One of the main signs of chronic pain is inflammation. Recently, in a research report published in the international journal of Neuron, scientists from the University of North Carolina School of Medicine and other institutions have discovered through research that anti-inflammatory cells called MRC1+ macrophages may be dysfunctional in a mouse model of neuropathic pain. Promoting these cells to return to their normal state may be expected to help treat body pain caused by nerve damage or nervous system dysfunction. Researchers have shown that stimulating the expression of an anti-inflammatory protein called CD163 may reduce signs of neuroinflammation in the spinal cord of mice with neuropathic pain.
Researchers have discovered that a type of anti-inflammatory macrophages may help relieve pain; but neuropathic pain seems to make these macrophages lose their function, but fortunately, they will not lose their function permanently. Because researchers can usually induce them to increase the body's anti-inflammatory activity to reduce the occurrence of neuropathic pain; the researchers speculate that by enhancing the activity of these macrophages may be expected to help develop new therapies for neuropathic pain.
According to US CDC data, about one-fifth of Americans suffer from chronic pain. The underlying cause is not clear to researchers. Patients often need to reduce body pain to live a normal life, although opioids can effectively treat pain in the short term, long-term use of the drug will produce serious side effects, such as addiction, respiratory depression, dizziness, nausea, and death from overdose.
Why powerful painkillers work well but produce significant side effects may be related to a basic biological fact, that is, pain involves a variety of cells, and current therapies lack the specificity of cell types. Therefore, any drug may be able to solve the undesirable changes in some cells and relieve the body's pain, but the drug may also increase the specific functions of other cells, leading to undesirable side effects.
In this study, the researchers used single-cell RNA sequencing technology to analyze thousands of cells at a time to observe which cells have changed during chronic pain in the body, and which methods of cells have changed. Knowing which cells can be targeted may be expected to help design specific therapies; theoretically, targeted therapies tend to produce fewer adverse side effects. To clarify which cells are changing and how they are changing, the researchers performed single-cell RNA sequencing on spinal cord cells in mice with neuropathic pain (a type of chronic pain caused by nerve damage). The spinal cord undergoes many long-term changes that induce neuropathic pain; researchers have discovered that a type of anti-inflammatory cells called MRC1+ macrophages may be malfunctioning.
Because long-term inflammation of the spinal cord is very common in animal models of neuropathic pain; as the identity of the new type of macrophages has been elucidated, researchers have also used a gene therapy to stimulate the anti-inflammatory protein called CD163 in MRC1+ macrophages. expression. Based on this method, one treatment can reduce the host's spinal cord inflammation, and can make this pain relief related behavior last up to a month. This study is very exciting for researchers because it implies a variety of different methods to enhance the function of these macrophages; and any kind of therapeutic method can provide a more precise strategy for the treatment of neuropathic pain.