Evidence map›Paper›PMID 10948142›Full record

ArticleInfection and immunity2000

Shiga toxin-induced tumor necrosis factor alpha expression: requirement for toxin enzymatic activity and monocyte protein kinase C and protein tyrosine kinases.

G H Foster, C S Armstrong, R Sakiri, V L Tesh

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 65 citations in OpenAlex.

  1. Cellular signaling pathway of Shiga toxin-induced ATP release.Frontiers in cellular and infection microbiology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Molecular Biology ofToxins · 2020
    Review
  7. Verotoxin Receptor-Based Pathology and Therapies.Frontiers in cellular and infection microbiology · 2020
    Review
  8. Review
  9. Review
  10. Role of Shiga/Vero toxins in pathogenesis.Microbiology spectrum · 2014
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Ricin and Shiga toxins: effects on host cell signal transduction.Current topics in microbiology and immunology · 2012
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  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 1 institution in 1 country.

G H FosterDepartment of Medical Microbiology and Immunology, Texas A&M University Health Science Center, College Station, Texas 77843-1114, USA.
C S Armstrong
R Sakiri
V L Tesh
Texas A&M Health Science Center · US

Funding

Pathogenic Mechanisms of Shiga ToxinsR01AI034530 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI TESH, VERNON L. · 2001 to 2010
$2.2M
PATHOGENIC MECHANISMS OF SHIGA AND SHIGA LIKE TOXINSR29AI034530 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI TESH, VERNON L. · 1995 to 1999
–
NIAID NIH HHS AI-34530NIAID NIH HHS R01 AI034530NIAID NIH HHS R29 AI034530
6 · The paper itself

Abstract

Infections with Shiga toxin (Stx)-producing bacteria cause bloody diarrhea which may progress to life-threatening complications, including acute renal failure and neurological abnormalities. The precise mechanism of disease progression is unclear, although evidence suggests that the localized production of the host proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-1 may exacerbate toxin-mediated vascular damage. Purified Stxs have been demonstrated to elicit proinflammatory cytokine synthesis from human peripheral blood mononuclear cells and monocytic cell lines in vitro. To understand toxin-monocyte interactions required for cytokine synthesis, we have treated differentiated THP-1 cells with purified wild-type toxins, enzymatic mutants, or B subunits and measured TNF-alpha production. Our data suggest that A subunit enzymatic activity is essential for cytokine production. THP-1 cells were treated with a series of protein kinase C (PKC), PKA, and protein tyrosine kinase inhibitors to examine the role of intracellular signaling molecules in Stx-mediated cytokine production. Treatment of cells with PKC and tyrosine kinase inhibitors blocked TNF-alpha secretion by Stx-stimulated THP-1 cells. Stx treatment directly activated PKC, which occurred at a point upstream of transcriptional activation of the gene encoding TNF-alpha.

Indexed as

Bacterial ToxinsCyclic AMP-Dependent Protein KinasesHumansMonocytesProtein Kinase CProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA, MessengerShiga ToxinsTumor Cells, CulturedTumor Necrosis Factor-alphaBacterial ToxinsCyclic AMP-Dependent Protein KinasesProtein Kinase CProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA, MessengerShiga ToxinsTumor Necrosis Factor-alpha

Identifiers

PMID10948142
PMCPMC101776
OpenAlexW2152425239

What OpenQuestion holds

Textmetadata
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.