in HS and may provide a rationale for targeting IL-17 in the disease.
The mean IL-17 serum level of patients with HS was 3.68 ± 2.08 pg/mL, which was significantly elevated (P < .0001) compared with that found in healthy volunteers (2.5 ± 1.11 pg/mL).