New research from University of Kentucky reportedly may shed some light on the opportunities to modulate the responses from macrophages after spinal cord injury.

This response, according to a press release from University of Kentucky, may potentially reduce, or even reverse, damage and the resulting side effects after the injury.

Macrophages are defined in the release as cellular sentinels in the body that are assigned to identify “attacks” from viruses, bacteria, or fungi, and sound the alarm when they are present.

However, the release continues, they are a double-edged sword in spinal cord injury, as they provide both neural repair-promoting properties and pathological functions that destroy neuronal tissue.

In a recent Featured Article in the Journal of Neuroscience, John Gensel PhD, assistant professor of physiology in the Spinal Cord and Brain Injury Research Center at the University of Kentucky, along with Phillip Popovich, PhD, professor in the department of neuroscience and director of the Center for Brain and Spinal Cord Repair (CBSCR) at The Ohio State University, explored the mechanisms governing the positive and negative processes that occur in macrophages following spinal cord injury, the release explains.

“On the cellular level, the body’s response to spinal cord injury is similar to the immune response to attacks by bacteria or viruses,” Gensel says in the release.

“The functions that macrophages adopt in response to these stimuli were the focus of our study,” he continues.

Gensel and Popovich looked at more than 50 animals with spinal cord injury to try to identify which macrophage receptors promoted neuronal repair and which directed the destructive process, per the release.

“We found that activating bacterial receptors boosted the macrophage response and limited damage to the spinal cord following injury, while activating fungal receptors actually contributed to pathology,” Gensel states in the release.

The release states that while this study reportedly oversimplifies the complex process by which macrophages promote repair and destruction of neuronal tissues, it nonetheless sheds light on opportunities to modulate macrophage responses after spinal cord injury, potentially reducing—or even reversing—damage and the resulting side effects.

“The implications are exciting: we now can look for treatments targeted to the receptors that jump-start the macrophage’s restorative effects without activating the receptors that modulate the destructive processes in that same cell,” Gensel and Popovich write, per the release.

[Source(s): University of Kentucky, Science Daily]