Cellular Communication Discovery Could Pave Way for Improved Neuropathic Pain Treatment

Scientists from King’s College London uncovered a new mechanism of cellular communication, between neurons and immune cells, in a discovery that could lead to new treatment targets for neuropathic pain.

Neuropathic pain is a type of chronic pain that is usually caused by an injury to nerves, but the pain persists long after the injury has healed. Neuropathic pain may occur after surgery or a car accident, or in some cases when a limb has been amputated. The cause of neuropathic pain is poorly understood, and current treatments are limited to opioids and antiepileptic drugs.

Using cellular and mouse models of neuropathic pain, the authors studied a cluster of neurons in the dorsal root ganglion (DRG), which are part of the sensory neurons that play an important role in communicating pain information to the brain.

They found that after nerve injury, pain neurons in this area released very small biological particles containing microRNA-21. These particles were then taken up by surrounding immune cells, ultimately leading to local inflammation and neuropathic pain.


When DRG pain neurons were blocked from releasing microRNA-21 in particles, this had an anti-inflammatory effect at a cellular level, which prevented neuropathic pain from occurring in mice.

These particles that contain agents that block microRNA-21 do not infiltrate the brain and lead to side effects.

In humans, a similar method could be applied to block pain neurons from releasing microRNA-21 in particles, which would prevent neuropathic pain from occurring. If successful, this would be the first drug to target neuropathic pain in specific areas without side effects, as opposed to the non-specific painkillers currently available.

The findings were published in Nature Communications.

Reference

Simeoli, R, Montague, K, Jones, H, et al. Exosomal cargo including microRNA regulates sensory neuron to macrophage communication after nerve trauma. Nature Co. 2017(8);1778. Published November 24, 2017. Accessed December 18, 2017. DOI: 10.1038/s41467-017-01841-5