Interleukin-32 is highly expressed in lesions of hidradenitis suppurativa.

Abstract

Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease. Its immunopathogenic mechanisms are still poorly understood. Previous studies demonstrated that the proinflammatory cytokine interleukin (IL)-32 is implicated in the pathogenesis of other inflammatory diseases. To investigate the tissue expression and systemic levels of IL-32, as well as its cellular sources, in patients with HS in comparison with healthy donors and patients with two other inflammatory skin diseases: psoriasis and atopic dermatitis (AD). Tissue samples were obtained from healthy skin and lesional HS, psoriatic and AD skin to analyse the expression of IL-32 by immunohistochemistry and semiquantitative real-time polymerase chain reaction. The cellular source of the cytokine was determined by double immunofluorescence staining. Serum from the four donor groups was used to measure systemic levels of IL-32 by enzyme-linked immunosorbent assay. IL-32 was upregulated in patients with HS in both lesional skin and serum when compared with healthy donors and patients with AD or psoriasis. In HS, IL-32 was found to be expressed by natural killer cells, T cells, macrophages and dendritic cells in highly infiltrated areas of the dermis. High IL32 mRNA levels in lesional HS skin coincided with high amounts of T cells and macrophages. Additionally, IL32 mRNA levels in lesional HS skin correlate positively with interferon-γ and IL-17A and negatively with IL-13. Our findings suggest that IL-32 is overexpressed in HS. Targeting IL-32 may therefore represent a new therapeutic option for the treatment of this recalcitrant disease.