Evidence map›Paper›PMID 27720803›Full record

ArticleJournal of hepatology2017

The gut microbiota contributes to a mouse model of spontaneous bile duct inflammation.

Elisabeth Schrumpf, Martin Kummen, Laura Valestrand, Thomas U Greiner, Kristian Holm, Velmurugesan Arulampalam, Henrik M Reims, John Baines, Fredrik Bäckhed, Tom H Karlsen and 3 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of hepatology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.0field-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

40 citing papers in PubMed, 74 citations in OpenAlex.

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  9. The gut-liver axis in hepatobiliary diseases.Inflammation and regeneration · 2024
    Review
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  14. The microbiota and the gut-liver axis in primary sclerosing cholangitis.Nature reviews. Gastroenterology & hepatology · 2023
    Review
  15. Primary Sclerosing Cholangitis and Inflammatory Bowel Disease: A Review.Journal of clinical and translational hepatology · 2022
    Review
  16. 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

13 authors at 6 institutions in 4 countries.

Elisabeth SchrumpfNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Martin KummenNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Laura ValestrandNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Section of Gastroenterology, Division of Surgery, Inflammatory Medicine and Transplantation, Surgery, and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Thomas U GreinerThe Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
Kristian HolmNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Velmurugesan ArulampalamCore Facility for Germfree Research (CFGR), Department of Comparative Medicine and Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Stockholm, Sweden.
Henrik M ReimsDepartment of Pathology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
John BainesMax Planck Institute for Evolutionary Biology, Plön, Germany; Institute for Experimental Medicine, Christian-Albrechts-University of Kiel, Kiel, Germany.
Fredrik BäckhedThe Wallenberg Laboratory and Sahlgrenska Center for Cardiovascular and Metabolic Research, Department of Molecular and Clinical Medicine, Institute of Medicine, University of Gothenburg, Gothenburg, Sweden.
Tom H KarlsenNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Section of Gastroenterology, Division of Surgery, Inflammatory Medicine and Transplantation, Surgery, and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Richard S BlumbergDivision of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Johannes R HovNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Section of Gastroenterology, Division of Surgery, Inflammatory Medicine and Transplantation, Surgery, and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway.
Espen MelumNorwegian PSC Research Center, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; K.G. Jebsen Inflammation Research Centre and Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Research Institute of Internal Medicine, Division of Surgery, Inflammatory Medicine and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Section of Gastroenterology, Division of Surgery, Inflammatory Medicine and Transplantation, Surgery, and Transplantation, Oslo University Hospital, Rikshospitalet, Oslo, Norway. Electronic address: espen.melum@medisin.uio.no.
Oslo University Hospital · NOUniversity of Gothenburg · SEUniversity of Oslo · NOBrigham and Women's Hospital · USKarolinska Institutet · SEKiel University · DE

Funding

STRUCTURE-FUNCTION RELATIONSHIPS IN THE ALIMENTARY TRACTP30DK034854 · NIDDK · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI WAYNE I LENCER · 1986 to 2026
$32.4M
MOLECULAR CHARACTERIZATION OF MUCOSAL LYMPHOCYTESR01DK044319 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI Richard S Blumberg · 1992 to 2026
$10.4M
Characterization of Mucosal LymphocytesR37DK044319 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BLUMBERG, RICHARD S · 2005 to 2014
$7.2M
NIDDK NIH HHS P30 DK034854NIDDK NIH HHS R01 DK044319NIDDK NIH HHS R37 DK044319
6 · The paper itself

Abstract

BACKGROUND &

aimsA strong association between human inflammatory biliary diseases and gut inflammation has led to the hypothesis that gut microbes and lymphocytes activated in the intestine play a role in biliary inflammation. The NOD.c3c4 mouse model develops spontaneous biliary inflammation in extra- and intrahepatic bile ducts. We aimed to clarify the role of the gut microbiota in the biliary disease of NOD.c3c4 mice.

methodsWe sampled cecal content and mucosa from conventionally raised (CONV-R) NOD.c3c4 and NOD control mice, extracted DNA and performed 16S rRNA sequencing. NOD.c3c4 mice were rederived into a germ free (GF) facility and compared with CONV-R NOD.c3c4 mice. NOD.c3c4 mice were also co-housed with NOD mice and received antibiotics from weaning.

resultsThe gut microbial profiles of mice with and without biliary disease were different both before and after rederivation (unweighted UniFrac-distance). GF NOD.c3c4 mice had less distended extra-hepatic bile ducts than CONV-R NOD.c3c4 mice, while antibiotic treated mice showed reduction of biliary infarcts. GF animals also showed a reduction in liver weight compared with CONV-R NOD.c3c4 mice, and this was also observed in antibiotic treated NOD.c3c4 mice. Co-housing of NOD and NOD.c3c4 mice indicated that the biliary phenotype was neither transmissible nor treatable by co-housing with healthy mice.

conclusionsNOD.c3c4 and NOD control mice show marked differences in the gut microbiota. GF NOD.c3c4 mice develop a milder biliary affection compared with conventionally raised NOD.c3c4 mice. Our findings suggest that the intestinal microbiota contributes to disease in this murine model of biliary inflammation. LAY SUMMARY: Mice with liver disease have a gut microflora (microbiota) that differs substantially from normal mice. In a normal environment, these mice spontaneously develop disease in their bile ducts. However, when these mice, are raised in an environment devoid of bacteria, the disease in the bile ducts diminishes. Overall this clearly indicates that the bacteria in the gut (the gut microbiota) influences the liver disease in these mice.

Indexed as

IntestinesAnimalsBile DuctsCholangitisDisease Models, AnimalGastrointestinal MicrobiomeLymphocyte ActivationMiceAnti-bacterial agentsGastrointestinal microbiomeGerm freeinbred NODInflammationLiverMiceMicrobiotaMucous membraneNOD.c3c4PBCPSC

Identifiers

PMID27720803
PMCPMC5250551
OpenAlexW2529609590

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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.