Evidence map›Paper›PMID 32289500›Full record

ArticleCellular and molecular gastroenterology and hepatology2020

Colitis-Induced Microbial Perturbation Promotes Postinflammatory Visceral Hypersensitivity.

Nicolas Esquerre, Lilian Basso, Manon Defaye, Fernando A Vicentini, Nina Cluny, Dominique Bihan, Simon A Hirota, Alana Schick, Humberto B Jijon, Ian A Lewis and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cellular and molecular gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% 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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Microbial dysbiosis alters serotonin signaling in a postinflammatory murine model of visceral pain.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
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  6. Review
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  8. Article
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  12. Article
  13. Neuroimmunophysiology of the gastrointestinal tract.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Review
  14. Review
  15. The Gut Microbiota and Chronic Pain.Current pain and headache reports · 2024
    Review
  16. Review
  17. Article
  18. Article
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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 2 institutions in 2 countries.

Nicolas EsquerreSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary.
Lilian BassoSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary.
Manon DefayeSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary.
Fernando A VicentiniSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary; Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary.
Nina ClunySnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary; Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary.
Dominique BihanDepartment of Biological Sciences, University of Calgary.
Simon A HirotaSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary.
Alana SchickInternational Microbiome Centre, Cumming School of Medicine, University of Calgary.
Humberto B JijonSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Division of Gastroenterology and Hepatology, Department of Medicine, University of Calgary.
Ian A LewisDepartment of Biological Sciences, University of Calgary.
Markus B GeukingSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Microbiology, Immunity and Infectious Diseases, Cumming School of Medicine, University of Calgary.
Keith A SharkeySnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary; Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary.
Christophe AltierSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Department of Physiology and Pharmacology, Cumming School of Medicine, University of Calgary; Alberta Children's Hospital Research Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta, Canada.
Yasmin NasserSnyder Institute for Chronic Diseases, Cumming School of Medicine, University of Calgary; Division of Gastroenterology and Hepatology, Department of Medicine, University of Calgary. Electronic address: ynasser@ucalgary.ca.
University of Calgary · CAAllen Institute for Brain Science · US

Funding

CIHR
6 · The paper itself

Abstract

BACKGROUND &

aimsDespite achieving endoscopic remission, more than 20% of inflammatory bowel disease patients experience chronic abdominal pain. These patients have increased rectal transient receptor potential vanilloid-1 receptor (TRPV1) expression, a key transducer of inflammatory pain. Because inflammatory bowel disease patients in remission exhibit dysbiosis and microbial manipulation alters TRPV1 function, our goal was to examine whether microbial perturbation modulated transient receptor potential function in a mouse model.

methodsMice were given dextran sodium sulfate (DSS) to induce colitis and were allowed to recover. The microbiome was perturbed by using antibiotics as well as fecal microbial transplant (FMT). Visceral and somatic sensitivity were assessed by recording visceromotor responses to colorectal distention and using hot plate/automated Von Frey tests, respectively. Calcium imaging of isolated dorsal root ganglia neurons was used as an in vitro correlate of nociception. The microbiome composition was evaluated via 16S rRNA gene variable region V4 amplicon sequencing, whereas fecal short-chain fatty acids (SCFAs) were assessed by using targeted mass spectrometry.

resultsPostinflammatory DSS mice developed visceral and somatic hyperalgesia. Antibiotic administration during DSS recovery induced visceral, but not somatic, hyperalgesia independent of inflammation. FMT of postinflammatory DSS stool into antibiotic-treated mice increased visceral hypersensitivity, whereas FMT of control stool reversed antibiotics' sensitizing effects. Postinflammatory mice exhibited both increased SCFA-producing species and fecal acetate/butyrate content compared with controls. Capsaicin-evoked calcium responses were increased in naive dorsal root ganglion neurons incubated with both sodium butyrate/propionate alone and with colonic supernatants derived from postinflammatory mice.

conclusionsThe microbiome plays a central role in postinflammatory visceral hypersensitivity. Microbial-derived SCFAs can sensitize nociceptive neurons and may contribute to the pathogenesis of postinflammatory visceral pain.

Indexed as

AnimalsColitis, UlcerativeColonDextran SulfateDisease Models, AnimalDysbiosisFatty Acids, VolatileFecesGastrointestinal MicrobiomeHumansIntestinal MucosaMaleMiceNociceptionNociceptorsTRPV Cation ChannelsDextran SulfateFatty Acids, VolatileTRPV1 protein, mouseTRPV Cation ChannelsCalcium ImagingDorsal Root GanglionDSS ColitisMicrobiomeShort-Chain Fatty AcidsVisceral Pain

Identifiers

PMID32289500
PMCPMC7301239
OpenAlexW3015694861

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.