Evidence map›Paper›PMID 30531979›Full record

ArticleNature microbiology2019

A multicomponent toxin from Bacillus cereus incites inflammation and shapes host outcome via the NLRP3 inflammasome.

Anukriti Mathur, Shouya Feng, Jenni A Hayward, Chinh Ngo, Daniel Fox, Ines I Atmosukarto, Jason D Price, Kristina Schauer, Erwin Märtlbauer, Avril A B Robertson and 5 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

83 citing papers in PubMed, 122 citations in OpenAlex.

  1. Virulence · 2026
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  3. The gasdermin family: from pyroptosis mechanisms to therapeutic targets.Signal transduction and targeted therapy · 2026
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  7. HypervirulentMicrobiology spectrum · 2026
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  18. Article
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23 more citing papers are in PubMed but not listed here.

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

15 authors at 6 institutions in 3 countries.

Anukriti MathurDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Shouya FengDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Jenni A HaywardDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Chinh NgoDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Daniel FoxDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Ines I AtmosukartoLipotek Pty Ltd, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Jason D PriceLipotek Pty Ltd, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Kristina SchauerDepartment of Veterinary Sciences, Faculty of Veterinary Medicine, Ludwig-Maximilians-Universität München, Oberschleißheim, Germany.ORCID http://orcid.org/0000-0002-1453-9002
Erwin MärtlbauerDepartment of Veterinary Sciences, Faculty of Veterinary Medicine, Ludwig-Maximilians-Universität München, Oberschleißheim, Germany.
Avril A B RobertsonSchool of Chemistry and Molecular Biosciences, The University of Queensland, Brisbane, Queensland, Australia.ORCID http://orcid.org/0000-0002-9652-8357
Gaetan BurgioDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.
Edward M FoxCommonwealth Scientific and Industrial Research Organisation (CSIRO) Agriculture and Food, Werribee, Victoria, Australia.
Stephen H LepplaMicrobial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Nadeem O KaakoushSchool of Medical Sciences, UNSW Sydney, Sydney, New South Wales, Australia.
Si Ming ManDepartment of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia. siming.man@anu.edu.au.ORCID http://orcid.org/0000-0002-5079-2857
Australian National University · AULudwig-Maximilians-Universität München · DECommonwealth Scientific and Industrial Research Organisation · AUNational Institutes of Health · USThe University of Queensland · AUUNSW Sydney · AU

Funding

Pathophysiological Actions of the Anthrax ToxinsZIAAI001032 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LEPPLA, STEPHEN · 2009 to 2025
$10.9M
Molecular Genetics and Pathogenesis of AnthraxZIAAI001030 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LEPPLA, STEPHEN · 2009 to 2025
$9.5M
Intramural NIH HHS ZIA AI001030
6 · The paper itself

Abstract

Host recognition of microbial components is essential in mediating an effective immune response. Cytosolic bacteria must secure entry into the host cytoplasm to facilitate replication and, in doing so, liberate microbial ligands that activate cytosolic innate immune sensors and the inflammasome. Here, we identified a multicomponent enterotoxin, haemolysin BL (HBL), that engages activation of the inflammasome. This toxin is highly conserved among the human pathogen Bacillus cereus. The three subunits of HBL bind to the cell membrane in a linear order, forming a lytic pore and inducing activation of the NLRP3 inflammasome, secretion of interleukin-1β and interleukin-18, and pyroptosis. Mechanistically, the HBL-induced pore results in the efflux of potassium and triggers the activation of the NLRP3 inflammasome. Furthermore, HBL-producing B. cereus induces rapid inflammasome-mediated mortality. Pharmacological inhibition of the NLRP3 inflammasome using MCC950 prevents B. cereus-induced lethality. Overall, our results reveal that cytosolic sensing of a toxin is central to the innate immune recognition of infection. Therapeutic modulation of this pathway enhances host protection against deadly bacterial infections.

Indexed as

InflammationAnimalsBacillus cereusBacterial ProteinsCell MembraneCells, CulturedCulture Media, ConditionedEnterotoxinsFemaleHemolysin ProteinsImmunity, InnateInflammasomesMacrophagesMaleMiceMice, Mutant StrainsBacterial ProteinsCulture Media, ConditionedEnterotoxinshemolysin BL protein, BacillusHemolysin ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePotassium

Identifiers

PMID30531979
PMCPMC7685251
OpenAlexW2902435763

What OpenQuestion holds

Textmetadata
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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.