Evidence map›Paper›PMID 26860464›Full record

ArticleScientific reports2016

Inflammasome components ASC and AIM2 modulate the acute phase of biomaterial implant-induced foreign body responses.

Susan N Christo, Kerrilyn R Diener, Jim Manavis, Michele A Grimbaldeston, Akash Bachhuka, Krasimir Vasilev, John D Hayball

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

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Prevention of the foreign body response to implantable medical devices by inflammasome inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Review
  6. A spike in inflammation.Nature nanotechnology · 2018
    Article
  7. Inflammatory osteolysis: a conspiracy against bone.The Journal of clinical investigation · 2017
    Review
  8. 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

7 authors at 4 institutions in 1 country.

Susan N ChristoExperimental Therapeutics Laboratory, Sansom Institute and Hanson Institute, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, 5000, Australia.
Kerrilyn R DienerExperimental Therapeutics Laboratory, Sansom Institute and Hanson Institute, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, 5000, Australia.
Jim ManavisCentre for Neurological Diseases, SA Pathology, Adelaide, SA 5000, Australia.
Michele A GrimbaldestonCentre for Cancer Biology, University of South Australia and SA Pathology, SA 5000, Australia.
Akash BachhukaMawson Institute, University of South Australia, Adelaide, SA 5095, Australia.
Krasimir VasilevMawson Institute, University of South Australia, Adelaide, SA 5095, Australia.
John D HayballExperimental Therapeutics Laboratory, Sansom Institute and Hanson Institute, School of Pharmacy and Medical Science, University of South Australia, Adelaide, SA, 5000, Australia.
University of South Australia · AUCentre for Cancer Biology · AUSouth Australia Pathology · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Detailing the inflammatory mechanisms of biomaterial-implant induced foreign body responses (FBR) has implications for revealing targetable pathways that may reduce leukocyte activation and fibrotic encapsulation of the implant. We have adapted a model of poly(methylmethacrylate) (PMMA) bead injection to perform an assessment of the mechanistic role of the ASC-dependent inflammasome in this process. We first demonstrate that ASC(-/-) mice subjected to PMMA bead injections had reduced cell infiltration and altered collagen deposition, suggesting a role for the inflammasome in the FBR. We next investigated the NLRP3 and AIM2 sensors because of their known contributions in recognising damaged and apoptotic cells. We found that NLRP3 was dispensable for the fibrotic encapsulation; however AIM2 expression influenced leukocyte infiltration and controlled collagen deposition, suggesting a previously unexplored link between AIM2 and biomaterial-induced FBR.

Indexed as

Acute DiseaseAdsorptionAnimalsApoptosis Regulatory ProteinsBiocompatible MaterialsBlood ProteinsCARD Signaling Adaptor ProteinsCollagen Type ICollagen Type IICytokinesDNA-Binding ProteinsEnzyme-Linked Immunosorbent AssayForeign BodiesImmunity, InnateImmunophenotypingInflammasomesAim2 protein, mouseApoptosis Regulatory ProteinsBiocompatible MaterialsBlood ProteinsCARD Signaling Adaptor ProteinsCollagen Type ICollagen Type IICytokinesDNA-Binding ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePolymethyl MethacrylatePycard protein, mouse

Identifiers

PMID26860464
PMCPMC4748295
OpenAlexW2405632856

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.