Evidence map›Paper›PMID 32120337›Full record

ReviewCurrent opinion in microbiology2020

The pyrin inflammasome in host-microbe interactions.

Nicole A Loeven, Natasha P Medici, James B Bliska

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in microbiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 65 citations in OpenAlex.

  1. ThePlants (Basel, Switzerland) · 2026
    Article
  2. ThebioRxiv : the preprint server for biology · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. IFI204 RestrictsMicroorganisms · 2025
    Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. The role of actin cytoskeleton component Arp2/3 in inflammatory response.Frontiers in cell and developmental biology · 2025
    Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. An Update on Familial Mediterranean Fever.International journal of molecular sciences · 2023
    Review
  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 1 institution in 1 country.

Nicole A LoevenDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03768, United States.
Natasha P MediciDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03768, United States; Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, NY 11794, United States.
James B BliskaDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, NH, 03768, United States. Electronic address: James.Bliska@dartmouth.edu.
Dartmouth College · US

Funding

Regulation of host innate and adaptive immunity by bacterial type III effectorsR01AI099222 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BLISKA, JAMES B · 2012 to 2025
$5.9M
Dartmouth Cystic Fibrosis Training ProgramT32HL134598 · NHLBI · DARTMOUTH COLLEGE · PI George A. O'Toole · 2017 to 2026
$1.7M
NHLBI NIH HHS T32 HL134598NIAID NIH HHS R01 AI099222
6 · The paper itself

Abstract

Pyrin is an inflammasome sensor in phagocytes that is activated in response to bacterial toxins and effectors that modify RhoA. Pathogen effector-triggered pyrin activation is analogous to an indirect guard mechanism in plants. Pyrin activation appears to be triggered when RhoA GTPases in a host cell are prevented from binding downstream signaling proteins (transducers). RhoA transducers that control this response include PRK kinases, which negatively regulate pyrin by phosphorylation and binding of 14-3-3 proteins. Microtubules regulate pyrin at different levels and may serve as a platform for inflammasome nucleation. Pyrin increases inflammation in the lung, gut or systemically during infection or intoxication in mouse models and protects against systemic infection by decreasing bacterial loads. Pathogenic Yersinia spp. overcome this protective response using effectors that inhibit the pyrin inflammasome. Gain of function mutations in MEFV, the gene encoding pyrin, cause the autoinflammatory disease Familial Mediterranean Fever. Yersinia pestis may have selected for gain of function MEFV mutations in the human population.

Indexed as

Host Microbial InteractionsActin CytoskeletonAnimalsBacteriaBacterial InfectionsBacterial ToxinsHost-Pathogen InteractionsHumansInflammasomesMicePyrinrhoA GTP-Binding ProteinBacterial ToxinsInflammasomesPyrinrhoA GTP-Binding Protein

Identifiers

PMID32120337
PMCPMC7247927
OpenAlexW3007086876

What OpenQuestion holds

Textmetadata
LicenceTDM
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.