Thursday, September 22nd
4:30pm-6:00pm EDT


Topical Workshop | Virtual Program




718 A

Chemokines and Lipid Mediators Modulate the Resolution of Inflammatory Arthritis Pain

Pain is a persistent feature of rheumatoid arthritis and sensory neuron-macrophage crosstalk in the dorsal root ganglia (DRG) plays a fundamental role for the establishment and maintenance of RA pain. In the K/BxN serum-transfer model of inflammatory arthritis, we observed that hind paw hypersensitivity (allodynia) persists after joint swelling is resolved. This phase is associated with the presence of CX3CR1-macrophages into the DRG and an imbalance in lipid mediators. Specifically, we found no difference in prostaglandins PGD2 and PGE2 levels, but a significant decrease in the pro-resolving lipid mediator Maresin1 (MaR1). The administration of MaR1 reversed K/BxN serum-transfer allodynia and this effect was maintained for 2 weeks after the last administration. Analysis of leukocytes in the DRG revealed that MaR1 treatment was associated with lower numbers of pro-inflammatory macrophages. Altogether these observations suggest that MaR1 treatment attenuates allodynia in inflammatory arthritis and reduces macrophage infiltration. I will discuss the proposal that inflammatory pain and pain that persists when inflammation is resolving may be reliant on partially distinct mechanisms, both involving monocytes/macrophages and biosynthesis of lipid mediators. CX3CR1-mediated mechanisms and lipid mediator biosynthesis facilitate such crosstalk and may constitute novel targets for the resolution of RA pain.

This Session is Available in Virtual Congress


Professor Marzia Malcangio

Professor of Neuropharmacology
King's College London