However, the cells can survive if interleukin 1b activity is quickly suppressed by macrophages. The gene produces a signal protein and this prolonged activity causes the primed regenerative cells to die. The experiments show that several genes involved in inflammation – including one called interleukin 1b – were active over longer periods of time in the mutant fish compared with normal zebrafish. – who include several researchers involved in the 2015 study – used genetic approaches to investigate the role of inflammation in tissue regeneration in zebrafish. Many immune cells have roles in fighting infection and in responding to tissue damage.When a tissue is damaged, the area often becomes inflamed as white blood cells called macrophages flock to the damaged area to protect it from infection and remove damaged cells. This is because the cells that are primed to regenerate die instead, but it was not clear why this happens. In 2015, a team of researchers found that some mutant zebrafish that lack blood cells including immune cells are unable to regenerate lost tissues. Zebrafish are particularly good at this to the extent that they can replace damaged or lost body parts with exact replicas of the originals. Our study reveals that proper levels of Il1b signaling and tissue inflammation, which are tuned by macrophages, play a crucial role in tissue regeneration.Īnimals and other multicellular organisms all have at least some ability to regenerate lost or wounded tissues. We further show that Il1b plays an essential role in normal fin fold regeneration by regulating expression of regeneration-induced genes.
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. Here, we found that the apoptosis phenotype is induced by prolonged expression of interleukin 1 beta ( il1b). We have previously reported that myeloid-defective zebrafish mutants display apoptosis of regenerative cells during fin fold regeneration.
Cellular responses to injury are crucial for complete tissue regeneration, but their underlying processes remain incompletely elucidated.