Evidence map›Paper›PMID 27933701›Full record

ArticleHelicobacter2017

CCR2 mediates Helicobacter pylori-induced immune tolerance and contributes to mucosal homeostasis.

Xia Sun, Min Zhang, Mohamad El-Zaatari, Gray B Huffnagle, John Y Kao

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Helicobacter, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

1 citing paper in PubMed, 10 citations in OpenAlex.

  1. Article
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 3 institutions in 2 countries.

Xia SunDepartment of Pharmacology, School of Medicine, Shandong University, Jinan, Shandong, China.
Min ZhangDepartment of Internal Medicine, Division of Gastroenterology, University of Michigan Health System, Ann Arbor, MI, USA.
Mohamad El-ZaatariDepartment of Internal Medicine, Division of Gastroenterology, University of Michigan Health System, Ann Arbor, MI, USA.
Gray B HuffnagleDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan Health System, Ann Arbor, MI, USA.
John Y KaoDepartment of Internal Medicine, Division of Gastroenterology, University of Michigan Health System, Ann Arbor, MI, USA.
Michigan Medicine · USShandong University · CNUniversity of Michigan–Ann Arbor · US

Funding

Role of Dendritic Cells in H pylori-induced Treg-mediated Host Immune ToleranceR01DK087708 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAO, JOHN Y · 2011 to 2015
$2.0M
NIDDK NIH HHS R01 DK087708
6 · The paper itself

Abstract

backgroundWe previously demonstrated that H. pylori infection leads to increased induction of regulatory T cells in local and systemic immune compartments. Here, we investigate the role of CCR2 in the tolerogenic programing of dendritic cells in a mouse model of H. pylori infection. MATERIALS AND

methodsCCR2 deficient (CCR2KO) mice and wild-type (Wt) mice infected with H. pylori SS1 strain were analyzed by qPCR and FACS analysis. In vitro, bone marrow-derived DC on day 6 from CCR2KO and Wt mice cocultured with or without H. pylori were examined to determine the impact of CCR2 signaling on dendritic cells function by qPCR, ELISA, and FACS analyses.

resultsAcute H. pylori infection was associated with a threefold increase in CCR2 mRNA expression in the gastric mucosa. H. pylori-infected CCR2KO mice exhibited a higher degree of mucosal inflammation, that is, increased gastritis scores and pro-inflammatory cytokine mRNA levels, but lower degree of H. pylori gastric colonization compared to infected Wt mice. Peripheral H. pylori-specific immune response measured in the CCR2KO spleen was characterized by a higher Th17 response and a lower Treg response. In vitro, CCR2KO bone marrow-derived DC was less mature and shown a lower Treg/Th17 ratio. Moreover, blockade of CCR2 signaling by MCP-1 neutralizing antibody inhibited H. pylori-stimulated bone marrow-derived DC maturation.

conclusionsOur results indicate that CCR2 plays an essential role in H. pylori-induced immune tolerance and shed light on a novel mechanism of CCR2-dependent DC Treg induction, which appears to be important in maintaining mucosal homeostasis during H. pylori infection.

Indexed as

Immune ToleranceAnimalsDendritic CellsDisease Models, AnimalEnzyme-Linked Immunosorbent AssayFlow CytometryHelicobacter InfectionsHelicobacter pyloriHomeostasisMaleMice, Inbred C57BLMice, KnockoutReal-Time Polymerase Chain ReactionReceptors, CCR2T-Lymphocytes, RegulatoryCcr2 protein, mouseReceptors, CCR2adaptive immunityChemokine receptor 2dendritic cellsimmatureimmune tolerance

Identifiers

PMID27933701
PMCPMC5352485
OpenAlexW2559981308

What OpenQuestion holds

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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.