Evidence map›Paper›PMID 26168305›Full record

ArticlePloS one2015

Defining the Roles of IFN-γ and IL-17A in Inflammation and Protection against Helicobacter pylori Infection.

Louise Sjökvist Ottsjö, Carl-Fredrik Flach, Staffan Nilsson, Rene de Waal Malefyt, Anna K Walduck, Sukanya Raghavan

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.8field-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

11 citing papers in PubMed, 38 citations in OpenAlex.

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  8. Identification of Two Lpp20 CD4Frontiers in microbiology · 2018
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 4 institutions in 3 countries.

Louise Sjökvist OttsjöDepartment of Microbiology & Immunology, University of Gothenburg, Gothenburg, Sweden.
Carl-Fredrik FlachDepartment of Microbiology & Immunology, University of Gothenburg, Gothenburg, Sweden.
Staffan NilssonDepartment of Mathematical Sciences, Chalmers University of Technology, Gothenburg, Sweden.
Rene de Waal MalefytDepartment of Immunology, Merck Research Laboratories, Palo Alto, California, United States of America.
Anna K WalduckSchool of Applied Sciences, RMIT University, Bundoora, Victoria, Australia.
Sukanya RaghavanDepartment of Microbiology & Immunology, University of Gothenburg, Gothenburg, Sweden.
University of Gothenburg · SEChalmers University of Technology · SEMerck & Co., Inc., Rahway, NJ, USA (United States) · USRMIT University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD4+ T cells have been shown to be essential for vaccine-induced protection against Helicobacter pylori infection. However, the effector mechanisms leading to reductions in the gastric bacterial loads of vaccinated mice remain unclear. We have investigated the function of IFN-γ and IL-17A for vaccine-induced protection and inflammation (gastritis) using IFN-γ-gene-knockout (IFN-γ-/-) mice, after sublingual or intragastric immunization with H. pylori lysate antigens and cholera toxin. Bacteria were enumerated in the stomachs of mice and related to the gastritis score and cellular immune responses. We report that sublingually and intragastrically immunized IFN-γ-/- mice had significantly reduced bacterial loads similar to immunized wild-type mice compared to respective unimmunized infection controls. The reduction in bacterial loads in sublingually and intragastrically immunized IFN-γ-/- mice was associated with significantly higher levels of IL-17A in stomach extracts and lower gastritis scores compared with immunized wild-type mice. To study the role of IL-17A for vaccine-induced protection in sublingually immunized IFN-γ-/- mice, IL-17A was neutralized in vivo at the time of infection. Remarkably, the neutralization of IL-17A in sublingually immunized IFN-γ-/- mice completely abolished protection against H. pylori infection and the mild gastritis. In summary, our results suggest that IFN-γ responses in the stomach of sublingually immunized mice promote vaccine-induced gastritis, after infection with H. pylori but that IL-17A primarily functions to reduce the bacterial load.

Indexed as

AnimalsAntigens, BacterialCell ProliferationGene Expression RegulationHelicobacter InfectionsHelicobacter pyloriImmunizationInflammationInterferon-gammaInterleukin-17Lymph NodesMice, Inbred C57BLNeutralization TestsSpleenStomachAntigens, BacterialInterferon-gammaInterleukin-17

Identifiers

PMID26168305
PMCPMC4500503
OpenAlexW2160807406

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.