Immune dysfunction after spinal cord injury – A review of autonomic and neuroendocrine mechanisms

Curr Opin Pharmacol, 2022 · DOI: 10.1016/j.coph.2022.102230 · Published: June 1, 2022

Simple Explanation

Spinal cord injury (SCI) can lead to a higher risk of infections, which can worsen neurological outcomes and increase mortality. This is because SCI disrupts the body's normal control of immune cells, leading to a condition called “SCI-Induced Immune Deficiency Syndrome” (SCI-IDS). The review focuses on how autonomic dysfunction and impaired neuroendocrine signaling contribute to SCI-IDS. Autonomic dysfunction refers to issues with the autonomic nervous system, which controls involuntary functions like heart rate and immune responses. The review also explores how SCI affects the development and movement of immune cell precursors in the bone marrow, suggesting that a “bone marrow failure syndrome” may be an early sign of SCI-IDS.

Study Duration

Not specified

Participants

Not specified

Evidence Level

Review

Key Findings

1
SCI disrupts neural and humoral control of immune cells, leading to SCI-IDS.
2
Autonomic dysfunction and impaired neuroendocrine signaling are key determinants of SCI-IDS.
3
SCI impairs the development and mobilization of immune cell precursors in bone marrow, potentially leading to a “bone marrow failure syndrome”.

Research Summary

Infections impair neurological outcome and increase mortality after spinal cord injury (SCI). Emerging data show that pathogens more easily infect individuals with SCI because SCI disrupts neural and humoral control of immune cells, culminating with the development of “SCI-Induced Immune Deficiency Syndrome” (SCI-IDS). New data indicate that SCI impairs the development and mobilization of immune cell precursors in bone marrow. Thus, this review will also explore how the post-injury acquisition of a “bone marrow failure syndrome” may be the earliest manifestation of SCI-IDS.

Practical Implications

Therapeutic Targets

Modulation of sympathetic-neuroendocrine signaling may prevent infections after SCI.

Early Intervention

Identifying and addressing bone marrow dysfunction early after SCI may mitigate immune deficiency.

Clinical Management

Understanding the mechanisms underlying SCI-IDS can lead to new interventions for treating or preventing infections after SCI.

Study Limitations

1
The review is based on existing literature and may be limited by the scope and quality of the included studies.
2
Further research is needed to fully understand the mechanisms underlying SCI-IDS and to develop effective interventions.
3
The review primarily focuses on autonomic and neuroendocrine mechanisms and may not fully address other factors that contribute to immune dysfunction after SCI.

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