Evidence map›Paper›PMID 25690155›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2015

Reciprocal Regulation of Substance P and IL-12/IL-23 and the Associated Cytokines, IFNγ/IL-17: A Perspective on the Relevance of This Interaction to Multiple Sclerosis.

Janek Vilisaar, Kiyokazu Kawabe, Manjit Braitch, Jehan Aram, Yasemin Furtun, Angela J Fahey, Mark Chopra, Radu Tanasescu, Patrick J Tighe, Bruno Gran and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  14. IL-23 mediates murine liver transplantation ischemia-reperfusion injury via IFN-γ/IRF-1 pathway.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  15. Article
  16. Article
  17. Neuropeptide substance P and the immune response.Cellular and molecular life sciences : CMLS · 2016
    Review
  18. Review
  19. Article
  20. 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

12 authors at 3 institutions in 3 countries.

Janek VilisaarDivision of Clinical Neurology, University of Nottingham, Nottingham, UK.
Kiyokazu Kawabe
Manjit Braitch
Jehan Aram
Yasemin Furtun
Angela J Fahey
Mark Chopra
Radu Tanasescu
Patrick J Tighe
Bruno Gran
Charalabos Pothoulakis
Cris S Constantinescu
University of Nottingham · GBQueen's Medical Centre · GBUniversity of California, Los Angeles · US

Funding

SUBSTANCE P AND INTESTINAL INFLAMMATIONR01DK047343 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI POTHOULAKIS, CHARALABOS · 1994 to 2014
$4.2M
NIDDK NIH HHS R01 DK047343
6 · The paper itself

Abstract

unlabelledThe neuropeptide substance P (SP) exhibits cytokine-like properties and exerts different effects in autoimmune inflammation. Various immune cells express SP and its neurokinin-1 receptor (NK1R) isoforms. A role for SP has been demonstrated in a number of autoimmune conditions, including multiple sclerosis (MS). In this work, we studied the role of SP and NK1R in human immune cells with a focus on their relationship with IL-12/IL-23 family cytokines and the associated IFN-γ/IL-17.

aims(1) To determine the role of SP mediated effects on induction of various inflammatory cytokines in peripheral blood mononuclear cells (PBMC); (2) to investigate the expression of SP and its receptor in T cells and the effects of stimulation with IL-12 and IL-23. Quantitative real-time PCR, flow cytometry, ELISA, promoter studies on PBMC and primary T cells from healthy volunteers, and Jurkat cell line. Treatment with SP significantly increased the expression of IL-12/IL-23 subunit p40, IL-23 p19 and IL-12 p35 mRNA in human PBMC. Expression of NK1R and SP in T cells was upregulated by IL-23 but a trend was observed with IL-12. The IL-23 effect likely involves IL-17 production that additionally mediates IL-23 effects. Mutual interactions exist with SP enhancing the cytokines IL-23 and IL-12, and SP and NK1R expression being differentially but potentially synergistically regulated by these cytokines. These findings suggest a proinflammatory role for SP in autoimmune inflammation. We propose a model whereby immunocyte derived SP stimulates Th1 and Th17 autoreactive cells migrating to the central nervous system (CNS), enhances their crossing the blood brain barrier and perpetuates inflammation in the CNS by being released from damaged nerves and activating both resident glia and infiltrating immune cells. SP may be a therapeutic target in MS.

Indexed as

Cell LineHealthy VolunteersHumansInterferon-gammaInterleukin-12Interleukin-12 Subunit p35Interleukin-12 Subunit p40Interleukin-17Interleukin-23Interleukin-23 Subunit p19Leukocytes, MononuclearReceptors, Neurokinin-1Substance PT-LymphocytesInterferon-gammaInterleukin-12Interleukin-12 Subunit p35Interleukin-12 Subunit p40Interleukin-17Interleukin-23Interleukin-23 Subunit p19Receptors, Neurokinin-1Substance P

Identifiers

PMID25690155
PMCPMC4543419
OpenAlexW2045656994

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.