Evidence map›Paper›PMID 31220184›Full record

ArticlePLoS pathogens2019

Blowing epithelial cell bubbles with GumB: ShlA-family pore-forming toxins induce blebbing and rapid cellular death in corneal epithelial cells.

Kimberly M Brothers, Jake D Callaghan, Nicholas A Stella, Julianna M Bachinsky, Mohammed AlHigaylan, Kara L Lehner, Jonathan M Franks, Kira L Lathrop, Elliot Collins, Deanna M Schmitt and 2 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Article
  3. Differential virulence potential of different clades of multidrug-resistantmedRxiv : the preprint server for health sciences · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Bacterial pore-forming toxins.Microbiology (Reading, England) · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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  20. Article
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

12 authors at 2 institutions in 1 country.

Kimberly M BrothersDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.
Jake D CallaghanDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.
Nicholas A StellaDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.
Julianna M BachinskyDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.ORCID 0000-0001-6400-9520
Mohammed AlHigaylanDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.ORCID 0000-0001-6990-7565
Kara L LehnerDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.
Jonathan M FranksCenter for Biological Imaging, University of Pittsburgh, Pittsburgh, PA United States of America.ORCID 0000-0002-5758-185X
Kira L LathropDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.
Elliot CollinsDepartment of Natural Sciences and Mathematics, West Liberty University, West Liberty, WV United States of America.
Deanna M SchmittDepartment of Natural Sciences and Mathematics, West Liberty University, West Liberty, WV United States of America.ORCID 0000-0001-6644-9124
Joseph HorzempaDepartment of Natural Sciences and Mathematics, West Liberty University, West Liberty, WV United States of America.ORCID 0000-0003-0867-5099
Robert M Q ShanksDepartment of Ophthalmology, University of Pittsburgh, Pittsburgh, PA United States of America.ORCID 0000-0002-7699-5396
University of Pittsburgh · USWest Liberty University · US

Funding

WV INBRE: The Inhibitor of Growth Family Member 4 (ING4) inhibits L-Type Amino Acid Transporter 1 (LAT1) expression to suppress Breast CancerP20GM103434 · NIGMS · MARSHALL UNIVERSITY · PI Travis Salisbury · 2012 to 2026
$61.1M
Virus Production and Manipulation of Protein/Gene Expression ModuleP30EY008098 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Ethan A Rossi · 1989 to 2026
$17.8M
Interdisciplinary Visual Sciences (IVS) Traininig ProgramT32EY017271 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Marlene Behrmann, Paul R. Kinchington · 2008 to 2026
$3.6M
NOT-NS-20-030: Use of anchored biologics to treat vesicant induced neovascularizationR01EY027331 · NEI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHANKS, ROBERT M · 2017 to 2021
$1.8M
NEI NIH HHS P30 EY008098NEI NIH HHS R01 EY027331NEI NIH HHS T32 EY017271NIGMS NIH HHS P20 GM103434
6 · The paper itself

Abstract

Medical devices, such as contact lenses, bring bacteria in direct contact with human cells. Consequences of these host-pathogen interactions include the alteration of mammalian cell surface architecture and induction of cellular death that renders tissues more susceptible to infection. Gram-negative bacteria known to induce cellular blebbing by mammalian cells, Pseudomonas and Vibrio species, do so through a type III secretion system-dependent mechanism. This study demonstrates that a subset of bacteria from the Enterobacteriaceae bacterial family induce cellular death and membrane blebs in a variety of cell types via a type V secretion-system dependent mechanism. Here, we report that ShlA-family cytolysins from Proteus mirabilis and Serratia marcescens were required to induce membrane blebbling and cell death. Blebbing and cellular death were blocked by an antioxidant and RIP-1 and MLKL inhibitors, implicating necroptosis in the observed phenotypes. Additional genetic studies determined that an IgaA family stress-response protein, GumB, was necessary to induce blebs. Data supported a model where GumB and shlBA are in a regulatory circuit through the Rcs stress response phosphorelay system required for bleb formation and pathogenesis in an invertebrate model of infection and proliferation in a phagocytic cell line. This study introduces GumB as a regulator of S. marcescens host-pathogen interactions and demonstrates a common type V secretion system-dependent mechanism by which bacteria elicit surface morphological changes on mammalian cells. This type V secretion-system mechanism likely contributes bacterial damage to the corneal epithelial layer, and enables access to deeper parts of the tissue that are more susceptible to infection.

Indexed as

AnimalsBacterial ToxinsCell DeathEpithelial CellsEpithelium, CornealHumansMicePerforinProteusProteus InfectionsRAW 264.7 CellsSerratia InfectionsSerratia marcescensSwineType V Secretion SystemsBacterial ToxinsPerforinType V Secretion Systems

Identifiers

PMID31220184
PMCPMC6586354
OpenAlexW2950731903

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.