Role of macrophages and activated microglia in neuropathic pain associated with chronic progressive spinal cord compression

Scientific Reports, 2019 · DOI: 10.1038/s41598-019-52234-1 · Published: October 15, 2019

Spinal Cord Injury Immunology Pain Management

Simple Explanation

This study investigates the causes of neuropathic pain (NeP) related to long-term spinal cord compression, focusing on the roles of microglia and macrophages. By using a mouse model with progressive spinal cord compression, the researchers analyzed how these immune cells contribute to pain development. The research found that as spinal cord compression worsened, more microglia were activated and macrophages infiltrated the spinal cord tissue. These cells, along with damage to the blood-spinal cord barrier (BSCB), appear to play a significant role in causing neuropathic pain. Additionally, the study identified specific molecular pathways (MAPK signaling) in these immune cells that are activated during spinal cord compression. This suggests that targeting these pathways could be a potential approach to alleviate neuropathic pain in patients with similar conditions.

Study Duration

12, 18, and 24 weeks

Participants

Spinal hyperostotic ttw/ttw mice (12-week-old, n = 37, 18-week-old, n = 37, 24-week-old, n = 34), ICR mice (n = 9)

Evidence Level

Not specified

Key Findings

1
The severity of spinal cord compression correlated with the proportion of activated microglia and hematogenous macrophages in the spinal cord.
2
Spinal cord compression was associated with overexpression of mitogen-activated protein kinases (MAPKs) in infiltrating macrophages.
3
Reversible blood-spinal cord barrier (BSCB) disruption was observed in the dorsal horns, suggesting a mechanism for immune cell infiltration.

Research Summary

This study investigated the roles of activated microglia and infiltrating macrophages in neuropathic pain (NeP) associated with chronic progressive spinal cord compression using a mouse model. The main findings indicated that the severity of spinal cord compression correlated with increased accumulation of activated microglia and macrophages, as well as disruption of the blood-spinal cord barrier (BSCB). The study also found that mitogen-activated protein kinases (MAPKs) were overexpressed in infiltrating macrophages, suggesting a potential therapeutic target for alleviating chronic neuropathic pain associated with compressive myelopathy.

Practical Implications

Therapeutic Targets

Targeting microglial activation and macrophage migration could provide new avenues for neuropathic pain treatment.

Diagnostic Markers

Identifying markers of BSCB disruption can aid in early diagnosis and intervention for compressive myelopathy.

Drug Delivery Strategies

Understanding BSCB permeability changes can help optimize drug delivery to the spinal cord.

Study Limitations

1
The study was conducted in a specific mouse model (ttw/ttw), which may not fully replicate the complexity of human compressive myelopathy.
2
The mechanisms of BSCB dysfunction and neuroinflammatory responses were only partially elucidated.
3
The long-term effects of microglial activation and macrophage infiltration were not fully explored.

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