Evidence map›Paper›PMID 32150572›Full record

ArticlePLoS pathogens2020

Interferon inducible GBPs restrict Burkholderia thailandensis motility induced cell-cell fusion.

David E Place, Benoit Briard, Parimal Samir, Rajendra Karki, Anannya Bhattacharya, Clifford S Guy, Jennifer L Peters, Sharon Frase, Peter Vogel, Geoffrey Neale and 2 more

Abstract read
In one paragraph

Article in PLoS pathogens, 2020. 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
–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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Significance of the cGAS-STING Pathway in Health and Disease.International journal of molecular sciences · 2023
    Review
  9. Human GBP1 Is Involved in the Repair of Damaged Phagosomes/Endolysosomes.International journal of molecular sciences · 2023
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. MicroRNA-30e-5p Regulates SOCS1 and SOCS3 During Bacterial Infection.Frontiers in cellular and infection microbiology · 2020
    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.

David E PlaceDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Benoit BriardDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Parimal SamirDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Rajendra KarkiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Anannya BhattacharyaDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.ORCID 0000-0001-6385-4028
Clifford S GuyDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Jennifer L PetersCell and Tissue Imaging Center, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Sharon FraseCell and Tissue Imaging Center, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.
Peter VogelVeterinary Pathology Core, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.ORCID 0000-0002-7535-0545
Geoffrey NealeHartwell Center for Bioinformatics & Biotechnology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.ORCID 0000-0003-3776-0858
Masahiro YamamotoDepartment of Immunoparasitology, Osaka University, 3-1 Yamadaoka, Suita, Osaka, Japan.
Thirumala-Devi KannegantiDepartment of Immunology, St. Jude Children's Research Hospital, Memphis, Tennessee, United States of America.ORCID 0000-0002-6395-6443

Funding

Viral Vector Technology (VVTSR)P30CA021765 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI CHARLES ROBERTS · 1985 to 2026
$166.9M
Role of NLR Inflammasomes in Autoinflammatory Diseases and Host DefenseR01AR056296 · NIAMS · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2008 to 2022
$5.9M
The Non-Inflammasome NLRs in Immunity and Host defenseR01AI124346 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2016 to 2026
$5.8M
Inflammatory Caspases in Innate Immunity and InflammationR37AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI Thirumala-Devi Kanneganti · 2017 to 2026
$4.9M
NLR signaling in colitis and colorectal tumorigenesisR01CA163507 · NCI · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2020
$3.5M
Inflammatory Caspases in Innate Immunity and InflammationR01AI101935 · NIAID · ST. JUDE CHILDREN'S RESEARCH HOSPITAL · PI KANNEGANTI, THIRUMALA-DEVI · 2012 to 2016
$2.2M
NCI NIH HHS P30 CA021765NCI NIH HHS R01 CA163507NIAID NIH HHS R01 AI101935NIAID NIH HHS R01 AI124346NIAID NIH HHS R37 AI101935NIAMS NIH HHS R01 AR056296
6 · The paper itself

Abstract

Innate immunity responds to pathogens by producing alarm signals and activating pathways that make host cells inhospitable for pathogen replication. The intracellular bacterium Burkholderia thailandensis invades the cytosol, hijacks host actin, and induces cell fusion to spread to adjacent cells, forming multinucleated giant cells (MNGCs) which promote bacterial replication. We show that type I interferon (IFN) restricts macrophage MNGC formation during B. thailandensis infection. Guanylate-binding proteins (GBPs) expressed downstream of type I IFN were required to restrict MNGC formation through inhibition of bacterial Arp2/3-dependent actin motility during infection. GTPase activity and the CAAX prenylation domain were required for GBP2 recruitment to B. thailandensis, which restricted bacterial actin polymerization required for MNGC formation. Consistent with the effects in in vitro macrophages, Gbp2-/-, Gbp5-/-, GbpChr3-KO mice were more susceptible to intranasal infection with B. thailandensis than wildtype mice. Our findings reveal that IFN and GBPs play a critical role in restricting cell-cell fusion and bacteria-induced pathology during infection.

Indexed as

AnimalsBurkholderiaBurkholderia InfectionsCell FusionGiant CellsGTP-Binding ProteinsInterferon Type IMacrophagesMiceMice, KnockoutNose DiseasesProtein PrenylationGTP-Binding ProteinsInterferon Type I

Identifiers

PMID32150572
PMCPMC7082077

What OpenQuestion holds

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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.