The following is a summary of “Unraveling the neuroimmune interface in chronic pain—the association between cytokines in the cerebrospinal fluid and pain in patients with lumbar disk herniation or degenerative disk disease,” published in the July 2024 issue of Pain by Rosenstrom et al.

Recent studies highlight the complex role of nerve-immune system interactions in chronic pain, suggesting both pain-promoting and pain-reducing mechanisms.

Researchers conducted a retrospective study investigating the link between cytokine levels, symptom severity, and potential pathways for peripheral-to-CNS communication.

They performed quantitative sensory testing, administered pain and functional disability questionnaires, and collected both blood and CSF samples. Utilizing proximity extension assay (PEA), levels of 92 inflammatory proteins in CSF and serum were assessed across 160 patients and controls. Albumin quotients in CSF/serum were also determined for individuals with degenerative disk disease (DDD) and lumbar disk herniation (LDH).

The results showed neuroimmune activation in the CNS among both patient groups despite the absence of systemic inflammation. Significant correlations were observed between several cytokines and the albumin quotient, suggesting peripheral-to-CNS neuroimmune communication, despite at subclinical levels. Specifically, cytokines CCL11, CD5, IL8, and MMP-10 exhibited elevated levels in CSF, demonstrated positive correlations between CSF and serum, and displayed nonlinear associations with back pain intensity in the LDH group but not in the DDD group.

Investigators concluded that neuroimmune activation in the CNS of patients with DDD and LDH indicated disease-specific relationships between CSF cytokines and back pain intensity, suggesting potential targeted therapies for chronic pain management.

Source: journals.lww.com/pain/fulltext/2024/07000/unraveling_the_neuroimmune_interface_in_chronic.25.aspx