Evidence map›Paper›PMID 32973786›Full record

ReviewFrontiers in immunology2020

Caspase-11 Non-canonical Inflammasomes in the Lung.

Changhoon Oh, Ambika Verma, Youssef Aachoui

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. LPS-aggregating proteins GBP1 and GBP2 are each sufficient to enhance caspase-4 activation both in cellulo and in vitro.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Review
  10. Article
  11. Caspase-4/11 exacerbates disease severity in SARS-CoV-2 infection by promoting inflammation and immunothrombosis.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Epithelial Pyroptosis in Host Defense.Journal of molecular biology · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. iScience · 2021
    Article
  17. Article
  18. 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.

Changhoon OhDepartment of Microbiology and Immunology, Center for Microbial Pathogenesis and Host Responses, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
Ambika VermaDepartment of Microbiology and Immunology, Center for Microbial Pathogenesis and Host Responses, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
Youssef AachouiDepartment of Microbiology and Immunology, Center for Microbial Pathogenesis and Host Responses, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
University of Arkansas for Medical Sciences · US

Funding

Study of the Cell-specific Inflammasome Responses During Defense Against Gram-negative BacteriaP20GM103625 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI AACHOUI, YOUSSEF · 2012 to 2021
$21.5M
Mechanisms of Inflammasome Defense against Cytosol-invasive BacteriaK22AI132489 · NIAID · UNIV OF ARKANSAS FOR MED SCIS · PI AACHOUI, YOUSSEF · 2018 to 2019
$269k
NIAID NIH HHS K22 AI132489NIGMS NIH HHS P20 GM103625
6 · The paper itself

Abstract

The airway epithelium and underlying innate immune cells comprise the first line of host defense in the lung. They recognize pathogen-associated molecular patterns (PAMPs) using membrane-bound receptors, as well as cytosolic receptors such as inflammasomes. Inflammasomes activate inflammatory caspases, which in turn process and release the inflammatory cytokines IL-1β and IL-18. Additionally, inflammasomes trigger a form of lytic cell death termed pyroptosis. One of the most important inflammasomes at the host-pathogen interface is the non-canonical caspase-11 inflammasome that responds to LPS in the cytosol. Caspase-11 is important in defense against Gram-negative pathogens, and can drive inflammatory diseases such as LPS-induced sepsis. However, pathogens can employ evasive strategies to minimize or evade host caspase-11 detection. In this review, we present a comprehensive overview of the function of the non-canonical caspase-11 inflammasome in sensing of cytosolic LPS, and its mechanism of action with particular emphasis in the role of caspase-11 in the lung. We also explore some of the strategies pathogens use to evade caspase-11.

Indexed as

Immunity, InnateAnimalsCaspase 1CaspasesGram-Negative BacteriaHost-Pathogen InteractionsHumansInflammasomesLipopolysaccharidesLungPneumonia, BacterialPyroptosisSignal TransductionCaspase 1caspase 11, humanCaspasesInflammasomesLipopolysaccharidesBurkholderia thailandensis lung defensecaspase-11gasdermin DGbpsinflammasomesLPSpore intracellular traps (PIT)

Identifiers

PMID32973786
PMCPMC7472987
OpenAlexW3080792270

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.