Evidence map›Paper›PMID 28704649›Full record

ArticleCell host & microbe2017

Indoleacrylic Acid Produced by Commensal Peptostreptococcus Species Suppresses Inflammation.

Marta Wlodarska, Chengwei Luo, Raivo Kolde, Eva d'Hennezel, John W Annand, Cortney E Heim, Philipp Krastel, Esther K Schmitt, Abdifatah S Omar, Elizabeth A Creasey and 12 more

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

Article in Cell host & microbe, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 509 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
509citing papers in PubMed, 1 pooled it
17.1field-weighted citation impact, top 1% 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

509 citing papers in PubMed, 1 synthesis or guideline pooled it, 836 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Article
  6. Article
  7. Review
  8. Gut microbes · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Microbiota-derived indole limitsScience advances · 2026
    Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Article

449 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

22 authors at 4 institutions in 2 countries.

Marta WlodarskaThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Chemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Chengwei LuoThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Raivo KoldeCenter for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Eva d'HennezelChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
John W AnnandChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Cortney E HeimThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Chemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Philipp KrastelNovartis Institutes for BioMedical Research, Novartis Campus, 4056 Basel, Switzerland.
Esther K SchmittNovartis Institutes for BioMedical Research, Novartis Campus, 4056 Basel, Switzerland.
Abdifatah S OmarThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Elizabeth A CreaseyCenter for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
Ashley L GarnerThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Sina MohammadiChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Daniel J O'ConnellThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Sahar AbubuckerChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Timothy D ArthurThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Eric A FranzosaThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Curtis HuttenhowerThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA 02115, USA.
Leon O MurphyChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Henry J HaiserChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Hera VlamakisThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Jeffrey A PorterChemical Biology and Therapeutics, Novartis Institutes for BioMedical Research, Cambridge, MA 02139, USA.
Ramnik J XavierThe Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA; Center for Computational and Integrative Biology, Massachusetts General Hospital, Boston, MA 02114, USA; Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA. Electronic address: xavier@molbio.mgh.harvard.edu.
Broad Institute · USHarvard University · USMassachusetts General Hospital · USNovartis Institutes for BioMedical Research

Funding

Pilot & Feasibility ProgramP30DK043351 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI RAYMOND T CHUNG · 1991 to 2026
$35.3M
NIDDK NIH HHS P30 DK043351
6 · The paper itself

Abstract

Host factors in the intestine help select for bacteria that promote health. Certain commensals can utilize mucins as an energy source, thus promoting their colonization. However, health conditions such as inflammatory bowel disease (IBD) are associated with a reduced mucus layer, potentially leading to dysbiosis associated with this disease. We characterize the capability of commensal species to cleave and transport mucin-associated monosaccharides and identify several Clostridiales members that utilize intestinal mucins. One such mucin utilizer, Peptostreptococcus russellii, reduces susceptibility to epithelial injury in mice. Several Peptostreptococcus species contain a gene cluster enabling production of the tryptophan metabolite indoleacrylic acid (IA), which promotes intestinal epithelial barrier function and mitigates inflammatory responses. Furthermore, metagenomic analysis of human stool samples reveals that the genetic capability of microbes to utilize mucins and metabolize tryptophan is diminished in IBD patients. Our data suggest that stimulating IA production could promote anti-inflammatory responses and have therapeutic benefits.

Indexed as

SymbiosisAnimalsAnti-Inflammatory AgentsBacteriaBacteroidesColonCytokinesDysbiosisEubacterialesHumansIndolesInflammationInflammatory Bowel DiseasesIntestinal MucosaIntestinesMiceAnti-Inflammatory AgentsCytokinesindoleacrylic acidIndolesMucin-2Mucinsindoleacrylic acidindolepropionic acidMuc2mucusorganoidPeptostreptococcus

Identifiers

PMID28704649
PMCPMC5672633
OpenAlexW2735584664

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.