Evidence map›Paper›PMID 25889599›Full record

ArticleJournal of neuroinflammation2015

Prolactin in combination with interferon-β reduces disease severity in an animal model of multiple sclerosis.

Simon Zhornitsky, Trina A Johnson, Luanne M Metz, Samuel Weiss, V Wee Yong

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  11. Review
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  13. Review
  14. Prolactin: Friend or Foe in Central Nervous System Autoimmune Inflammation?International journal of molecular sciences · 2016
    Review
  15. Article
  16. Review
  17. Therapeutic Advances and Future Prospects in Progressive Forms of Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016
    Review
  18. 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

5 authors at 1 institution in 1 country.

Simon ZhornitskyHotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada. simon.zhornitsky@albertahealthservices.ca.
Trina A JohnsonHotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada. trina.johnson@mcgill.ca.
Luanne M MetzHotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada. luanne.metz@albertahealthservices.ca.
Samuel WeissHotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada. weiss@ucalgary.ca.
V Wee YongHotchkiss Brain Institute and the Department of Clinical Neurosciences, Cumming School of Medicine, University of Calgary, 3330 Hospital Drive NW, Calgary, AB, T2N 4N1, Canada. vyong@ucalgary.ca.
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous work has demonstrated that the hormone prolactin promotes oligodendrocyte precursor proliferation and remyelination following lysolecithin-induced demyelination of the mouse spinal cord. Prolactin, however, can elicit pro-inflammatory responses, and its use in the prototypical demyelinating and inflammatory condition, multiple sclerosis (MS), should thus be approached cautiously. Here, we sought to determine whether recombinant prolactin could alter the course of experimental autoimmune encephalomyelitis (EAE), an inflammatory animal model of MS. Consistent with previous literature, we found that prolactin activated leukocytes in vitro. Daily treatment with prolactin from around the time of onset of clinical signs, for 9 (days 9 to 17) or 25 (days 9 to 33) days did not increase clinical or histological signs of EAE over that of vehicle-treated mice. Instead, the combination of prolactin and a suboptimal dose of recombinant murine interferon-β resulted in (days 9 to 17 group) or trended towards (days 9 to 33 group), a greater amelioration of clinical signs of EAE, compared to either treatment alone or to vehicle controls. Histological analyses corroborated the clinical EAE data. These results suggest that prolactin may be beneficial when administered in combination with interferon-β in MS.

Indexed as

AnimalsAntigen-Presenting CellsCell ProliferationDisease Models, AnimalDrug Therapy, CombinationFemaleImmunologic FactorsInterferon-betaMiceMice, Inbred C57BLMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsProlactinSpinal CordTime FactorsImmunologic FactorsInterferon-betaMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsProlactin

Identifiers

PMID25889599
PMCPMC4367923
OpenAlexW2096708063

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.