Researchers from Washington University School of Medicine, St. Louis, report that receptors on immune cells may be a more effective therapeutic target than nerve cells for the delivery of analgesia for chronic pain. The discovery arose from an investigation into the mechanism of action of a nonopioid drug called EMA401 that has been tested in mouse models and found effective for the treatment of nerve pain following shingles infection. Principal investigator D.P. Mohapatra, PhD, associate professor of anesthesiology, commented, “Generally, scientists have the understanding that targets for treating pain must be within the nervous system. It turns out that the target here is not on nerve cells, but on immune cells called macrophages.” The findings were reported last week in Journal of Neuroscience.
The investigational drug affects the action of angiotensin, a hormone that causes blood vessels to constrict. Co-investigator Andrew Shepherd, PhD, said, “We found that the receptor the drug affected wasn’t on the nerve cells; it was on macrophages, the immune cells. When we added macrophages to the dish alongside the nerve cells, the angiotensin could ‘talk’ to the macrophages, and then the macrophages ‘talked’ to the nerve cells, which then transmitted pain signals.” Dr. Mohapatra noted that broadening the range of targets to include receptors on immune cells may open the way to new analgesics that have fewer side effects. “The beauty of this drug is that, unlike an opioid, it doesn’t cross the blood-brain barrier, so right away you eliminate a number of potentially harmful side effects, including addiction and the potential for abuse,” he said. “And by widening the scope of potential targets to macrophages, it may be possible to develop more effective therapies for chronic, neuropathic pain.”
Read about the research findings.
The journal abstract may be read here.
Posted on July 12, 2018