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
Affiliations
Tomoya Hasegawa
School of Bioscience and Biotechnology, Tokyo Institute of Technology, Midori-ku, Japan
Christopher J Hall
Department of Molecular Medicine and Pathology, School of Medical Sciences, University of Auckland, Auckland, New Zealand
Philip S Crosier
Department of Molecular Medicine and Pathology, School of Medical Sciences, University of Auckland, Auckland, New Zealand
Gembu Abe
Division of Molecular and Developmental Biology, National Institute of Genetics, and Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Japan
Division of Molecular and Developmental Biology, National Institute of Genetics, and Department of Genetics, SOKENDAI (The Graduate University for Advanced Studies), Mishima, Japan
Akira Kudo
School of Bioscience and Biotechnology, Tokyo Institute of Technology, Midori-ku, Japan
Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated. We have previously reported that myeloid-defective 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.
