Immune dysfunction and chronic inflammation following spinal cord injury

Abstract

Study design: Review article. Objectives: The objective of this study is to provide an overview of the many factors that contribute to the chronic inflammatory state typically observed following spinal cord injury (SCI). Methods: Literature review. Results: Not applicable. Conclusion: SCI is typically characterized by a low-grade inflammatory state due to a number of factors. As bidirectional communication exists between the nervous, endocrine and immune systems, damage to the spinal cord may translate into both endocrinal and immune impairment. Damage to the autonomic nervous system may induce immune dysfunction directly, through the loss of neural innervation of lymphoid organs, or indirectly by inducing endocrinal impairment. In addition, damage to the somatic nervous system and the corresponding loss of motor and sensory function increases the likelihood of developing a number of secondary health complications and metabolic disorders associated with a state of inflammation. Lastly, numerous related disorders associated with a state of chronic inflammation have been found to be at a substantially higher prevalence following SCI. Together, such factors help explain the chronic inflammatory state and immune impairment typically observed following SCI. An understanding of the interactions between systems, both in health and disease, and the many causes of chronic inflammation may aid in the effective future treatment of immune dysfunction and related disorders following SCI.

miR-136-5p Regulates the Inflammatory Response by Targeting the IKKβ/NF-κB/A20 Pathway After Spinal Cord Injury

“…Some scholars have confirmed the role of an immunoinflammatory response in SCI and its repair process through animal experiments [26,27]. In addition, some studies have proposed intervening in the immunoinflammatory response to promote interventions after SCI [28].…”

Activation and Regulation of NLRP3 Inflammasome by Intrathecal Application of SDF-1a in a Spinal Cord Injury Model

“…The migrating and invading macrophages represent an integral and specific feature, since the sequential activation and composition of pro-inflammatory M1 macrophages and alternatively stimulated M2a, M2b, and M2c macrophage subtypes occur during wound healing and facilitate the transition between inflammation, proliferation, and tissue remodeling [22]. Generally, SCI induces a low-grade inflammatory state which is characterized by bidirectional communication between the nervous, endocrine, and immune system [30]. Microglia accumulation peaks in the lesion on 3-7 days post SCI throughout the gray and white matter at the epicenter of the injury site [31].…”

Association between Cervical Spondylosis and Migraine: A Nationwide Retrospective Cohort Study

“…The findings indicated that inflammatory cascade might serve the potential molecular mechanisms underlying the pathogenesis of cervical spondylotic myelopathy, leading to migraine attack. Second, increased inflammation in the cervical spine due to the proinflammatory molecules release into the bloodstream upregulated the hypothalamicpituitary-adrenal axis, causing the hypothalamic dysfunction 32 . This process intensified the sensitivity to pain in the brain, which may lead to predisposition to migraine.…”