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Interleukin‐32 is highly expressed in lesions of hidradenitis suppurativa
Author(s) -
Thomi R.,
Yerly D.,
Yawalkar N.,
Simon D.,
Schlapbach C.,
Hunger R.E.
Publication year - 2017
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.15458
Subject(s) - dermis , psoriasis , hidradenitis suppurativa , medicine , proinflammatory cytokine , cytokine , pathogenesis , pathology , interleukin , immunology , tumor necrosis factor alpha , atopic dermatitis , inflammation , disease
Summary Background 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. Objectives 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 ). Methods 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. Results 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 IL 32 mRNA levels in lesional HS skin coincided with high amounts of T cells and macrophages. Additionally, IL 32 mRNA levels in lesional HS skin correlate positively with interferon‐γ and IL ‐17A and negatively with IL ‐13. Conclusions 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.