title: Interleukin-32 is highly expressed in lesions of hidradenitis suppurativa.
abstract: 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.
  
  
  OBJECTIVE
  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 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.
  
  
  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.
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
authors.forename: R
authors.identifier: http://orcid.org/0000-0002-8260-6449
authors.initials: R
authors.lastname: Thomi
authors.affiliation: Department of Rheumatology, Immunology and Allergology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
authors.forename: D
authors.initials: D
authors.lastname: Yerly
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
authors.forename: N
authors.initials: N
authors.lastname: Yawalkar
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
authors.forename: D
authors.identifier: http://orcid.org/0000-0001-8965-9407
authors.initials: D
authors.lastname: Simon
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
authors.forename: C
authors.initials: C
authors.lastname: Schlapbach
authors.affiliation: Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
authors.forename: R E
authors.initials: RE
authors.lastname: Hunger
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D003713:Dendritic Cells / Q000378:metabolism; D005260:Female; D017497:Hidradenitis Suppurativa / Q000378:metabolism*; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism*; D007694:Killer Cells, Natural / Q000378:metabolism; D008264:Macrophages / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000378:metabolism; D013601:T-Lymphocytes / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
chemical_list: C496971:IL32 protein, human; D020381:Interleukin-17; D007378:Interleukins; D012333:RNA, Messenger; D007371:Interferon-gamma