Evidence map›Paper›PMID 39858411›Full record

ArticleBiomolecules2024

IL-18 Blockage Reduces Neuroinflammation and Promotes Functional Recovery in a Mouse Model of Spinal Cord Injury.

Easmin Begum, Md Rashel Mahmod, Md Mahbobur Rahman, Fumiko Fukuma, Takeshi Urano, Yuki Fujita

Abstract read
In one paragraph

Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. The spleen-brain axis in Alzheimer's disease and related dementias: Integrating immune and metabolic regulation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025
    Review
  13. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Easmin BegumDepartment of Anatomy and Developmental Biology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.
Md Rashel MahmodDepartment of Anatomy and Developmental Biology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.
Md Mahbobur RahmanDepartment of Anatomy and Developmental Biology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.
Fumiko FukumaDepartment of Anatomy and Developmental Biology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.
Takeshi UranoCenter for Vaccines and Therapeutic Antibodies for Emerging Infectious Diseases, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.
Yuki FujitaDepartment of Anatomy and Developmental Biology, Faculty of Medicine, Shimane University, 89-1 Enya-cho, Izumo 693-8501, Shimane, Japan.

Funding

Japan Society for the Promotion of Science Grant 23H04169
6 · The paper itself

Abstract

The prognosis of spinal cord injury (SCI) is closely linked to secondary injury processes, predominantly driven by neuroinflammation. Interleukin-18 (IL-18) plays a pivotal role in this inflammatory response. In previous work, we developed an anti-IL-18 antibody capable of neutralizing the active form of IL-18. This study evaluated the functional effects of this antibody in a mouse model of SCI. IL-18 expression was significantly upregulated in the spinal cord following injury. In a mouse model of SCI (C57BL/6J strain), mice were administered 150 μg of the anti-IL-18 antibody intraperitoneally. IL-18 inhibition via antibody treatment facilitated motor functional recovery post-injury. This intervention reduced neuronal death, reactive gliosis, microglia/macrophage activation, and neutrophil infiltration. Additionally, IL-18 inhibition lowered the expression of pro-inflammatory factors, such as IL-1β and the M1 microglia/macrophage marker Ccl17, while enhancing the expression of the M2 microglia/macrophage marker Arginase 1. Collectively, our findings demonstrate that IL-18 inhibition promotes motor recovery and facilitates the polarization of M1 microglia/macrophages to the M2 phenotype, thereby fostering a neuroprotective immune microenvironment in mice with SCI.

Indexed as

Interleukin-18Neuroinflammatory DiseasesRecovery of FunctionSpinal Cord InjuriesAnimalsDisease Models, AnimalMacrophagesMiceMice, Inbred C57BLMicrogliaInterleukin-18cytokinesgene expressiongliaIL-18inflammatory responseneuroinflammationneuronneuroprotectionspinal cord injurytraumatic injury

Identifiers

PMID39858411
PMCPMC11761924

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.