Directing Neutrophil Fate via Sensory-Immune Interactions Accelerates Diabetic Bone Healing - PubMed
4 hours ago
- #neuroimmune interactions
- #diabetic bone healing
- #neutrophil polarization
- Diabetic bone defects are primarily caused by disrupted inflammation.
- Reduced sensory innervation in diabetic bone defects leads to impaired immune dynamics, including delayed neutrophil chemotaxis and abnormal neutrophil retention due to reduced macrophage efferocytosis.
- A scaffold with microspheres enabling burst IL-8 release and a matrix providing sustained nerve growth factor release was designed to address these issues.
- Timely neutrophil chemotaxis induced by IL-8 promotes bone healing via stem cell recruitment, further enhanced by sensory innervation through neutrophil N2 polarization.
- Macrophages form synapse-like structures with growing neurites, restoring efferocytosis driven by neuronal Galectin-3.
- Spatiotemporally regulating neuroimmune circuits improves mandibular bone regeneration in diabetic rats, highlighting therapeutic potential.