Evidence map›Paper›PMID 35715845›Full record

ArticleJournal of neuroinflammation2022

Electrical stimulation of the splenic nerve bundle ameliorates dextran sulfate sodium-induced colitis in mice.

David J Brinkman, Thomas Simon, Anne S Ten Hove, Konstantina Zafeiropoulou, Olaf Welting, Patricia H P van Hamersveld, Rose A Willemze, Andrew Y F Li Yim, Caroline Verseijden, Theodorus B M Hakvoort and 4 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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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 5 institutions in 3 countries.

David J Brinkman *Tytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands. d.j.brinkman@amsterdamumc.nl.ORCID http://orcid.org/0000-0003-1862-9256
Thomas Simon *Institut de Pharmacologie Moléculaire et Cellulaire, Université Côte d'Azur, CNRS, Nice, France.
Anne S Ten HoveTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Konstantina ZafeiropoulouTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Olaf WeltingTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Patricia H P van HamersveldTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Rose A WillemzeTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Andrew Y F Li YimTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Caroline VerseijdenTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Theodorus B M HakvoortTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Misha D LuyerDepartment of Surgery, Catharina Hospital, Eindhoven, The Netherlands.
Margriet J VervoordeldonkTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Philippe BlancouInstitut de Pharmacologie Moléculaire et Cellulaire, Université Côte d'Azur, CNRS, Nice, France.
Wouter J de JongeTytgat Institute for Liver and Intestinal Research, Gastroenterology and Hepatology, Amsterdam Gastroenterology Endocrinology Metabolism, Amsterdam UMC, University of Amsterdam, Room S2-162, Meibergdreef 69, 1105 BK, Amsterdam, The Netherlands.
Amsterdam University Medical Centers · NLCentre National de la Recherche Scientifique · FRRadboud University Nijmegen · NLEmma Kinderziekenhuis · NLUniversity of Bonn · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVagus nerve stimulation has been suggested to affect immune responses, partly through a neuronal circuit requiring sympathetic innervation of the splenic nerve bundle and norepinephrine (NE) release. Molecular and cellular mechanisms of action remain elusive. Here, we investigated the therapeutic value of this neuromodulation in inflammatory bowel disease (IBD) by applying electrical splenic nerve bundle stimulation (SpNS) in mice with dextran sulfate sodium (DSS)-induced colitis.

methodsCuff electrodes were implanted around the splenic nerve bundle in mice, whereupon mice received SpNS or sham stimulation. Stimulation was applied 6 times daily for 12 days during DSS-induced colitis. Colonic and splenic tissues were collected for transcriptional analyses by qPCR and RNA-sequencing (RNA-seq). In addition, murine and human splenocytes were stimulated with lipopolysaccharide (LPS) in the absence or presence of NE. Single-cell RNA-seq data from publicly available data sets were analyzed for expression of β-adrenergic receptors (β-ARs).

resultsColitic mice undergoing SpNS displayed reduced colon weight/length ratios and showed improved Disease Activity Index scores with reduced Tumor Necrosis Factor α mRNA expression in the colon compared with sham stimulated mice. Analyses of splenocytes from SpNS mice using RNA-seq demonstrated specific immune metabolism transcriptome profile changes in myeloid cells. Splenocytes showed expression of β-ARs in myeloid and T cells. Cytokine production was reduced by NE in mouse and human LPS-stimulated splenocytes.

conclusionsTogether, our results demonstrate that SpNS reduces clinical features of colonic inflammation in mice with DSS-induced colitis possibly by inhibiting splenic myeloid cell activation. Our data further support exploration of the clinical use of SpNS for patients with IBD.

Indexed as

ColitisInflammatory Bowel DiseasesAnimalsColonDextran SulfateDisease Models, AnimalElectric StimulationHumansLipopolysaccharidesMiceMice, Inbred C57BLDextran SulfateLipopolysaccharidesInflammatory bowel diseaseRNA-sequencingSplenic nerve stimulation

Identifiers

PMID35715845
PMCPMC9204975
OpenAlexW4283029852

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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.