Evidence map›Paper›PMID 28666018›Full record

ArticlePloS one2017

Indole-3-carbinol, a plant nutrient and AhR-Ligand precursor, supports oral tolerance against OVA and improves peanut allergy symptoms in mice.

Christiane Hammerschmidt-Kamper, Daniel Biljes, Katja Merches, Irina Steiner, Thomas Daldrup, Marianne Bol-Schoenmakers, Raymond H H Pieters, Charlotte Esser

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  5. AhR signaling in skin-resident CD207Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  20. Mechanisms by which gut microorganisms influence food sensitivities.Nature reviews. Gastroenterology & hepatology · 2019
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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

8 authors at 3 institutions in 2 countries.

Christiane Hammerschmidt-KamperIUF - Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.
Daniel BiljesIUF - Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.
Katja MerchesIUF - Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.
Irina SteinerInstitute of Legal Medicine, Department of Forensic Toxicology, University Hospital of Düsseldorf, Düsseldorf, Germany.
Thomas DaldrupInstitute of Legal Medicine, Department of Forensic Toxicology, University Hospital of Düsseldorf, Düsseldorf, Germany.
Marianne Bol-SchoenmakersInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.
Raymond H H PietersInstitute for Risk Assessment Sciences, Utrecht University, Utrecht, The Netherlands.
Charlotte EsserIUF - Leibniz Research Institute for Environmental Medicine, Düsseldorf, Germany.ORCID http://orcid.org/0000-0002-2957-4636
Leibniz Institute of Environmental Medicine · DEDüsseldorf University Hospital · DEUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In general, dietary antigens are tolerated by the gut associated immune system. Impairment of this so-called oral tolerance is a serious health risk. We have previously shown that activation of the ligand-dependent transcription factor aryl hydrocarbon receptor (AhR) by the environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects both oral tolerance and food allergy. In this study, we determine whether a common plant-derived, dietary AhR-ligand modulates oral tolerance as well. We therefore fed mice with indole-3-carbinole (I3C), an AhR ligand that is abundant in cruciferous plants. We show that several I3C metabolites were detectable in the serum after feeding, including the high-affinity ligand 3,3´-diindolylmethane (DIM). I3C feeding robustly induced the AhR-target gene CYP4501A1 in the intestine; I3C feeding also induced the aldh1 gene, whose product catalyzes the formation of retinoic acid (RA), an inducer of regulatory T cells. We then measured parameters indicating oral tolerance and severity of peanut-induced food allergy. In contrast to the tolerance-breaking effect of TCDD, feeding mice with chow containing 2 g/kg I3C lowered the serum anti-ovalbumin IgG1 response in an experimental oral tolerance protocol. Moreover, I3C feeding attenuated symptoms of peanut allergy. In conclusion, the dietary compound I3C can positively influence a vital immune function of the gut.

Indexed as

Administration, OralAnimalsEnzyme-Linked Immunosorbent AssayIndolesMiceMice, Inbred C57BLOvalbuminPeanut HypersensitivityReceptors, Aryl Hydrocarbonindole-3-carbinolIndolesOvalbuminReceptors, Aryl Hydrocarbon

Identifiers

PMID28666018
PMCPMC5493375
OpenAlexW2731789252

What OpenQuestion holds

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LicenceCC BY
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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.