Evidence map›Paper›PMID 32657447›Full record

ArticleThe EMBO journal2020

A unique bacterial tactic to circumvent the cell death crosstalk induced by blockade of caspase-8.

Hiroshi Ashida, Chihiro Sasakawa, Toshihiko Suzuki

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 58 citations in OpenAlex.

  1. Mechanisms, regulation and clinical relevance of necroptosis.Nature reviews. Molecular cell biology · 2026
    Review
  2. Review
  3. Harnessing PANoptosis for Innate Immune Response.Current pharmaceutical design · 2026
    Article
  4. Differential targeting of human pyroptotic Caspase-5 and Caspase-4 bybioRxiv : the preprint server for biology · 2025
    Article
  5. mBio · 2025
    Article
  6. Article
  7. Review
  8. Manipulating the PANoptosome: baseless hype or a newfound hope for human immunity?Apoptosis : an international journal on programmed cell death · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Necroptosis in bacterial infections.Frontiers in immunology · 2024
    Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Hiroshi AshidaDepartment of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0003-1408-6864
Chihiro SasakawaMedical Mycology Research Center, Chiba University, Chiba, Japan.ORCID 0000-0002-6919-1832
Toshihiko SuzukiDepartment of Bacterial Infection and Host Response, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University (TMDU), Tokyo, Japan.ORCID 0000-0003-3853-0106
Tokyo Medical and Dental University · JPChiba University Hospital · JP

Funding

AMED 19gm6010009h0003Astellas Foundation for Research on Metabolic DisordersGrant-in-Aid for Scientific Research 16H05186GSK Japan Research Grant 2016Hamaguchi Foundation for the Advancement of BiochemistryJapan Foundation for Pediatric ResearchKawano Masanori Memorial Foundation for Promotion of PediatricsNaito FoundationSenri Life Science FoundationTakeda Science FoundationTERUMO FOUNDATION for LIFE SCIENCES and ARTSUehara Memorial Foundation
6 · The paper itself

Abstract

Upon invasive bacterial infection of colonic epithelium, host cells induce several types of cell death to eliminate pathogens. For instance, necroptosis is a RIPK-dependent lytic cell death that serves as a backup system to fully eliminate intracellular pathogens when apoptosis is inhibited; this phenomenon has been termed "cell death crosstalk". To maintain their replicative niche and multiply within cells, some enteric pathogens prevent epithelial cell death by delivering effectors via the type III secretion system. In this study, we found that Shigella hijacks host cell death crosstalk via a dual mechanism: inhibition of apoptosis by the OspC1 effector and inhibition of necroptosis by the OspD3 effector. Upon infection by Shigella, host cells recognize blockade of caspase-8 apoptosis signaling by OspC1 effector as a key danger signal and trigger necroptosis as a backup form of host defense. To counteract this backup defense, Shigella delivers the OspD3 effector, a protease, to degrade RIPK1 and RIPK3, preventing necroptosis. We believe that blockade of host cell death crosstalk by Shigella is a unique intracellular survival tactic for prolonging the bacterium's replicative niche.

Indexed as

NecroptosisBacterial Outer Membrane ProteinsCaspase 8HCT116 CellsHeLa CellsHT29 CellsHumansPeptide HydrolasesReceptor-Interacting Protein Serine-Threonine KinasesShigella flexneriBacterial Outer Membrane ProteinsCASP8 protein, humanCaspase 8Peptide HydrolasesReceptor-Interacting Protein Serine-Threonine KinasesRIPK1 protein, humanRIPK3 protein, humanapoptosiseffectornecroptosisShigella

Identifiers

PMID32657447
PMCPMC7459423
OpenAlexW3041706475

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.