The Journal of Clinical Investigation · 9 authors, 7 centres
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This preclinical mouse study used a femoral fracture model to show that fracture healing is improved by a pathway where callus γδ T cells increase gut permeability, leading to the expansion and migration of intestinal Th17 cells (induced by segmented filamentous bacteria) to the fracture site.
The study employed a stabilized mouse femoral fracture model to investigate the role of specific T cell populations and the gut microbiome in fracture repair. Fractures were shown to expand γδ T cells in the callus, which promoted systemic inflammation and increased gut permeability. In mice harboring the Th17 cell-inducing bacterium segmented filamentous bacteria (SFB), this was followed by the expansion and egress of intestinal Th17 cells, mediated by the S1P receptor 1, and their homing to the callus via CCL20. This pathway improved fracture repair, as evidenced by higher bone volume and mechanical strength at specific time points. Impairment of fracture healing was demonstrated through deletion of γδ T cells, microbiome depletion via antibiotics, blockade of Th17 cell egress, or neutralization of Th17 cell influx into the callus. The findings highlight a preclinical mechanism linking local immune response, gut microbiota, and T cell trafficking to bone regeneration.
