Evidence map›Paper›PMID 24220299›Full record

ArticleMucosal immunology2014

Contrasting immune responses mediate Campylobacter jejuni-induced colitis and autoimmunity.

A Malik, D Sharma, J St Charles, L A Dybas, L S Mansfield

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

42 citing papers in PubMed, 60 citations in OpenAlex.

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  17. IL-23 Contributes toFrontiers in immunology · 2020
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  18. Review
  19. Fecal Microbiota Transplantation in Neurological Disorders.Frontiers in cellular and infection microbiology · 2020
    Review
  20. Human Immunity AgainstImmune network · 2019
    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

5 authors at 1 institution in 1 country.

A Malik1] Comparative Enteric Diseases Laboratory, Michigan State University, East Lansing, Michigan, USA [2] Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA.
D SharmaDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA.
J St Charles1] Comparative Enteric Diseases Laboratory, Michigan State University, East Lansing, Michigan, USA [2] Comparative Medicine and Integrative Biology Program, Michigan State University, East Lansing, Michigan, USA.
L A DybasComparative Enteric Diseases Laboratory, Michigan State University, East Lansing, Michigan, USA.
L S Mansfield1] Comparative Enteric Diseases Laboratory, Michigan State University, East Lansing, Michigan, USA [2] Department of Microbiology and Molecular Genetics, Michigan State University, East Lansing, Michigan, USA.
Michigan State University · US

Funding

The Impact of Microbiome Composition, Diversity, and Function on Enteric DiseaseU19AI090872 · NIAID · MICHIGAN STATE UNIVERSITY · PI MANSFIELD, LINDA S. · 2010 to 2014
$7.1M
NIAID NIH HHS N01 AI030058NIAID NIH HHS N01-AI-30058NIAID NIH HHS U19 AI090872NIAID NIH HHS U19AI090872
6 · The paper itself

Abstract

Campylobacter jejuni is a leading cause of foodborne enteritis that has been linked to the autoimmune neuropathy, Guillain Barré syndrome (GBS). C57BL/6 interleukin (IL)-10(+/+) and congenic IL-10(-/-) mice serve as C. jejuni colonization and colitis models, respectively, but a mouse model for GBS is lacking. We demonstrate that IL-10(-/-) mice infected with a C. jejuni colitogenic human isolate had significantly upregulated type 1 and 17 but not type 2 cytokines in the colon coincident with infiltration of phagocytes, T cells and innate lymphoid cells (ILCs). Both ILC and T cells participated in interferon-γ (IFN-γ), IL-17, and IL-22 upregulation but in a time- and organ-specific manner. T cells were, however, necessary for colitis as mice depleted of Thy-1(+) cells were protected while neither Rag1(-/-) nor IL-10R blocked Rag1(-/-) mice developed colitis after infection. Depleting IFN-γ, IL-17, or both significantly ameliorated colitis and drove colonic responses toward type 2 cytokine and antibody induction. In contrast, C. jejuni GBS patient strains induced mild colitis associated with blunted type 1/17 but enhanced type 2 responses. Moreover, the type 2 but not type 1/17 antibodies cross-reacted with peripheral nerve gangliosides demonstrating autoimmunity.

Indexed as

AutoimmunityAnimalsAntibodies, BacterialCampylobacter InfectionsCampylobacter jejuniColitisCytokinesDisease Models, AnimalImmunity, CellularImmunity, InnateImmunoglobulin Class SwitchingImmunoglobulin GInterleukin-10MiceMice, KnockoutSeverity of Illness IndexAntibodies, BacterialCytokinesImmunoglobulin GInterleukin-10

Identifiers

PMID24220299
PMCPMC4112758
OpenAlexW2029782308

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.