Transient inflammatory response mediated by interleukin-1β is required for proper regeneration in zebrafish fin fold

Tomoya Hasegawa, Christopher J. Hall, Philip S. Crosier, Gembu Abe, Koichi Kawakami, Akira Kudo, Atsushi Kawakami

    Research output: Contribution to journalArticlepeer-review

    53 Citations (Scopus)

    Abstract

    Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloiddefective zebrafish mutants display apoptosis of regenerative cells during fin fold regeneration. Here, we found that the apoptosis phenotype is induced by prolonged expression of interleukin 1 beta (il1b). Myeloid cells are considered to be the principal source of Il1b, but we show that epithelial cells express il1b in response to tissue injury and initiate the inflammatory response, and that its resolution by macrophages is necessary for survival of regenerative cells. We further show that Il1b plays an essential role in normal fin fold regeneration by regulating expression of regeneration-induced genes. Our study reveals that proper levels of Il1b signaling and tissue inflammation, which are tuned by macrophages, play a crucial role in tissue regeneration.

    Original languageEnglish
    Article numbere22716
    JournaleLife
    Volume6
    DOIs
    Publication statusPublished - 2017 Feb 23

    ASJC Scopus subject areas

    • Neuroscience(all)
    • Immunology and Microbiology(all)
    • Biochemistry, Genetics and Molecular Biology(all)

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