Immune–tracheal intercellular signalling coordinates the muscle injury response in Drosophila

Effective tissue adaptation to damage requires precise coordination among diverse cell types. In skeletal muscle, injury-responsive cells play a pivotal role in repair, yet the molecular and cellular mechanisms governing their coordinated activity remain incompletely understood. Here, we identify adultDrosophilaimmune cells-hemocytes-as key mediators of the muscle injury response. Following damage, hemocytes are rapidly recruited to affected fibers, where they perform dual functions. First, they promote tracheal (respiratory cell) branching by depositing the FGF ligand Branchless (Bnl) along damaged muscle, which activates its receptor, FGFR/Breathless (Btl), on tracheal cells, stimulating their outgrowth toward the injury and supporting oxygen delivery. Second, hemocytes contribute to structural stabilization by supplying key extracellular matrix (ECM) components, including SPARC and Collagen IV, to the damaged fiber. Together, these findings uncover a coordinated injury response in which immune cells act as central mediators of metabolic and structural adaptation in response to damage.