Evidence map›Paper›PMID 32191733›Full record

ArticlePloS one2020

Prolonged inflammation leads to ongoing damage after spinal cord injury.

Jacek M Kwiecien, Wojciech Dabrowski, Beata Dąbrowska-Bouta, Grzegorz Sulkowski, Wendy Oakden, Christian J Kwiecien-Delaney, Jordan R Yaron, Liqiang Zhang, Lauren Schutz, Barbara Marzec-Kotarska and 4 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
9.9field-weighted citation impact, top 1% of its field
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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.

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  19. Imaging Demyelinated Axons After Spinal Cord Injuries with PET Tracer [Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025
    Article
  20. Article

15 more citing papers are in PubMed but not listed here.

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

14 authors at 6 institutions in 3 countries.

Jacek M KwiecienDepartment of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.ORCID 0000-0002-0128-9307
Wojciech DabrowskiDepartment of Anaesthesiology and Intensive Therapy, Medical University of Lublin, Lublin, Poland.
Beata Dąbrowska-BoutaLaboratory of Pathoneurochemistry, Mossakowski Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.
Grzegorz SulkowskiLaboratory of Pathoneurochemistry, Mossakowski Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.
Wendy OakdenPhysical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
Christian J Kwiecien-DelaneyFaculty of Science, McMaster University, Hamilton, Ontario, Canada.
Jordan R YaronCenters for Personalized Diagnostics and Immunotherapy, Vaccines and Virotherapy, Biodesign Institute, Arizona State University, Tempe, Arizona, United States of America.ORCID 0000-0002-4133-474X
Liqiang ZhangCenters for Personalized Diagnostics and Immunotherapy, Vaccines and Virotherapy, Biodesign Institute, Arizona State University, Tempe, Arizona, United States of America.
Lauren SchutzCenters for Personalized Diagnostics and Immunotherapy, Vaccines and Virotherapy, Biodesign Institute, Arizona State University, Tempe, Arizona, United States of America.
Barbara Marzec-KotarskaDepartment of Clinical Pathomorphology, Medical University of Lublin, Lublin, Poland.
Greg J StaniszPhysical Sciences, Sunnybrook Research Institute, Toronto, Ontario, Canada.
John P KarisDepartment of Neuroradiology, Barrow Neurological Institute, Dignity Health St. Joseph's Hospital and Medical Center, Phoenix, Arizona, United States of America.ORCID 0000-0003-4181-4185
Lidia StruzynskaLaboratory of Pathoneurochemistry, Mossakowski Medical Research Center, Polish Academy of Sciences, Warsaw, Poland.
Alexandra R LucasCenters for Personalized Diagnostics and Immunotherapy, Vaccines and Virotherapy, Biodesign Institute, Arizona State University, Tempe, Arizona, United States of America.
Arizona State University · USMossakowski Medical Research Institute, Polish Academy of Sciences · PLMcMaster University · CAMedical University of Lublin · PLSunnybrook Health Science Centre · CABarrow Neurological Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of spinal cord injury (SCI) remains poorly understood and treatment remains limited. Emerging evidence indicates that post-SCI inflammation is severe but the role of reactive astrogliosis not well understood given its implication in ongoing inflammation as damaging or neuroprotective. We have completed an extensive systematic study with MRI, histopathology, proteomics and ELISA analyses designed to further define the severe protracted and damaging inflammation after SCI in a rat model. We have identified 3 distinct phases of SCI: acute (first 2 days), inflammatory (starting day 3) and resolution (>3 months) in 16 weeks follow up. Actively phagocytizing, CD68+/CD163- macrophages infiltrate myelin-rich necrotic areas converting them into cavities of injury (COI) when deep in the spinal cord. Alternatively, superficial SCI areas are infiltrated by granulomatous tissue, or arachnoiditis where glial cells are obliterated. In the COI, CD68+/CD163- macrophage numbers reach a maximum in the first 4 weeks and then decline. Myelin phagocytosis is present at 16 weeks indicating ongoing inflammatory damage. The COI and arachnoiditis are defined by a wall of progressively hypertrophied astrocytes. MR imaging indicates persistent spinal cord edema that is linked to the severity of inflammation. Microhemorrhages in the spinal cord around the lesion are eliminated, presumably by reactive astrocytes within the first week post-injury. Acutely increased levels of TNF-alpha, IL-1beta, IFN-gamma and other pro-inflammatory cytokines, chemokines and proteases decrease and anti-inflammatory cytokines increase in later phases. In this study we elucidated a number of fundamental mechanisms in pathogenesis of SCI and have demonstrated a close association between progressive astrogliosis and reduction in the severity of inflammation.

Indexed as

AnimalsAnti-Inflammatory AgentsArachnoiditisAstrocytesCytokinesDisease Models, AnimalGliosisHumansMacrophagesMagnetic Resonance ImagingMaleMyelin SheathRatsSeverity of Illness IndexSpinal CordSpinal Cord InjuriesAnti-Inflammatory AgentsCytokines

Identifiers

PMID32191733
PMCPMC7081990
OpenAlexW3010706193

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.