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Reducing inflammation by removing a specific receptor in immune cells and brain support cells
Updated
Abstract
Systemic administration of lipopolysaccharide resulted in a significant reduction in plasma cytokine and chemokine induction in EP2-deficient mice.
- EP2 signaling in myeloid lineage cells is associated with proinflammatory responses to lipopolysaccharide.
- Conditional deletion of the EP2 receptor in myeloid cells reduced systemic inflammatory responses and transmission to the brain.
- Decreased hippocampal inflammatory gene expression and lower levels of IL-6 in the cerebral cortex were observed following EP2 deletion.
- Microglial and astrocytic inflammatory responses to the neurotoxin MPTP were significantly blunted with the absence of EP2 signaling.
- Ablation of microglial EP2 receptor led to downregulation of inflammatory pathways, suggesting a role in modulating inflammation.
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