Evidence map›Paper›PMID 27682622›Full record

ArticleEuropean journal of immunology2016

IL-1β, IL-18, and eicosanoids promote neutrophil recruitment to pore-induced intracellular traps following pyroptosis.

Ine Jorgensen, Joseph P Lopez, Stefan A Laufer, Edward A Miao

Open access · bronzeAbstract read
In one paragraph

Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 160 citations in OpenAlex.

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  11. Salmonella spvC gene suppresses macrophage/neutrophil antibacterial defense mediated by gasdermin D.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
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  17. Molecular Mechanisms of Pyroptosis.Methods in molecular biology (Clifton, N.J.) · 2023
    Review
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  19. Article
  20. Review

27 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Ine JorgensenDepartment of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Joseph P LopezDepartment of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Stefan A LauferDepartment of Pharmaceutical/Medicinal Chemistry, Institute of Pharmacy, University of Tübingen, Tübingen, Germany.
Edward A MiaoDepartment of Microbiology and Immunology, Center for Gastrointestinal Biology and Disease, and Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
University of North Carolina at Chapel Hill · USUniversity of Tübingen · DE

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Deborah F. Tate · 1985 to 2026
$201.5M
Variation in Human Innate ImmunityU54AI057141 · NIAID · UNIVERSITY OF WASHINGTON · PI COOKSON, BRAD T · 2003 to 2013
$102.3M
GASTROENTEROLOGY RESEARCH TRAININGT32DK007737 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEHZAD Z. SHEIKH · 1996 to 2026
$7.8M
Inflammasome Response to Bacterial InfectionR01AI097518 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MIAO, EDWARD A · 2012 to 2016
$2.0M
Role of caspase-11 in innate immunityR01AI119073 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MIAO, EDWARD A · 2015 to 2019
$1.7M
NCI NIH HHS P30 CA016086NIAID NIH HHS R01 AI097518NIAID NIH HHS R01 AI119073NIAID NIH HHS U54 AI057141NIDDK NIH HHS T32 DK007737
6 · The paper itself

Abstract

Inflammasomes activate caspase-1, initiating a lytic form of programmed cell death termed pyroptosis, which is an important innate immune defense mechanism against intracellular infections. We recently demonstrated in a mouse infection model of pyroptosis that instead of releasing bacteria into the extracellular space, bacteria remain trapped within the pyroptotic cell corpse, termed the pore-induced intracellular trap (PIT). This trapping mediates efferocytosis of the PIT and associated bacteria by neutrophils; bacteria are subsequently killed via neutrophil ROS. Using this pyroptosis model, we now show that the pro-inflammatory cytokines IL-1β and IL-18 and inflammatory lipid mediators termed eicosanoids are required for effective clearance of bacteria downstream of pyroptosis. We further show that IL-1β, IL-18, and eicosanoids affect this in part by mediating neutrophil recruitment to the PIT. This is in addition to our prior findings that complement is also important to attract neutrophils. Thus, the PIT initiates a robust and coordinated innate immune response involving multiple mediators that attract neutrophils to efferocytose the PIT and its entrapped bacteria.

Indexed as

AnimalsCaspase 1Cell MovementCells, CulturedEicosanoidsExtracellular TrapsGram-Positive Bacterial InfectionsImmunity, InnateInflammasomesInterleukin-18Interleukin-1betaMiceMice, Inbred C57BLMice, KnockoutNeutrophilsPorinsCaspase 1EicosanoidsInflammasomesInterleukin-18Interleukin-1betaPorinsReactive Oxygen SpeciesCaspase-1InflammasomeNeutrophil recruitmentPore-induced intracellular trapPyroptosis

Identifiers

PMID27682622
PMCPMC5138142
OpenAlexW2525203665

What OpenQuestion holds

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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.