Evidence map›Paper›PMID 36323778›Full record

ArticleNature2022

Inulin fibre promotes microbiota-derived bile acids and type 2 inflammation.

Mohammad Arifuzzaman, Tae Hyung Won, Ting-Ting Li, Hiroshi Yano, Sreehaas Digumarthi, Andrea F Heras, Wen Zhang, Christopher N Parkhurst, Sanchita Kashyap, Wen-Bing Jin and 10 more

Open access · greenAbstract read
In one paragraph

Article in Nature, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 papers.

0numbers the graph read from it
0cells of the map it votes in
141citing papers in PubMed
16.1field-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

141 citing papers in PubMed, 197 citations in OpenAlex.

  1. Trial
  2. mSystems · 2025
    Trial
  3. Trial
  4. Trial
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Review

81 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

20 authors at 1 institution in 1 country.

Mohammad ArifuzzamanJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.ORCID http://orcid.org/0000-0002-2730-1247
Tae Hyung WonBoyce Thompson Institute, Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, USA.
Ting-Ting LiJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Hiroshi YanoJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.ORCID http://orcid.org/0000-0002-3098-2629
Sreehaas DigumarthiJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Andrea F HerasGale and Ira Drukier Institute for Children's Health, Department of Pediatrics, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Wen ZhangJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Christopher N ParkhurstJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Sanchita KashyapJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Wen-Bing JinJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Gregory Garbès PutzelJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Amy M TsouJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Coco ChuJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Qianru WeiJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.ORCID http://orcid.org/0000-0002-6684-7904
Alex GrierJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA.
JRI IBD Live Cell Bank Consortium
Stefan WorgallGale and Ira Drukier Institute for Children's Health, Department of Pediatrics, Weill Cornell Medicine, Cornell University, New York, NY, USA.
Chun-Jun GuoJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA. chg4001@med.cornell.edu.
Frank C SchroederBoyce Thompson Institute, Department of Chemistry and Chemical Biology, Cornell University, Ithaca, NY, USA. schroeder@cornell.edu.ORCID http://orcid.org/0000-0002-4420-0237
David ArtisJill Roberts Institute for Research in Inflammatory Bowel Disease, Division of Gastroenterology and Hepatology, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, Cornell University, New York, NY, USA. dartis@med.cornell.edu.ORCID http://orcid.org/0000-0002-1753-4100
Cornell University · US

Funding

Institutional Career Development CoreKL2TR002385 · NCATS · WEILL MEDICAL COLL OF CORNELL UNIV · PI YUAN-SHAN ZHU · 2017 to 2026
$13.3M
Regulation of protective immunity following enteric viral infectionU01AI095608 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID, SONNENBERG, GREGORY F · 2011 to 2025
$11.0M
Multidisciplinary Approach Training in Respiratory ResearchT32HL134629 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI Robert J Kaner, Heather Winona Stout Delgado · 2018 to 2026
$5.2M
Small molecule signaling in C. elegansR35GM131877 · NIGMS · BOYCE THOMPSON INST FOR PLANT RESEARCH · PI Frank Clemens Schroeder · 2019 to 2026
$5.0M
Microbiota-derived metabolites and the regulation of host immunity and inflammation (Diversity Supplement)R01AI172027 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI David Artis, Chun-Jun Guo · 2022 to 2026
$4.4M
Neuroimmune Regulation of Atopic DermatitisR01AR070116 · NIAMS · WASHINGTON UNIVERSITY · PI KIM, BRIAN · 2016 to 2021
$3.8M
Regulation and function of innate lymphoid cells in the gutR01AI095466 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID · 2011 to 2022
$3.7M
Neuropeptide-mediated regulation of antihelminth immunityR01AI151599 · NIAID · RUTGERS BIOMEDICAL AND HEALTH SCIENCES · PI ARTIS, DAVID, SIRACUSA, MARK CHRISTOPHER · 2020 to 2024
$3.2M
Neuro-immune regulation of intestinal inflammationR01DK126871 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID · 2020 to 2024
$3.2M
Dietary Regulation of Intestinal Inflammation and RepairR01DK132244 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI ARTIS, DAVID, GUO, CHUN-JUN · 2022 to 2025
$2.7M
An integrative and generalizable approach to modulate microbiota small molecules in the hostDP2HD101401 · NICHD · WEILL MEDICAL COLL OF CORNELL UNIV · PI GUO, CHUN-JUN · 2019 to 2019
$2.5M
Rhinovirus respiratory infection and sphingolipid metabolismR21AI140724 · NIAID · WEILL MEDICAL COLL OF CORNELL UNIV · PI WORGALL, STEFAN · 2018 to 2019
$479k
Howard Hughes Medical InstituteNCATS NIH HHS KL2 TR002385NHLBI NIH HHS T32 HL134629NIAID NIH HHS R01 AI095466NIAID NIH HHS R01 AI151599NIAID NIH HHS R01 AI172027NIAID NIH HHS R21 AI140724NIAID NIH HHS U01 AI095608NIAMS NIH HHS R01 AR070116NICHD NIH HHS DP2 HD101401NIDDK NIH HHS R01 DK126871NIDDK NIH HHS R01 DK132244NIGMS NIH HHS R35 GM131877
6 · The paper itself

Abstract

Dietary fibres can exert beneficial anti-inflammatory effects through microbially fermented short-chain fatty acid metabolites<sup>1,2</sup>, although the immunoregulatory roles of most fibre diets and their microbiota-derived metabolites remain poorly defined. Here, using microbial sequencing and untargeted metabolomics, we show that a diet of inulin fibre alters the composition of the mouse microbiota and the levels of microbiota-derived metabolites, notably bile acids. This metabolomic shift is associated with type 2 inflammation in the intestine and lungs, characterized by IL-33 production, activation of group 2 innate lymphoid cells and eosinophilia. Delivery of cholic acid mimics inulin-induced type 2 inflammation, whereas deletion of the bile acid receptor farnesoid X receptor diminishes the effects of inulin. The effects of inulin are microbiota dependent and were reproduced in mice colonized with human-derived microbiota. Furthermore, genetic deletion of a bile-acid-metabolizing enzyme in one bacterial species abolishes the ability of inulin to trigger type 2 inflammation. Finally, we demonstrate that inulin enhances allergen- and helminth-induced type 2 inflammation. Taken together, these data reveal that dietary inulin fibre triggers microbiota-derived cholic acid and type 2 inflammation at barrier surfaces with implications for understanding the pathophysiology of allergic inflammation, tissue protection and host defence.

Indexed as

Bile Acids and SaltsDietary FiberGastrointestinal MicrobiomeInflammationInulinAnimalsCholic AcidEosinophilsHumansImmunity, InnateInterleukin-33IntestinesLungLymphocytesMetabolomicsMiceBile Acids and SaltsCholic AcidDietary FiberInterleukin-33InulinReceptor, Farnesoid X-Activated

Identifiers

PMID36323778
PMCPMC10576985
OpenAlexW4307931817

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.