According to a new study by researchers at The Ohio State University Wexner Medical Center and collaborators in Germany, Switzerland, and Canada, patients recuperating from a serious spinal cord injury can develop an immune deficit, putting them at risk of contracting life-threatening infections. The findings were published in the journal Brain.
The deficiency, known as spinal cord damage-induced immune deficiency syndrome, was first discovered in animal models. According to the findings of this investigation, immunological insufficiency is also likely in patients. Monocytes, white blood cells necessary to fight bacterial infections, were shown to be deactivated quickly after spinal cord damage in 111 patients. It also discovered decreases in blood levels of antibody and immunoglobulins, both of which are components of the body’s “learned” or adaptive immunity.
Furthermore, these immune-deficiency indications were linked to the degree of spinal-cord injury. That is, they were “neurogenic,” and they were added to the other effects of spinal-cord damage that decrease the immune system, such as being bedridden, having anesthesia, or undergoing surgery.
The findings, according to the researchers, could lead to improvements in spinal-cord injury care by assessing a patient’s susceptibility to infection. This would aid in identifying people with compromised immune systems and in the development of new medicines to minimize infection susceptibility early on.
“Infections and subsequent sepsis are the main cause of death after spinal-cord injury,” said co-corresponding author Jan Schwab, MD, Ph.D., the William E. Hunt & Charlotte M. Curtis Chair and a professor of neurology and neurosciences at the Ohio State College of Medicine.
“Our study provides evidence for an immune deficiency that sets spinal-cord injured patients up to develop infections,” said Schwab, who is also medical director of the Belford Center for Spinal Cord Injury and a Scholar of the Chronic Brain Injury Initiative at Ohio State.
The findings revealed that the risk of developing an immune deficiency syndrome was highest in patients with complete, higher-level injury (fourth thoracic vertebra or above), compared to patients with incomplete, lower-level injury (fifth thoracic vertebra or lower), and compared to a control group of patients with vertebral fracture that did not involve the spinal cord.
With a complete spinal-cord injuries, all motor and sensory function below the level of injury is lost; with an incomplete spinal-cord injury, some function persists below the level of injury.
“Those patients with complete injuries and consequent loss of central nervous system control over immune system function displayed the highest odds for an immune deficiency,” Schwab said.
The study included 111 patients who were included in the SCIentinel project, an international prospective multi-center cohort study. The researchers assessed the amounts of a cell-surface protein called mHLA-DR on monocytes to detect the existence and degree of immune suppression in patients’ blood.
A low number of mHLA-DR molecules is a well-known and quantitative measure for monocyte deactivation, and it has been proven to predict sepsis susceptibility in critically ill patients.
Among the key findings are:
- Patients with severe total damage experienced the most lung and urinary tract infections, including recurrent infections.
- Within two weeks of injury, patients with infections had mHLA-DR levels below the “immune suppression” reference range.
Patients with early infection (in the first or second week) showed mHLA-DR levels in the “borderline immunoparalysis” range 15 hours after injury. - A decrease in immunoglobulin (IgG and IgA) levels following spinal cord damage suggested a reduction in humoral immunity as well. This was especially noticeable in severely wounded individuals
- Both cellular and non-cellular immune defense mechanisms were reduced in injured patients, which was associated with early infection initiation.
“Overall, our study suggests that a neurogenic immune deficiency syndrome drives infection susceptibility in spinal-cord injury patients, and it does so in a severity-dependent manner,” Schwab said.
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