Evidence map›Paper›PMID 26455347›Full record

ArticleImmunology2016

Interleukin-23 (IL-23), independent of IL-17 and IL-22, drives neutrophil recruitment and innate inflammation during Clostridium difficile colitis in mice.

Andrew J McDermott, Nicole R Falkowski, Roderick A McDonald, Chinmay R Pandit, Vincent B Young, Gary B Huffnagle

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.5field-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

50 citing papers in PubMed, 61 citations in OpenAlex.

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  17. Host Immune Responses toTropical medicine and infectious disease · 2023
    Review
  18. Review
  19. Article
  20. Microbiology (Reading, England) · 2023
    Review
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

6 authors at 1 institution in 1 country.

Andrew J McDermottDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Nicole R FalkowskiDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Roderick A McDonaldDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Chinmay R PanditDivision of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI, USA.
Vincent B YoungDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
Gary B HuffnagleDepartment of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, MI, USA.
University of Michigan–Ann Arbor · US

Funding

University of Michigan Center for Gastrointestinal ResearchP30DK034933 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI OWYANG, CHUNG · 1986 to 2021
$22.5M
The Interplay Between Host Immunity and Clostridium difficile PathogenesisU19AI090871 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI YOUNG, VINCENT B · 2010 to 2014
$7.5M
NIAID NIH HHS U19 AI090871NIDDK NIH HHS P30 DK034933
6 · The paper itself

Abstract

Our objective was to determine the role of the inflammatory cytokine interleukin-23 (IL-23) in promoting neutrophil recruitment, inflammatory cytokine expression and intestinal histopathology in response to Clostridium difficile infection. Wild-type (WT) and p19(-/-) (IL-23KO) mice were pre-treated with cefoperazone in their drinking water for 5 days, and after a 2-day recovery period were challenged with spores from C. difficile strain VPI 10463. Interleukin-23 deficiency was associated with significant defects in both the recruitment of CD11b(High) Ly6G(H) (igh) neutrophils to the colon and the expression of neutrophil chemoattractants and stabilization factors including Cxcl1, Cxcl2, Ccl3 and Csf3 within the colonic mucosa as compared with WT animals. Furthermore, the expression of inflammatory cytokines including Il33, Tnf and Il6 was significantly reduced in IL-23-deficient animals. There was also a trend towards less severe colonic histopathology in the absence of IL-23. The induction of Il17a and Il22 was also significantly abrogated in IL-23KO mice. Inflammatory cytokine expression and neutrophilic inflammation were not reduced in IL-17a-deficient mice or in mice treated with anti-IL-22 depleting monoclonal antibody. However, induction of RegIIIg was significantly reduced in animals treated with anti-IL-22 antibody. Taken together, these data indicate that IL-23, but not IL-17a or IL-22, promotes neutrophil recruitment and inflammatory cytokine and chemokine expression in the colon in response to C. difficile infection.

Indexed as

Immunity, InnateNeutrophil InfiltrationAnimalsAntibodies, MonoclonalClostridioides difficileColonDisease Models, AnimalEnterocolitis, PseudomembranousFemaleInflammation MediatorsInterleukin-17Interleukin-22Interleukin-23 Subunit p19InterleukinsIntestinal MucosaMaleAntibodies, MonoclonalIl17a protein, mouseIl23a protein, mouseInflammation MediatorsInterleukin-17Interleukin-22Interleukin-23 Subunit p19InterleukinsPancreatitis-Associated ProteinsProteinsReg3g protein, mouseClostridium difficilecolitisinnate inflammationmucosal inflammationneutrophils

Identifiers

PMID26455347
PMCPMC4693884
OpenAlexW1963308907

What OpenQuestion holds

Textmetadata
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.