Evidence map›Paper›PMID 31632394›Full record

ArticleFrontiers in immunology2019

Nigericin Promotes NLRP3-Independent Bacterial Killing in Macrophages.

Heather Armstrong, Michael Bording-Jorgensen, Richard Chan, Eytan Wine

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Role of NLRP3 inflammasome-mediated neuronal pyroptosis and neuroinflammation in neurodegenerative diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  8. Review
  9. GSDMD-mediated pyroptosis restrains intracellularFrontiers in cellular and infection microbiology · 2023
    Article
  10. Role of NLRP3 inflammasome in systemic sclerosis.Arthritis research & therapy · 2022
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. ASC-Mediated Inflammation and Pyroptosis AttenuatesPathogens (Basel, Switzerland) · 2020
    Article
  16. Cellular Models and Assays to Study NLRP3 Inflammasome Biology.International journal of molecular sciences · 2020
    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

4 authors at 1 institution in 1 country.

Heather ArmstrongDepartment of Pediatrics, University of Alberta, Edmonton, AB, Canada.
Michael Bording-JorgensenCentre of Excellence for Gastrointestinal Inflammation and Immunity Research (CEGIIR), University of Alberta, Edmonton, AB, Canada.
Richard ChanCentre of Excellence for Gastrointestinal Inflammation and Immunity Research (CEGIIR), University of Alberta, Edmonton, AB, Canada.
Eytan WineDepartment of Pediatrics, University of Alberta, Edmonton, AB, Canada.
University of Alberta · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered microbiota has been associated with a number of diseases, including inflammatory bowel diseases, diabetes, and cancer. This dysregulation is thought to relate the host inflammatory response to enteric pathogens. Macrophages play a key role in host response to microbes and are involved in bacterial killing and clearance. This process is partially mediated through the potassium efflux-dependent, cytosolic, PYCARD-containing inflammasome protein complex. Surprisingly, we discovered an alternative mechanism for bacterial killing, independent of the NLRP3 inflammasome/PYCARD. Using the NLRP3 inflammasome-deficient Raw 264.7 and PYCARD-deficient J77 macrophages, which both lack PYCARD, we found that the potassium efflux activator nigericin enhances bacterial killing. Macrophage response to nigericin was examined by RT gene profiling and subsequent qPCR, which demonstrated altered expression of a series of genes involved in the IL-18 bacterial killing pathway. Based on our results we propose a model of bacterial killing, unrelated to NLRP3 inflammasome activation in macrophage cells. Improving understanding of the molecular pathways driving bacterial clearance within macrophage cells will aid in the development of novel immune-targeted therapeutics in a number of diseases.

Indexed as

AnimalsAnti-Bacterial AgentsBacteriaCytotoxicity, ImmunologicHost-Pathogen InteractionsImmunity, InnateInflammasomesMacrophagesMiceMicrobial ViabilityModels, BiologicalNigericinNLR Family, Pyrin Domain-Containing 3 ProteinPhagocytosisRAW 264.7 CellsSignal TransductionAnti-Bacterial AgentsInflammasomesNigericinNLR Family, Pyrin Domain-Containing 3 ProteinCitrobacter rodentiuminflammasomeinflammatory bowel diseasesnigericinNLRP3

Identifiers

PMID31632394
PMCPMC6779719
OpenAlexW2978794097

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.