Spine Injury Patients At High Risk for Immunodeficiency – Neuroscience News

Summary: Patients recovering from severe spinal cord injuries are more prone to immune deficiencies.

Such a deficiency, known as spinal cord injury-induced immune deficiency syndrome, can expose patients to life-threatening infections. This immune deficiency is closely related to the severity of spinal cord injury and can further impair the immune system.

This research could pave the way for better patient care by identifying severely immunosuppressed patients and designing new treatments to curb susceptibility to infection.

Key Facts:

  1. Patients recovering from severe spinal cord injuries may develop immune deficiencies, increasing the risk of life-threatening infections.
  2. The severity of spinal cord injury is directly correlated with the degree of immune deficiency, leading to further weakening of the immune system.
  3. These findings may contribute to improving spinal cord injury care by identifying patients with overt immune suppression and establishing treatments to reduce susceptibility to infection.

Source: Ohio State University

Patients recovering from severe spinal cord injuries can develop immune deficiencies that put them at risk for life-threatening infections, according to a new study by researchers at The Ohio State University Wexner Medical Center and collaborators in Germany, Switzerland and Canada.

This study is reported in the journal Brain.

The deficiency, called spinal cord injury-induced immune deficiency syndrome, was originally identified in an experimental model. The findings of this study suggest that immune deficiency is also a possibility in these patients.

It shows an outline of a person with the spinal cord highlighted.
In addition, this indicator of immune deficiency is associated with the severity of spinal cord injury. Credits: Neuroscience News

The study of 111 patients found that monocytes, white blood cells needed to fight bacterial infections, were deactivated shortly after spinal cord injury. He also found decreased levels of antibodies and immunoglobulins in the blood, which are part of the body’s “learned” or adaptive immunity.

In addition, this indicator of immune deficiency is associated with the severity of spinal cord injury. That is, they are “neurogenic,” and they add to the other consequences of a spinal cord injury that also weakens the immune system such as being bedridden, receiving anesthesia or undergoing surgery.

The researchers stated that the findings could lead to improvements in the treatment of spinal cord injuries through the stages of a patient’s susceptibility to infection. This will help to identify immunocompromised patients and the development of new treatments to reduce susceptibility to infection early on.

“Infection and subsequent sepsis are the leading causes of death after spinal cord injury,” said correspondent author Jan Schwab, MD, Ph.D., William E. Hunt & Charlotte M. Curtis Chair and a professor of neurology and neuroscience at Ohio State College of medicine.

“Our study provides evidence of an immune deficiency that predisposes spinal cord injury patients to infection,” said Schwab, who is also medical director of the Belford Center for Spinal Cord Injury and Scholar of the Chronic Brain Injury Initiative at Ohio State. .

Findings indicated that the risk of developing an immunodeficiency syndrome was greatest in patients with complete high-grade injuries (fourth thoracic vertebra or higher), compared with patients with incomplete low-grade injuries (fifth thoracic vertebra or lower), and compared with a reference group of patients with spinal fractures that do not involve the spinal cord.

Total spinal cord injury results in total loss of motor and sensory function below the level of injury; with an incomplete spinal cord injury, some function remains below the level of the injury.

“Patients with total injury and consequent loss of central nervous system control over immune system function show the highest likelihood of immune deficiency,” said Schwab.

The study included 111 patients enrolled in a prospective international multi-center cohort study known as the SCIentinel study. To detect the presence and severity of immune suppression in patients’ blood, the researchers measured the levels of a cell surface molecule called mHLA-DR in monocytes.

Low mHLA-DR molecule counts are a recognized and measurable marker of monocyte deactivation and have been shown to predict susceptibility to sepsis in critically ill patients.

Key findings include:

  • Patients with high total injury have the highest burden of pulmonary and urinary tract infections, including recurrent infections;
  • Patients with infection had mHLA-DR levels below the reference value for “immune suppression” within two weeks of injury;
  • Patients with early infection (in the first or second week) had very low mHLA-DR values ​​in the “borderline immunoparalysis” range already 15 hours after injury;
  • Decreased levels of immunoglobulins (IgG and IgA) after spinal cord injury suggest suppressed humoral immunity as well. It is most prominent in patients with severe injuries;
  • Cellular and non-cellular immune defense mechanisms are compromised in spinal cord injury patients and are associated with early infection.

“Overall, our study shows that neurogenic immune deficiency syndrome drives infection susceptibility in spinal cord injury patients, and that is dependent on severity,” said Schwab.

About this spinal cord injury and neurology research news

Author: Jan Schwab
Source: Ohio State University
Contact: Jan Schwab – Ohio State University
Picture: The image is credited to Neuroscience News

Original Research: Open access.
“Spine injury-induced immune deficiency syndrome: results of the SCIentinel study” by Jan Schwab et al. Brain


Spinal cord injury-induced immune deficiency syndrome: results of the SCIentinel study

Infection is common after spinal cord injury (SCI), is a major cause of death and is a confounder in rehabilitation associated with impaired recovery. We hypothesized that SCI causes acquired lesion-dependent (neurogenic) immune suppression as an underlying mechanism to facilitate infection.

International prospective multicenter cohort study (SCIentinel; protocol registration DRKS00000122; N = 111 patients) was designed to differentiate neurogenic from general trauma-related effects on the immune system. Therefore, SCI patient groups differ based on neurological level, i.e. high SCI [thoracic (Th)4 or higher]; Low SCI (Th5 or lower) and severity (complete SCI; incomplete SCI), compared to a reference group of spine fracture (VF) patients without SCI.

The primary outcome was quantitative monocytic Human Leukocyte Antigen-DR (mHLA-DR, synonym MHC II) expression, a validated marker for immune suppression in critically ill patients associated with infection susceptibility. mHLA-DR was assessed from Day 1 to 10 weeks after injury using standard flow cytometry procedures.

Secondary outcomes were leukocyte subpopulation counts, serum immunoglobulin levels, and clinically determined infection. A linear mixed model with multiple imputations was applied to evaluate the logarithmically transformed differences in parameter groups.

Quantitative mean mHLA-DR [ln (antibodies/cell)] the level at the primary endpoint 84 hours after injury showed an immune-suppressive state below the normative value of 9.62 in all groups, which further differed in dimension with the neurological grade: high SCI [8.95 (98.3% confidence interval, CI: 8.63; 9.26), n = 41]low SI [9.05 (98.3% CI: 8.73; 9.36), n = 29]and VF without SCI [9.25 (98.3% CI: 8.97; 9.53), n = 41, P = 0.003].

Post hoc analysis accounting for SCI severity revealed the strongest decrease in mHLA-DR [8.79 (95% CI: 8.50; 9.08)] in the complete and high SCI groups, further indicating delayed recovery of mHLA-DR [9.08 (95% CI: 8.82; 9.38)] and showed a difference from control VF −0.43 (95% CI: −0.66; −0.20) at 14 days.

Complete, high SCI patients also revealed persistently lower serum immunoglobulin G [−0.27 (95% CI: −0.45; −0.10)] and immunoglobulin A [−0.25 (95% CI: −0.49; −0.01)] level [ln (g/l × 1000)] up to 10 weeks after injury. Low mHLA-DR levels within the immunoparalytic limit range (below 9.21) were positively associated with earlier incidence and onset of infection, which is consistent with results from studies of stroke or major surgery.

Spinal cord injury patients may develop secondary neurogenic immune deficiency syndrome characterized by reduced expression of mHLA-DR and relative hypogammaglobulinemia (combined cellular and humoral immune deficiency). mHLA-DR expression provides a basis for stratifying the risk of infection in patients with SCI.

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