Related Experiment Video
Updated: May 31, 2025

09:38
Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
Published on: September 12, 2016
12.2K
IL-18 Blockage Reduces Neuroinflammation and Promotes Functional Recovery in a Mouse Model of Spinal Cord Injury
Easmin Begum1, Md Rashel Mahmod1, Md Mahbobur Rahman1
1Department of Anatomy and Developmental Biology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.
Biomolecules
|January 25, 2025
Summary
Targeting Interleukin-18 (IL-18) with a neutralizing antibody significantly improved motor function after spinal cord injury (SCI) in mice. This treatment reduced inflammation and neuronal death, promoting a neuroprotective environment.
Area of Science:
- Neuroscience
- Immunology
- Regenerative Medicine
Background:
- Spinal cord injury (SCI) prognosis is heavily influenced by secondary injury processes, particularly neuroinflammation.
- Interleukin-18 (IL-18) is a key mediator in the inflammatory response following SCI.
- Previous research developed an anti-IL-18 antibody to neutralize active IL-18.
Purpose of the Study:
- To evaluate the functional effects of an anti-IL-18 antibody in a mouse model of SCI.
- To investigate the impact of IL-18 inhibition on neuroinflammation and neuronal survival post-SCI.
Main Methods:
- Utilized a C57BL/6J mouse model of SCI.
- Administered 150 μg of anti-IL-18 antibody intraperitoneally post-injury.
- Assessed motor functional recovery, neuronal death, glial activation, and inflammatory markers.
Main Results:
- IL-18 expression was upregulated post-SCI.
- Anti-IL-18 antibody treatment significantly improved motor functional recovery.
- Inhibition reduced neuronal death, reactive gliosis, microglia/macrophage activation, and neutrophil infiltration.
- IL-18 inhibition decreased pro-inflammatory factors (IL-1β, Ccl17) and increased M2 microglia/macrophage markers (Arginase 1).
Conclusions:
- IL-18 inhibition promotes motor recovery following SCI in mice.
- The antibody treatment shifts microglia/macrophage polarization from M1 to M2 phenotype.
- Targeting IL-18 fosters a neuroprotective immune microenvironment, offering a potential therapeutic strategy for SCI.

