Macrophage migration inhibitory factor facilitates production of CCL5 in astrocytes following rat spinal cord injury

Journal of Neuroinflammation, 2018 · DOI: https://doi.org/10.1186/s12974-018-1297-z · Published: September 6, 2018

Simple Explanation

Following spinal cord injury, astrocytes, a type of brain cell, can release chemicals that cause inflammation. Macrophage migration inhibitory factor (MIF) is a protein that also contributes to this inflammation. This study investigates whether MIF influences astrocytes to release a specific inflammatory chemical called CCL5. The study found that MIF does indeed cause astrocytes to release CCL5. This release is facilitated by MIF interacting with a receptor called CD74 on the astrocyte surface. Blocking this interaction reduces the amount of CCL5 released. The released CCL5 then attracts immune cells to the site of injury, exacerbating inflammation. This suggests that targeting MIF or its interaction with CD74 could be a potential therapeutic strategy to reduce inflammation and improve recovery after spinal cord injury.

Study Duration

Not specified

Participants

Adult male Sprague–Dawley (SD) rats

Evidence Level

Not specified

Key Findings

1
CCL5 protein levels were increased in astrocytes of rat injured spinal cord, in parallel with the expression of MIF.
2
MIF facilitates CCL5 production of astrocytes through interaction with CD74 membrane receptor.
3
MIF induces CCL5 production of astrocytes through JNK signaling.

Research Summary

This study investigated the role of macrophage migration inhibitory factor (MIF) in the production of chemokine (C-C motif) ligand 5 (CCL5) in astrocytes following rat spinal cord injury. The results showed that MIF facilitates CCL5 production in astrocytes through interaction with the CD74 membrane receptor and activation of c-Jun N-terminal kinase (JNK). CCL5 released by astrocytes promoted the migration of M2 macrophages, contributing to excessive inflammation and affecting motor functional recovery after spinal cord injury.

Practical Implications

Therapeutic Target Identification

MIF and its receptor CD74 could be potential therapeutic targets for reducing inflammation after spinal cord injury.

Inflammation Management

Modulating CCL5 production in astrocytes may help manage the inflammatory response following SCI.

Cell-Specific Treatment

Targeting the JNK signaling pathway in astrocytes could be a cell-specific approach to reduce CCL5 production and inflammation.

Study Limitations

1
The study was conducted on a rat model, and the results may not be directly translatable to humans.
2
The study focused primarily on CCL5 and did not investigate the role of other chemokines and cytokines involved in spinal cord injury.
3
The precise mechanisms by which CCL5 facilitates M2 macrophage migration require further investigation.

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