Evidence map›Paper›PMID 20638366›Full record

ArticleBiochemical and biophysical research communications2010

Anthrax lethal toxin activates the inflammasome in sensitive rat macrophages.

Zachary L Newman, Devorah Crown, Stephen H Leppla, Mahtab Moayeri

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. TheMicrobiology spectrum · 2019
    Review
  9. Review
  10. Article
  11. Bacterial Exotoxins and the Inflammasome.Frontiers in immunology · 2015
    Review
  12. Article
  13. Review
  14. Article
  15. Small molecule inhibitors of anthrax lethal factor toxin.Bioorganic & medicinal chemistry · 2014
    Article
  16. NLRP3 inflammasome activation induced by engineered nanomaterials.Small (Weinheim an der Bergstrasse, Germany) · 2013
    Review
  17. Article
  18. Review
  19. Anthrax and the inflammasome.Microbes and infection · 2012
    Review
  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

4 authors at 2 institutions in 1 country.

Zachary L NewmanLaboratory of Bacterial Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 33 North Drive, Building 33, Room 1W20B, Bethesda, MD 20892, USA. newmanz@niaid.nih.gov
Devorah Crown
Stephen H Leppla
Mahtab Moayeri
National Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

Comparative Medicine Infectious Diseases- BethesdaZIGAI001047 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI ELKINS, WILLIAM · 2009 to 2025
$535.6M
Intramural NIH HHS Z99 AI999999
6 · The paper itself

Abstract

Anthrax lethal toxin (LT) is an important virulence factor for Bacillus anthracis. In mice, LT lyses macrophages from certain inbred strains in less than 2h by activating the Nlrp1b inflammasome and caspase-1, while macrophages from other strains remain resistant to the toxin's effects. We analyzed LT effects in toxin-sensitive and resistant rat macrophages to test if a similar pathway was involved in rat macrophage death. LT activates caspase-1 in rat macrophages from strains harboring LT-sensitive macrophages in a manner similar to that in toxin-sensitive murine macrophages. This activation of caspase-1 is dependent on proteasome activity, and sensitive macrophages are protected from LT's lytic effects by lactacystin. Proteasome inhibition also delayed the death of rats in response to LT, confirming our previous data implicating the rat Nlrp1 inflammasome in animal death. Quinidine, caspase-1 inhibitors, the cathepsin B inhibitor CA-074Me, and heat shock also protected rat macrophages from LT toxicity. These data support the existence of an active functioning LT-responsive Nlrp1 inflammasome in rat macrophages. The activation of the rat Nlrp1 inflammasome is required for LT-mediated rat macrophage lysis and contributes to animal death.

Indexed as

AcetylcysteineAdaptor Proteins, Signal TransducingAnimalsAntigens, BacterialApoptosis Regulatory ProteinsBacterial ToxinsCaspase 1Cell DeathCell LineCysteine Proteinase InhibitorsFemaleInflammationMacrophagesProteasome Endopeptidase ComplexRatsAcetylcysteineAdaptor Proteins, Signal Transducinganthrax toxinAntigens, BacterialApoptosis Regulatory ProteinsBacterial ToxinsCaspase 1Cysteine Proteinase InhibitorslactacystinNALP1 protein, mouseProteasome Endopeptidase Complex

Identifiers

PMID20638366
PMCPMC2925535
OpenAlexW2023324232

What OpenQuestion holds

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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.