Evidence map›Paper›PMID 32066975›Full record

ArticleNature medicine2020

Interleukin-22-mediated host glycosylation prevents Clostridioides difficile infection by modulating the metabolic activity of the gut microbiota.

Hiroko Nagao-Kitamoto, Jhansi L Leslie, Sho Kitamoto, Chunsheng Jin, Kristina A Thomsson, Merritt G Gillilland, Peter Kuffa, Yoshiyuki Goto, Robert R Jenq, Chiharu Ishii and 10 more

Open access · greenAbstract read
In one paragraph

Article in Nature medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 144 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
144citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 5% 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

144 citing papers in PubMed, 1 synthesis or guideline pooled it, 218 citations in OpenAlex.

  1. Pooled it
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  15. Protection or Vulnerability? The Context-Dependent Memory of Intestinal Inflammation.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  16. World journal of gastroenterology · 2025
    Article
  17. Review
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  19. Review
  20. Article

84 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 6 institutions in 3 countries.

Hiroko Nagao-KitamotoDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.
Jhansi L LeslieDivision of Infectious Disease, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Sho KitamotoDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.ORCID http://orcid.org/0000-0003-3597-6647
Chunsheng JinInstitute of Biomedicine, Department of Medical Biochemistry, University of Gothenburg, Gothenburg, Sweden.ORCID http://orcid.org/0000-0002-0229-102X
Kristina A ThomssonInstitute of Biomedicine, Department of Medical Biochemistry, University of Gothenburg, Gothenburg, Sweden.
Merritt G GillillandDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.
Peter KuffaDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.
Yoshiyuki GotoDivision of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan.
Robert R JenqDepartment of Genomic Medicine, Division of Cancer Medicine, University of Texas MD Anderson Cancer Center, Houston TX, USA.
Chiharu IshiiInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan.
Akiyoshi HirayamaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan.
Anna M SeekatzDivision of Infectious Disease, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Eric C MartensDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Kathryn A EatonDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
John Y KaoDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.
Shinji FukudaInstitute for Advanced Biosciences, Keio University, Tsuruoka, Japan.ORCID http://orcid.org/0000-0001-5161-9880
Peter D R HigginsDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA.
Niclas G KarlssonInstitute of Biomedicine, Department of Medical Biochemistry, University of Gothenburg, Gothenburg, Sweden.
Vincent B YoungDivision of Infectious Disease, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Nobuhiko KamadaDivision of Gastroenterology, University of Michigan Medical School, Ann Arbor, MI, USA. nkamada@umich.edu.ORCID http://orcid.org/0000-0002-1980-4178
University of Michigan · USUniversity of Gothenburg · SEKeio University · JPChiba University · JPThe University of Texas MD Anderson Cancer Center · USUniversity of Tsukuba · JP

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OWYANG, CHUNG · 1986 to 2021
$22.5M
Statistics and Bioinformatics Core - WangU24DK097153 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI BURANT, CHARLES F · 2012 to 2017
$10.1M
Systems biology of Clostridium difficile infectionU01AI124255 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCHLOSS, PATRICK DAVID, YOUNG, VINCENT B · 2016 to 2020
$9.8M
The Metabolomics Data Center and Workbench (MDCW)U01DK097430 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SUBRAMANIAM, SHANKAR · 2012 to 2017
$7.4M
The role of IL-1ß-inducing pathobionts in the pathogenesis of Crohn’s diseaseR01DK108901 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Nobuhiko Kamada · 2017 to 2026
$3.8M
Mechanisms of gut epithelial DUOX-mediated intestinal homeostasisR01DK117565 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI GRASBERGER, HELMUT F, KAO, JOHN Y · 2018 to 2021
$2.0M
Dietary amino acids control the competition between pathogenic and commensal E. coli in inflamed gutR21DK110146 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAMADA, NOBUHIKO · 2016 to 2017
$426k
NIAID NIH HHS U01 AI124255NIDDK NIH HHS P30 DK034933NIDDK NIH HHS R01 DK108901NIDDK NIH HHS R01 DK117565NIDDK NIH HHS R21 DK110146NIDDK NIH HHS U01 DK097430NIDDK NIH HHS U24 DK097153
6 · The paper itself

Abstract

The involvement of host immunity in the gut microbiota-mediated colonization resistance to Clostridioides difficile infection (CDI) is incompletely understood. Here, we show that interleukin (IL)-22, induced by colonization of the gut microbiota, is crucial for the prevention of CDI in human microbiota-associated (HMA) mice. IL-22 signaling in HMA mice regulated host glycosylation, which enabled the growth of succinate-consuming bacteria Phascolarctobacterium spp. within the gut microbiome. Phascolarctobacterium reduced the availability of luminal succinate, a crucial metabolite for the growth of C. difficile, and therefore prevented the growth of C. difficile. IL-22-mediated host N-glycosylation is likely impaired in patients with ulcerative colitis (UC) and renders UC-HMA mice more susceptible to CDI. Transplantation of healthy human-derived microbiota or Phascolarctobacterium reduced luminal succinate levels and restored colonization resistance in UC-HMA mice. IL-22-mediated host glycosylation thus fosters the growth of commensal bacteria that compete with C. difficile for the nutritional niche.

Indexed as

AnimalsBacteriaClostridioides difficileClostridium InfectionsEnterocolitis, PseudomembranousFemaleGastrointestinal MicrobiomeGlycosylationHost Microbial InteractionsHumansInterleukin-22InterleukinsMaleMiceMice, Inbred C57BLMice, KnockoutInterleukin-22Interleukins

Identifiers

PMID32066975
PMCPMC7160049
OpenAlexW3006266099

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.