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Scientists identify an underlying cause of immune suppression following spinal cord injury

Researchers from Cincinnati Children’s Hospital Medical Center and The Ohio State University’s Wexner Medical Center have identified an underlying cause of immune suppression in people who have suffered a high level injury to their spinal cord. What’s more, they have been able to propose a possible treatment.

In their write up, published in a recent edition of Nature Neuroscience, the researchers explain that when the spinal cord is injured higher than thoracic level 5 (T5), this causes the circuitry of the autonomic nervous system to become highly plastic. This circuitry controls our unconscious bodily functions, such as respiration, heartbeat, digestion and function of the immune system.

Following such an injury, the body reacts to the damage by forming new nervous system circuitry, however this new circuitry is often abnormal.

By using mouse models of spinal cord injury, the researchers were able to see that this irregular circuitry causes responses that go beyond the segments in the thoracic spine. In uninjured mice, the circuitry would normally feed nerves to the secondary lymphoid tissues which assist in the generation of immune cells. As a result of these extended responses, the bladder and/or bowel activate abnormal spinal interneurons, resulting in the formation of an overlarge network of neural circuitry, which in turn, sets off an anti-inflammatory and immune suppressive reflex.

Infection Biggest Threat To Those With Spinal Injuries

One of the consequences of immune suppression is infection, which is the main cause of death for people who suffer a spinal cord injury. Injury to the spinal cord has also been seen to cause autonomic dysreflexia, which results in episodes of high blood pressure, and which is potentially fatal for both patients and mouse models.

Patients who have suffered a high-level injury to their spinal cord go on to develop ‘spinal cord injury-induced immune suppression syndrome’. The mouse models in this study exhibited atrophied spleens and signs of leukopenia, which both indicate a low white blood cell count. As this abnormal spinal cord circuitry is likely to cause chronic immune suppression, it makes it more likely that patients will experience complications from common infections, such as pneumonia.

Armed with this information, the researchers looked at ways to develop a treatment by testing chemogenetic agents, that can either activate or deactivate these cells, on their mouse models. This enabled them to silence the signalling transmissions from the newly forming interneurons, which resulted in the reversal of the immune suppressive reflex. Furthermore the atrophy in the mice models’ spleens was reversed and the white blood cell count went up.

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