Interleukin-32 is highly expressed in lesions of hidradenitis suppurativa.
- Thomi R Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
- Yerly D Department of Rheumatology, Immunology and Allergology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
- Yawalkar N Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
- Simon D Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
- Schlapbach C Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
- Hunger RE Department of Dermatology, Inselspital, Bern University Hospital, University of Bern, 3010, Bern, Switzerland.
- 2017-03-17
Published in:
- The British journal of dermatology. - 2017
Adult
Case-Control Studies
Dendritic Cells
Female
Hidradenitis Suppurativa
Humans
Interferon-gamma
Interleukin-17
Interleukins
Killer Cells, Natural
Macrophages
Male
Middle Aged
RNA, Messenger
Skin
T-Lymphocytes
Up-Regulation
English
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 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.
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 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.
- Language
-
- English
- Open access status
- green
- Identifiers
-
- DOI 10.1111/bjd.15458
- PMID 28301691
- Persistent URL
- https://folia.unifr.ch/global/documents/89883
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