Evidence map›Paper›PMID 26456705›Full record

ArticleScientific reports2015

Induction of Mincle by Helicobacter pylori and consequent anti-inflammatory signaling denote a bacterial survival strategy.

Savita Devi, Eerappa Rajakumara, Niyaz Ahmed

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.0field-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

29 citing papers in PubMed, 50 citations in OpenAlex.

  1. [Molecular mechanisms of chronic gastric mucosal inflammation induced byZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
    Review
  2. Dysregulated macrophage immunity inFrontiers in immunology · 2025
    Review
  3. Review
  4. Review
  5. iScience · 2024
    Article
  6. Review
  7. Article
  8. Immune Biology and Persistence of Helicobacter pylori in Gastric Diseases.Current topics in microbiology and immunology · 2023
    Article
  9. Innate Immunity Crosstalk withInternational journal of molecular sciences · 2022
    Review
  10. Article
  11. Journal of oral microbiology · 2022
    Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Immunostimulation byThe Journal of biological chemistry · 2020
    Article
  17. C-Type Lectin Receptors in Host Defense Against Bacterial Pathogens.Frontiers in cellular and infection microbiology · 2020
    Review
  18. Article
  19. The Interaction ofJournal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  20. 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

3 authors at 2 institutions in 1 country.

Savita DeviPathogen Biology Laboratory, Department of Biotechnology and Bioinformatics, University of Hyderabad, Hyderabad, Telangana, India.
Eerappa RajakumaraDepartment of Biotechnology, Indian Institute of Technology Hyderabad, Yeddumailaram, Telangana, India.
Niyaz AhmedPathogen Biology Laboratory, Department of Biotechnology and Bioinformatics, University of Hyderabad, Hyderabad, Telangana, India.
University of Hyderabad · INIndian Institute of Technology Hyderabad · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evasion of innate immune recognition is one of the key strategies for persistence of Helicobacter pylori, by virtue of its ability to modulate or escape the host innate immune receptors and signaling pathways. C-type lectin receptors (CLRs) predominantly expressed by macrophages are pivotal in tailoring immune response against pathogens. The recognition of glyco or carbohydrate moieties by Mincle (Macrophage inducible C-type lectin) is emerging as a crucial element in anti-fungal and anti-mycobacterial immunity. Herein, we demonstrate the role of Mincle in modulation of innate immune response against H. pylori infection. Our results revealed an upregulated expression of Mincle which was independent of direct host cell contact. Upon computational modelling, Mincle was observed to interact with the Lewis antigens of H. pylori LPS and possibly activating an anti-inflammatory cytokine production, thereby maintaining a balance between pro- and anti-inflammatory cytokine production. Furthermore, siRNA mediated knockdown of Mincle in human macrophages resulted in up regulation of pro-inflammatory cytokines and consequent down regulation of anti-inflammatory cytokines. Collectively, our study demonstrates a novel mechanism employed by H. pylori to escape clearance by exploiting functional plasticity of Mincle to strike a balance between pro-and anti-inflammatory responses ensuring its persistence in the host.

Indexed as

Immune EvasionAmino Acid SequenceBinding SitesCell LineGene Expression RegulationHelicobacter pyloriHumansInterleukin-10Lectins, C-TypeLipopolysaccharidesMacrophage ActivationMacrophagesModels, MolecularMolecular Sequence DataProtein BindingProtein Interaction Domains and MotifsCLEC4D protein, humanIL10 protein, humanInterleukin-10Lectins, C-Typelipopolysaccharide, Helicobacter pyloriLipopolysaccharidesReceptors, ImmunologicRNA, Small InterferingTumor Necrosis Factor-alpha

Identifiers

PMID26456705
PMCPMC4601021
OpenAlexW1962130714

What OpenQuestion holds

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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.