Evidence map›Paper›PMID 28683091›Full record

ArticlePLoS pathogens2017

Endothelial cells are intrinsically defective in xenophagy of Streptococcus pyogenes.

Shiou-Ling Lu, Tsuyoshi Kawabata, Yi-Lin Cheng, Hiroko Omori, Maho Hamasaki, Tatsuya Kusaba, Ryo Iwamoto, Hirokazu Arimoto, Takeshi Noda, Yee-Shin Lin and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

16 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Increasing Rate of FatalMicroorganisms · 2024
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  6. Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  7. Eliminating the invading extracellular and intracellular FnBpFrontiers in cellular and infection microbiology · 2023
    Article
  8. Article
  9. Article
  10. Frontiers in cellular and infection microbiology · 2021
    Review
  11. Article
  12. Nicotinamide Increases Intracellular NADFrontiers in microbiology · 2020
    Article
  13. Article
  14. Group AMicrobiology spectrum · 2019
    Article
  15. Article
  16. 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

11 authors at 4 institutions in 2 countries.

Shiou-Ling LuDepartment of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Tsuyoshi KawabataDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Yi-Lin ChengDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Hiroko OmoriResearch Institute for Microbial Disease, Osaka University, Osaka, Japan.
Maho HamasakiDepartment of Genetics, Graduate School of Medicine, Osaka University, Osaka, Japan.
Tatsuya KusabaDepartment of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Ryo IwamotoDepartment of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.
Hirokazu ArimotoGraduate School of Life Sciences, Tohoku University, Sendai, Japan.ORCID http://orcid.org/0000-0002-0086-6117
Takeshi NodaGraduate School of Frontier Bioscience, Osaka University, Osaka, Japan.ORCID http://orcid.org/0000-0003-3581-7961
Yee-Shin LinDepartment of Microbiology and Immunology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Tamotsu YoshimoriDepartment of Intracellular Membrane Dynamics, Graduate School of Frontier Biosciences, Osaka University, Osaka, Japan.ORCID http://orcid.org/0000-0001-9787-3788
The University of Osaka · JPNational Cheng Kung University · TWNational Yang Ming Chiao Tung University · TWTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Group A Streptococcus (GAS) is deleterious pathogenic bacteria whose interaction with blood vessels leads to life-threatening bacteremia. Although xenophagy, a special form of autophagy, eliminates invading GAS in epithelial cells, we found that GAS could survive and multiply in endothelial cells. Endothelial cells were competent in starvation-induced autophagy, but failed to form double-membrane structures surrounding GAS, an essential step in xenophagy. This deficiency stemmed from reduced recruitment of ubiquitin and several core autophagy proteins in endothelial cells, as demonstrated by the fact that it could be rescued by exogenous coating of GAS with ubiquitin. The defect was associated with reduced NO-mediated ubiquitin signaling. Therefore, we propose that the lack of efficient clearance of GAS in endothelial cells is caused by their intrinsic inability to target GAS with ubiquitin to promote autophagosome biogenesis for xenophagy.

Indexed as

AutophagyCell LineEndothelial CellsEpithelial CellsHost-Pathogen InteractionsHumansPhagosomesStreptococcal InfectionsStreptococcus pyogenesUbiquitinUbiquitin

Identifiers

PMID28683091
PMCPMC5500369
OpenAlexW2732238029

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.