Evidence map›Paper›PMID 27573815›Full record

ArticleThe Journal of experimental medicine2016

Pyroptosis triggers pore-induced intracellular traps (PITs) that capture bacteria and lead to their clearance by efferocytosis.

Ine Jorgensen, Yue Zhang, Bryan A Krantz, Edward A Miao

Abstract read
In one paragraph

Article in The Journal of experimental medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 263 papers.

0numbers the graph read from it
0cells of the map it votes in
263citing papers in PubMed
–field-weighted citation impact
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

263 citing papers in PubMed.

  1. Disulfidptosis: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Delayed disulfiram targeting GSDMD-NETs axis rescues sepsis by limiting bacterial spread and lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  9. Review
  10. Article
  11. Review
  12. Infection strategies ofGut microbes reports · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Human non-canonical inflammasomes activate CASP3 to limit intracellularbioRxiv : the preprint server for biology · 2025
    Article
  17. Article
  18. Review
  19. Article
  20. Review

203 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.

Ine JorgensenDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.ORCID 0000-0002-4183-156X
Yue ZhangDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.
Bryan A KrantzDepartment of Microbial Pathogenesis, University of Maryland Dental School, Baltimore, MD 21201.ORCID 0000-0002-4911-5824
Edward A MiaoDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 Center for Gastrointestinal Biology and Disease, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599 emiao@med.unc.edu.ORCID 0000-0001-7295-3490

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
Variation in Human Innate ImmunityU54AI057141 · NIAID · UNIVERSITY OF WASHINGTON · PI HAYDEN, HILLARY · 2003 to 2013
$102.3M
GASTROENTEROLOGY RESEARCH TRAININGT32DK007737 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SHEHZAD Z. SHEIKH · 1996 to 2026
$7.8M
Physical Principles of Bacterial Toxin Translocation across MembranesR01AI077703 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI KRANTZ, BRYAN ANDREW · 2008 to 2017
$3.3M
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
ImageStreamX Mark IIS10OD017984 · OD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FISHER, NANCY C. · 2015 to 2015
$418k
NCI NIH HHS P30 CA016086NIAID NIH HHS R01 AI077703NIAID NIH HHS R01 AI097518NIAID NIH HHS R01 AI119073NIAID NIH HHS U54 AI057141NIDDK NIH HHS T32 DK007737NIH HHS S10 OD017984
6 · The paper itself

Abstract

Inflammasomes activate caspase-1 in response to cytosolic contamination or perturbation. This inflammatory caspase triggers the opening of the GSDMD pore in the plasma membrane, resulting in lytic cell death called pyroptosis. We had previously assumed that pyroptosis releases intracellular bacteria to the extracellular space. Here, we find that viable bacteria instead remain trapped within the cellular debris of pyroptotic macrophages. This trapping appears to be an inevitable consequence of how osmotic lysis ruptures the plasma membrane, and may also apply to necroptosis and some forms of nonprogrammed necrosis. Although membrane tears release soluble cytosolic contents, they are small enough to retain organelles and bacteria. We call this structure the pore-induced intracellular trap (PIT), which is conceptually parallel to the neutrophil extracellular trap (NET). The PIT coordinates innate immune responses via complement and scavenger receptors to drive recruitment of and efferocytosis by neutrophils. Ultimately, this secondary phagocyte kills the bacteria. Hence, caspase-1-driven pore-induced cell death triggers a multifaceted defense against intracellular bacteria facilitated by trapping the pathogen within the cellular debris. Bona fide intracellular bacterial pathogens, such as Salmonella, must prevent or delay pyroptosis to avoid being trapped in the PIT and subsequently killed by neutrophils.

Indexed as

PhagocytosisPyroptosisAnimalsComplement System ProteinsGreen Fluorescent ProteinsIntracellular SpaceMacrophagesMiceMice, Inbred C57BLMicrobial ViabilityNecrosisNeutrophilsReceptors, ScavengerSalmonella typhimuriumSolubilityComplement System ProteinsGreen Fluorescent ProteinsReceptors, Scavenger

Identifiers

PMID27573815
PMCPMC5030797

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Registered trials

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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.