Immunodeficiency potentiates the ability of decellularized muscle matrix to regenerate a volumetric muscle injury

Statement of Purpose: Volumetric muscle loss (VML) is the abrupt loss of skeletal muscle caused by blast, contusion, laceration, or tumor resection. VML injuries result in extensive scar formation and permanent loss of function. Current strategies to repair VML include autologous muscle transfers and physical therapy. Despite cosmetic improvements, muscle function is not regained. Animal models of VML are crucial in the development of novel strategies that recover muscle function. While athymic animals are often used to prevent immune rejection in cases where xenogeneic components are incorporated, reports indicate that T-cell deficiency in these animals suppresses inflammation, improving regeneration compared to immunocompetent controls. Furthermore, those T-cell deficient animals expressed a different composition of macrophage subtypes, which could contribute to altered regeneration (Grabowska et. al). We hypothesized that repair of a VML defect with an allogeneic decellularized muscle matrix (DMM) would lead to better structural and functional regeneration in athymic rats when compared to immunocompetent rats.