Epidermal RelA Specifically Restricts Contact Allergen-Induced Inflammation and Apoptosis in Skin (2014)

publicationsKumari S, Herzberg B, Pofahl R, Krieg T, Haase I; J Invest Dermatol. 2014 Apr 16. doi: 10.1038/jid.2014.193. [Epub ahead of print]

Abstract

 

Strong inhibition of NF-κB signaling in the epidermis results in spontaneous skin inflammation in mice and men. As there is evidence for linkage between polymorphisms within the NF-κB signaling pathway and human inflammatory skin phenotypes, we asked whether partial functional inhibition of NF-κB signaling in epidermal keratinocytes can modulate clinically relevant skin inflammation. We therefore mutated rela specifically in the epidermis of mice (RelAE-MUT mice). These mice show no inflammatory phenotype. Induction of contact allergy, but not croton oil-induced irritant dermatitis, resulted in stronger ear swelling and increased epidermal thickness in RelAE-MUT mice. Both contact allergen and croton oil treatment led to increased expression of calgranulins A and B (S100A8/ A9) in RelAE-MUT mice. Epidermal hyperproliferation in RelAE-MUT mice was non-cell autonomous as cultured primary epidermal keratinocytes from RelAE-MUT mice showed reduced proliferation compared with controls. These results demonstrate that epidermal RelA specifically regulates delayed-type hypersensitivity-induced skin inflammation. In addition, we describe here an essential but nonspecific function of RelA in the protection of epidermal keratinocytes from apoptosis. Our study identifies functions of NF-κB signaling in the epidermis and corroborates a specific role of epidermal keratinocytes in the regulation of skin inflammation.Journal of Investigative Dermatology advance online publication, 8 May 2014; doi:10.1038/jid.2014.193.

 

 

Pubmed

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