Laboratory for Optical and Computational Instrumentation, University of Wisconsin-Madison, Madison, United States
Julie Rindy
Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, United States
William Vincent
Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, United States; First Year Experience, Northern Arizona University, Flagstaff, United States
Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, United States; Department of Pediatrics, University of Wisconsin-Madison, Madison, United States
Wound repair is controlled temporally and spatially to restore tissue homeostasis. Previously we reported that thermal damage of the larval zebrafish fin disrupts collagen organization and wound healing compared to tail transection (LeBert et al., 2018). Here we characterize different injury models in larval zebrafish to dissect temporal and spatial dynamics of repair in complex damage. We found that each damage model triggers distinct inflammatory and tissue responses, with Stat3 and TGFβ playing key roles in the regulation of mesenchymal cells during simple repair. While thermal injury disrupts collagen fibers initially, healing is recovered as inflammation resolves, and mesenchymal cells and collagen fibers align. By contrast, infected wounds lead to persistent inflammation and loss of mesenchymal cells, resulting in minimal tissue repair. These wound models have broad physiological relevance, thereby providing a valuable advance in our toolkit to probe the dynamics of inflammation and wound repair in complex tissue damage.
