Inflammation rewires the enteric nervous system through neurogenic monocyte recruitment - PubMed
5 hours ago
- #neuroimmune axis
- #inflammation
- #enteric nervous system
- Inflammatory bowel disease (IBD) disrupts gastrointestinal (GI) functions, including bowel motility, with persistent motility disorders even during remission.
- Postinflammatory GI motility dysfunction results from structural remodeling of the enteric nervous system (ENS), involving neuronal loss and neurogenesis.
- During mucosal inflammation, enteric neurons upregulate CCL2, recruiting monocytes into the myenteric plexus, leading to excessive ENS remodeling.
- Monocyte-derived macrophages infiltrate the myenteric ganglia, contributing to postinflammatory motility dysfunction.
- A hypoxia-induced stress response in enteric neurons, mediated by HIF1α, counterbalances this neuroimmune axis.
- Enhancing the neuron-intrinsic hypoxia pathway can limit ENS remodeling and preserve motility.
- The study proposes a therapeutic strategy to maintain ENS integrity and function during inflammation.