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Ex vivo culture of mouse skin activates an interleukin 1 alpha‐dependent inflammatory response
Author(s) -
Zhou HongMing,
Slominski Radomir M.,
Seymour Leroy J.,
Bell Maria C.,
Dave Priya,
Atumonye Joseph,
Wright William,
Dawes Avery,
Griesenauer Brad,
Paczesny Sophie,
Kaplan Mark H.,
Spandau Dan F,
Turner Matthew J.
Publication year - 2020
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.14044
Subject(s) - ex vivo , cxcl1 , chemokine , immunology , interleukin , biology , interleukin 3 , in vivo , proinflammatory cytokine , cytokine , microbiology and biotechnology , inflammation , immune system , t cell , antigen presenting cell
Abstract Ex vivo culture of mouse and human skin causes an inflammatory response characterized by production of multiple cytokines. We used ex vivo culture of mouse tail skin specimens to investigate mechanisms of this skin culture‐induced inflammatory response. Multiplex assays revealed production of interleukin 1 alpha (IL‐1α), interleukin 1 beta (IL‐1β), interleukin 6 (IL‐6), chemokine C‐X‐C motif ligand 1 (CXCL1), granulocyte colony‐stimulating factor (G‐CSF) and granulocyte‐macrophage colony‐stimulating factor (GM‐CSF) during skin culture, and quantitative PCR revealed transcripts for these proteins were also increased. Ex vivo cultures of skin from myeloid differentiation primary response 88 deficient mice ( Myd88 −/− ) demonstrated significantly reduced expression of transcripts for the aforementioned cytokines. The same result was observed with skin from interleukin 1 receptor type 1 deficient mice ( Il1r1 −/− ). These data suggested the IL‐1R1/MyD88 axis is required for the skin culture‐induced inflammatory response and led us to investigate the role of IL‐1α and IL‐1β (the ligands for IL‐1R1) in this process. Addition of IL‐1α neutralizing antibody to skin cultures significantly reduced expression of Cxcl1 , Il6 and Csf3 . IL‐1β neutralization did not reduce levels of these transcripts. These studies suggest that IL‐1α promotes the skin the culture‐induced inflammatory response.