Evidence map›Paper›PMID 24662098›Full record

ArticleGut microbes

Discordance between changes in the gut microbiota and pathogenicity in a mouse model of spontaneous colitis.

Maria Elisa Perez-Muñoz, Kirk Bergstrom, Vincent Peng, Robert Schmaltz, Roberto Jimenez-Cardona, Nathan Marsteller, Sam McGee, Thomas Clavel, Ruth Ley, Jianxin Fu and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Gut microbes. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

32 citing papers in PubMed, 55 citations in OpenAlex.

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  12. C1GALT1 in health and disease.Oncology letters · 2021
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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

12 authors at 5 institutions in 3 countries.

Maria Elisa Perez-MuñozDepartment of Food Science and Technology; University of Nebraska; Lincoln, NE USA; Department of Pathology; Johns Hopkins University School of Medicine; Baltimore, MD USA.
Kirk BergstromOklahoma Medical Research Foundation; Oklahoma City, OK USA.
Vincent PengOklahoma Medical Research Foundation; Oklahoma City, OK USA.
Robert SchmaltzDepartment of Food Science and Technology; University of Nebraska; Lincoln, NE USA.
Roberto Jimenez-CardonaDepartment of Food Science and Technology; University of Nebraska; Lincoln, NE USA.
Nathan MarstellerDepartment of Food Science and Technology; University of Nebraska; Lincoln, NE USA.
Sam McGeeOklahoma Medical Research Foundation; Oklahoma City, OK USA.
Thomas ClavelJunior Research Group Intestinal Microbiome; ZIEL-Research Center for Nutrition and Food Sciences; Technische Universität München; Munich, Germany.
Ruth LeyDepartment of Microbiology; Cornell University; Ithaca, NY USA.
Jianxin FuOklahoma Medical Research Foundation; Oklahoma City, OK USA.
Lijun XiaOklahoma Medical Research Foundation; Oklahoma City, OK USA.
Daniel A PetersonDepartment of Food Science and Technology; University of Nebraska; Lincoln, NE USA; Department of Pathology; Johns Hopkins University School of Medicine; Baltimore, MD USA.
Oklahoma Medical Research Foundation · USUniversity of Nebraska–Lincoln · USCornell University · USFood & Nutrition · NLJohns Hopkins Medicine · US

Funding

Role of Mucin-type O-glycans in Intestinal InflammationR01DK085691 · NIDDK · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI David Casero, Lijun Xia · 2010 to 2026
$6.2M
The Microbiota in a Novel Mouse Model of Ulcerative ColitisR21AI097419 · NIAID · JOHNS HOPKINS UNIVERSITY · PI PETERSON, DANIEL A · 2012 to 2013
$449k
NIAID NIH HHS K08AI07660901NIAID NIH HHS R21 AI097419NIAID NIH HHS R21AI097419NIDDK NIH HHS R01 DK085691NIDDK NIH HHS R01DK085691
6 · The paper itself

Abstract

Under conventional conditions, mice deficient in core 1-derived O-glycans (TM-IEC C1galt1(-/-)), which have a defective mucus layer, experienced spontaneous inflammation of the colon. Analysis of fecal bacterial populations by pyrosequencing of 16S rRNA gene showed that disease in conventional TM-IEC C1galt1(-/-) was associated with shifts in the microbiota manifested by increases in Lactobacillus and Clostridium species, and decreases in unclassified Ruminococcaceae and Lachnospiraceae. Under germ-free (GF) conditions, TM-IEC C1galt1(-/-) presented decreased goblet cells, but did not develop inflammation. Monoassociation of GF TM-IEC C1galt1(-/-) revealed that bacterial species differ significantly in their ability to induce inflammatory changes. Bacteroides thetaiotaomicron caused inflammation, while Lactobacillus johnsonii (enriched during colitis) did not. These observations demonstrate that not all microbiota shifts that correlate with disease contribute to pathogenesis.

Indexed as

BiotaAnimalsBacteriaColitisColonDisease Models, AnimalDNA, BacterialDNA, RibosomalDysbiosisGalactosyltransferasesHumansMice, Inbred C57BLMice, KnockoutRNA, Ribosomal, 16SSequence Analysis, DNAC1galt1 protein, mouseDNA, BacterialDNA, RibosomalGalactosyltransferasesRNA, Ribosomal, 16SAkkermasia muciniphilaBacteroides sartoriiBacteroides thetaiotaomicronClostridiumcore 1 O-glycans deficient micedysbiosisgut microbiotaLactobacillus johnsoniipyrosequencingspontaneous colitis

Identifiers

PMID24662098
PMCPMC4153765
OpenAlexW1974483396

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.