Evidence map›Paper›PMID 22509021›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Induction of microRNA-155 is TLR- and type IV secretion system-dependent in macrophages and inhibits DNA-damage induced apoptosis.

Manuel Koch, Hans-Joachim Mollenkopf, Uwe Klemm, Thomas F Meyer

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Non-coding RNA Networks in Infection.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  3. Dysregulated macrophage immunity inFrontiers in immunology · 2025
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. MicroRNA Modulation of Host Immune Response and Inflammation Triggered byInternational journal of molecular sciences · 2021
    Review
  14. Article
  15. Four Chromosomal Type IV Secretion Systems inFrontiers in microbiology · 2020
    Review
  16. Deregulation of miRNA inJournal of clinical medicine · 2019
    Article
  17. Review
  18. Review
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Manuel KochDepartment of Molecular Biology, Max Planck Institute for Infection Biology, Berlin 10117, Germany.
Hans-Joachim Mollenkopf
Uwe Klemm
Thomas F Meyer
Max Planck Institute for Infection Biology · DEMax Planck Society · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Helicobacter pylori is a gastric pathogen responsible for a high disease burden worldwide. Deregulated inflammatory responses, possibly involving macrophages, are implicated in H. pylori-induced pathology, and microRNAs, such as miR-155, have recently emerged as crucial regulators of innate immunity and inflammatory responses. miR-155 is regulated by Toll-like receptor (TLR) ligands in monocyte-derived cells and has been shown to be induced in macrophages during H. pylori infection. Here, we investigated the regulation of miR-155 expression in primary murine bone marrow-derived macrophages (BMMs) during H. pylori infection and examined the downstream mRNA targets of this microRNA using microarray analysis. We report TLR2/4- and NOD1/2-independent up-regulation of miR-155, which was found to be dependent on the major H. pylori pathogenicity determinant, the type IV secretion system (T4SS). miR-155 expression was dependent on NF-κB signaling but was independent of CagA. Microarray analysis identified known gene targets of miR-155 in BMMs during H. pylori infection that are proapoptotic. We also identified and validated miR-155 binding sites in the 3' UTRs of the targets, Tspan14, Lpin1, and Pmaip1. We observed that H. pylori-infected miR-155(-/-) BMMs were significantly more susceptible to cisplatin DNA damage-induced apoptosis than were wild-type BMMs. Thus, our data suggest a function for the prototypical H. pylori pathogenicity factor, the T4SS, in the up-regulation of miR-155 in BMMs. We propose the antiapoptotic effects of miR-155 could enhance macrophage resistance to apoptosis induced by DNA damage during H. pylori infection.

Indexed as

ApoptosisAdaptor Proteins, Vesicular TransportAnimalsAntigens, BacterialBacterial ProteinsCell LineCells, CulturedDNA DamageFemaleGene Expression ProfilingHelicobacter pyloriHost-Pathogen InteractionsMacrophagesMaleMiceMice, Inbred C57BLAdaptor Proteins, Vesicular TransportAntigens, BacterialBacterial ProteinscagA protein, Helicobacter pyloriMicroRNAsMirn155 microRNA, mouseMyd88 protein, mouseMyeloid Differentiation Factor 88Receptor-Interacting Protein Serine-Threonine Kinase 2Receptor-Interacting Protein Serine-Threonine KinasesRipk2 protein, mouseTicam1 protein, mouseToll-Like Receptor 2Toll-Like Receptor 4Toll-Like ReceptorsVirulence Factors

Identifiers

PMID22509021
PMCPMC3358876
OpenAlexW2099350622

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.