Evidence map›Paper›PMID 29644622›Full record

ArticleEuropean journal of immunology2018

Microbial metabolites, short-chain fatty acids, restrain tissue bacterial load, chronic inflammation, and associated cancer in the colon of mice.

Myunghoo Kim, Leon Friesen, Jeongho Park, Hyungjin M Kim, Chang H Kim

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.3field-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

63 citing papers in PubMed, 111 citations in OpenAlex.

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  13. Microorganisms · 2025
    Article
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3 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Myunghoo KimDepartment of Comparative Pathobiology and Purdue Research Center for Cancer Research, Purdue University, West Lafayette, IN, USA.
Leon FriesenDepartment of Comparative Pathobiology and Purdue Research Center for Cancer Research, Purdue University, West Lafayette, IN, USA.
Jeongho ParkDepartment of Comparative Pathobiology and Purdue Research Center for Cancer Research, Purdue University, West Lafayette, IN, USA.
Hyungjin M KimDepartment of Biostatistics, University of Michigan, Ann Arbor, MI, USA.
Chang H KimDepartment of Comparative Pathobiology and Purdue Research Center for Cancer Research, Purdue University, West Lafayette, IN, USA.ORCID 0000-0003-4618-9139
Purdue University West Lafayette · USUniversity of Michigan · US

Funding

Homing of Functionally Distinct ILC SubsetsR01AI121302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIM, CHANG H · 2016 to 2020
$1.9M
FoxP3+ T cells of mucosal tissuesR01AI074745 · NIAID · PURDUE UNIVERSITY · PI KIM, CHANG H · 2008 to 2012
$1.7M
Migration and function of Th17 cells in the gutR01AI080769 · NIAID · PURDUE UNIVERSITY · PI KIM, CHANG H · 2010 to 2013
$1.3M
NIAID NIH HHS R01 AI074745NIAID NIH HHS R01 AI080769NIAID NIH HHS R01 AI121302
6 · The paper itself

Abstract

The intestinal immune system is regulated by microbes and their metabolites. The roles of gut microbial metabolites in regulating intestinal inflammation and tumorigenesis are incompletely understood. We systematically studied the roles of short-chain fatty acids (SCFAs) and their receptors (GPR43 or GPR41) in regulating tissue bacterial load, acute versus chronic inflammatory responses, and intestinal cancer development. SCFA receptor-, particularly GPR43-, deficient mice were defective in mounting appropriate acute immune responses to promote barrier immunity, and developed uncontrolled chronic inflammatory responses following epithelial damage. Further, intestinal carcinogenesis was increased in GPR43-deficient mice. Dietary fiber and SCFA administration suppressed intestinal inflammation and cancer in both GPR43-dependent and independent manners. The beneficial effect of GPR43 was not mediated by altered microbiota but by host tissue cells and hematopoietic cells to a lesser degree. We found that inability to suppress commensal bacterial invasion into the colonic tissue is associated with the increased chronic Th17-driven inflammation and carcinogenesis in the intestine of GPR43-deficient mice. In sum, our results reveal the beneficial function of the SCFA-GPR43 axis in suppressing bacterial invasion and associated chronic inflammation and carcinogenesis in the colon.

Indexed as

AnimalsBacterial LoadCarcinogenesisColitisColonColonic NeoplasmsDietary FiberFatty Acids, VolatileGastrointestinal MicrobiomeHumansImmunity, MucosalInflammationIntestinal MucosaMiceMice, KnockoutReceptors, G-Protein-CoupledDietary FiberFatty Acids, VolatileFfar2 protein, mouseGpcr41 protein, mouseReceptors, G-Protein-CoupledColon cancerDietary fiberInflammationShort-chain fatty acids

Identifiers

PMID29644622
PMCPMC6310065
OpenAlexW2797511628

What OpenQuestion holds

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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.