My name is Pall Karlsson, and I am a senior researcher at Aarhus University.
Immune cells are potential targets for effective therapy for painful diabetic polyneuropathy
It is difficult to treat neuropathic pain.
Pain research has largely focused on nerve cells that transmit pain signals.
Our new study, published in August in Journal of Neuroscience shows that targeting receptors
on immune cells may be more effective for chronic pain.
The background for our study was to understand how an investigational drug controls nerve pain.
The drug was believed to interact with nerve cells carrying pain signals.
But surprisingly, our study showed that the drug doesn't hit nerve cells, but macrophages.
We showed this in a 3-step process.
Step 1 – Cell culture.
The drug inhibits angiotensin II type 2 receptors.
When adding angiotensin hormone to mouse nerve cells, nothing happens – because there is
no angiotensin type 2 receptor on the sensory neurons and therefore there is no pain signal.
When we added macrophages to the culture, they talked to the nerve cells, which first
then started to transmit pain signals.
Step 2 – animal models.
When we injected angiotensin into the mice, they felt pain.
However, after reducing the number of macrophages in the mice, the mice didn't feel pain in
response to the injection.
After a few days, when the macrophages repopulated, the pain returned.
Step 3 – human patients.
Lastly, we also showed that patients with painful diabetic polyneuropathy also show
increased macrophage infiltration in the skin, alongside degenerated nerve fibers that transmit pain signals.
We have therefore widened the scope of potential targets to macrophages, thereby opening a
new possibility for more effective therapies, for example for painful diabetic polyneuropathy.
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