Evidence map›Paper›PMID 34951948›Full record

ArticleCell host & microbe2022

Virulence factors perforate the pathogen-containing vacuole to signal efferocytosis.

Hirotaka Hiyoshi, Bevin C English, Vladimir E Diaz-Ochoa, Tamding Wangdi, Lillian F Zhang, Miako Sakaguchi, Takeshi Haneda, Renée M Tsolis, Andreas J Bäumler

Open access · hybridAbstract read
In one paragraph

Article in Cell host & microbe, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 41 citations in OpenAlex.

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  13. Infection biology ofEcoSal Plus · 2024
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  18. Salmonella spvC gene suppresses macrophage/neutrophil antibacterial defense mediated by gasdermin D.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  19. Review
  20. Cell and Tissue Tropism of Brucella spp.Infection and immunity · 2023
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

Hirotaka HiyoshiDepartment of Bacteriology, Institute of Tropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan; Department of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Bevin C EnglishDepartment of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Vladimir E Diaz-OchoaDepartment of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Tamding WangdiDepartment of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Lillian F ZhangDepartment of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Miako SakaguchiCentral Laboratory, Institute of Tropical Medicine, Nagasaki University, 1-12-4 Sakamoto, Nagasaki 852-8523, Japan.
Takeshi HanedaLaboratory of Microbiology, School of Pharmacy, Kitasato University, 5-9-1, Shirokane, Minato-ku, Tokyo 108-8641, Japan.
Renée M TsolisDepartment of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA.
Andreas J BäumlerDepartment of Medical Microbiology and Immunology, University of California at Davis, One Shields Ave, Davis, CA 95616, USA. Electronic address: ajbaumler@ucdavis.edu.
University of California, Davis · USNagasaki University · JPKitasato University · JP

Funding

Virulence Factors of SalmonellaR01AI044170 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI BAUMLER, ANDREAS J · 1999 to 2022
$8.5M
Exacerbation of colitis by the microbiotaR01AI112445 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler · 2015 to 2026
$6.2M
Microbiota Outgrowth by SalmonellaR01AI096528 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2011 to 2025
$6.1M
Mechanism of Colonization ResistanceR01AI112949 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler · 2016 to 2026
$5.2M
Innate immune sensing of ER stress during bacterial infectionR01AI109799 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TSOLIS, RENEE M · 2014 to 2024
$3.6M
Neutrophil-intrinsic role of SLC11A1/NRAMP1 in control of bacterial infectionR01AI149632 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TSOLIS, RENEE M · 2019 to 2023
$2.4M
Salmonella Host interactionsR37AI044170 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Andreas J Baumler, Renee M Tsolis · 2025 to 2026
$1.2M
Role of NRAMP1/SLC11A1 in Salmonella pathogenesisR21AI143253 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TSOLIS, RENEE M · 2019 to 2020
$432k
Salmonella pathogenicity island 2 triggers pore-induced intracellular trap formation to evade killing by neutrophilsR21AI143929 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HIYOSHI, HIROTAKA · 2020 to 2021
$432k
Dietary copper reconfigures pathogen growthR21AI146432 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2019 to 2020
$432k
The pathogenesis of paratyphoid feverR21AI126080 · NIAID · WASHINGTON UNIVERSITY · PI WANGDI, TAMDING · 2016 to 2017
$426k
Citrobacter illuminates the mechanistic underpinnings of gut biogeographyR21AI153069 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BAUMLER, ANDREAS J · 2020 to 2021
$413k
NIAID NIH HHS R01 AI044170NIAID NIH HHS R01 AI096528NIAID NIH HHS R01 AI109799NIAID NIH HHS R01 AI112445NIAID NIH HHS R01 AI112949NIAID NIH HHS R01 AI149632NIAID NIH HHS R21 AI126080NIAID NIH HHS R21 AI143253NIAID NIH HHS R21 AI143929NIAID NIH HHS R21 AI146432NIAID NIH HHS R21 AI153069NIAID NIH HHS R37 AI044170NIAID NIH HHS R56 AI112949
6 · The paper itself

Abstract

Intracellular pathogens commonly reside within macrophages to find shelter from humoral defenses, but host cell death can expose them to the extracellular milieu. We find intracellular pathogens solve this dilemma by using virulence factors to generate a complement-dependent find-me signal that initiates uptake by a new phagocyte through efferocytosis. During macrophage death, Salmonella uses a type III secretion system to perforate the membrane of the pathogen-containing vacuole (PCV), thereby triggering complement deposition on bacteria entrapped in pore-induced intracellular traps (PITs). In turn, complement activation signals neutrophil efferocytosis, a process that shelters intracellular bacteria from the respiratory burst. Similarly, Brucella employs its type IV secretion system to perforate the PCV membrane, which induces complement deposition on bacteria entrapped in PITs. Collectively, this work identifies virulence factor-induced perforation of the PCV as a strategy of intracellular pathogens to generate a find-me signal for efferocytosis.

Indexed as

VacuolesVirulence FactorsPhagocytosisType III Secretion SystemsType IV Secretion SystemsType III Secretion SystemsType IV Secretion SystemsVirulence FactorsBrucellacomplementefferocytosismacrophageneutrophilSalmonella

Identifiers

PMID34951948
PMCPMC8831471
OpenAlexW4200582457

What OpenQuestion holds

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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.