Epidermal Expression and Regulation of Interleukin-33 during Homeostasis and Inflammation: Strong Species Differences

IL-33 is a novel IL-1 family member with a putative role in inflammatory skin disorders and a complex biology. Therefore, recent conflicting data regarding its function in experimental models justify a close assessment of its tissue expression and regulation. Indeed, we report here that there are st...

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Bibliographic Details
Published in:Journal of investigative dermatology 2015-07, Vol.135 (7), p.1771-1780
Main Authors: Sundnes, Olav, Pietka, Wojciech, Loos, Tamara, Sponheim, Jon, Rankin, Andrew L., Pflanz, Stefan, Bertelsen, Vibeke, Sitek, Jan C., Hol, Johanna, Haraldsen, Guttorm, Khnykin, Denis
Format: Article
Language:English
Subjects:
Adult
Animals
Biopsy, Needle
Blotting, Western
Dermatitis - genetics
Dermatitis - physiopathology
Disease Models, Animal
Epidermis - immunology
Epidermis - metabolism
Epidermis - pathology
Female
Gene Expression Regulation
Homeostasis - genetics
Homeostasis - physiology
Humans
Immunohistochemistry
Inflammation - genetics
Inflammation - physiopathology
Interleukin-33
Interleukins - genetics
Keratinocytes - immunology
Keratinocytes - metabolism
Mice
Mice, Inbred C57BL
Middle Aged
Real-Time Polymerase Chain Reaction - methods
Sampling Studies
Species Specificity
Sus scrofa
Swine
Tissue Culture Techniques
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Summary:IL-33 is a novel IL-1 family member with a putative role in inflammatory skin disorders and a complex biology. Therefore, recent conflicting data regarding its function in experimental models justify a close assessment of its tissue expression and regulation. Indeed, we report here that there are strong species differences in the expression and regulation of epidermal IL-33. In murine epidermis, IL-33 behaved similar to an alarmin, being constitutively expressed in keratinocyte nuclei and rapidly lost during acute inflammation. By contrast, human and porcine IL-33 were weakly expressed or absent in keratinocytes of noninflamed skin but induced during acute inflammation. To this end, we observed that expression of IL-33 in human keratinocytes but not murine keratinocytes was strongly induced by IFN-γ, and this upregulation completely depended on the presence of EGFR ligands. Accordingly, IFN-γ increased the expression of IL-33 in the basal layers of the epidermis in human ex vivo skin cultures only, despite good evidence of IFN-γ activity in cultures from both species. Together these findings demonstrate that a full understanding of IL-33 function in clinical settings must take species-specific differences into account.
ISSN:0022-202X
1523-1747
DOI:10.1038/jid.2015.85