Evidence map›Paper›PMID 30122655›Full record

ArticleCell host & microbe2018

Temporal Regulation of the Bacterial Metabolite Deoxycholate during Colonic Repair Is Critical for Crypt Regeneration.

Umang Jain, Chin-Wen Lai, Shanshan Xiong, Victoria M Goodwin, Qiuhe Lu, Brian D Muegge, George P Christophi, Kelli L VanDussen, Bethany P Cummings, Erick Young and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell host & microbe, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

39 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
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    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Umang JainDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Chin-Wen LaiDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Shanshan XiongDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Victoria M GoodwinDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Qiuhe LuDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Brian D MueggeDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
George P ChristophiDivision of Gastroenterology, Department of Medicine, Washington University School of Medicine, St. Louis, MO, 63110 USA.
Kelli L VanDussenDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Bethany P CummingsDepartment of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
Erick YoungResearch Beyond Borders, Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT 06877, USA.
John HamborResearch Beyond Borders, Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT 06877, USA.
Thaddeus S StappenbeckDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: stappenb@wustl.edu.
Washington University in St. Louis · USBoehringer Ingelheim (United States) · USCornell University · US

Funding

Tunable therapeutic modulation of the gut microbiome by engineered probioticsR01AT009741 · NCCIH · WASHINGTON UNIVERSITY · PI DANTAS, GAUTAM, MOON, TAE SEOK · 2018 to 2022
$3.5M
RESPONSES OF INTESTINAL STEM CELLS TO EPITHELIAL INJURYR01DK071619 · NIDDK · WASHINGTON UNIVERSITY · PI STAPPENBECK, THADDEUS S · 2008 to 2017
$3.2M
DEFINING THE BASIS OF EPITHELIAL DEFECTS IN CROHN'S DISEASE PATIENTSK01DK109081 · NIDDK · WASHINGTON UNIVERSITY · PI VANDUSSEN, KELLI LYNN · 2016 to 2020
$737k
NCCIH NIH HHS R01 AT009741NIDDK NIH HHS K01 DK109081NIDDK NIH HHS R01 DK071619
6 · The paper itself

Abstract

Colonic wound repair is an orchestrated process, beginning with barrier re-establishment and followed by wound channel formation and crypt regeneration. Elevated levels of prostaglandin E2 (PGE2) promote barrier re-establishment; however, we found that persistently elevated PGE2 hinders subsequent repair phases. The bacterial metabolite deoxycholate (DCA) promotes transition through repair phases via PGE2 regulation. During barrier re-establishment, DCA levels are locally diminished in the wound, allowing enhanced PGE2 production and barrier re-establishment. However, during transition to the wound channel formation phase, DCA levels increase to inhibit PGE2 production and promote crypt regeneration. Altering DCA levels via antibiotic treatment enhances PGE2 levels but impairs wound repair, which is rescued with DCA treatment. DCA acts via its receptor, farnesoid X receptor, to inhibit the enzyme cPLA2 required for PGE2 synthesis. Thus, colonic wound repair requires temporally regulated signals from microbial metabolites to coordinate host-associated signaling cascades. VIDEO ABSTRACT.

Indexed as

Wound HealingAnimalsBacteriaBiopsyColonCyclooxygenase 2Deoxycholic AcidDinoprostoneGastrointestinal MicrobiomeHydroxyprostaglandin DehydrogenasesIntestinal MucosaMiceMice, KnockoutNitrobenzenesPrimary Cell CultureSulfonamides15-hydroxyprostaglandin dehydrogenaseCyclooxygenase 2Deoxycholic AcidDinoprostoneHydroxyprostaglandin DehydrogenasesN-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamideNitrobenzenesPtgs2 protein, mouseSulfonamidesVancomycin

Identifiers

PMID30122655
PMCPMC6555552
OpenAlexW2886313842

What OpenQuestion holds

Textmetadata
LicenceTDM
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.