Evidence map›Paper›PMID 15102770›Full record

ArticleInfection and immunity2004

Regulation of proinflammatory cytokine expression by Shiga toxin 1 and/or lipopolysaccharides in the human monocytic cell line THP-1.

Lisa M Harrison, Wilhelmina C E van Haaften, Vernon L Tesh

Open access · greenAbstract readComparative Study
In one paragraph

Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 68 citations in OpenAlex.

  1. Decades Long Involvement of THP-1 Cells as a Model for Macrophage Research: A Comprehensive Review.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2024
    Review
  2. Review
  3. Review
  4. The Role ofToxins · 2020
    Review
  5. Molecular Biology ofToxins · 2020
    Review
  6. Article
  7. Comparative Transcriptomics of Shiga Toxin-Producing and CommensalFrontiers in cellular and infection microbiology · 2020
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Effect of shiga toxin and its subunits on cytokine induction in different cell lines.International journal of molecular and cellular medicine · 2014
    Article
  17. Review
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Lisa M HarrisonDepartment of Medical Microbiology and Immunology, Texas A&M University System Health Science Center, College Station, Texas 77843-1114, USA.
Wilhelmina C E van Haaften
Vernon L Tesh
Texas A&M University System · US

Funding

Pathogenic Mechanisms of Shiga ToxinsR01AI034530 · NIAID · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI TESH, VERNON L. · 2001 to 2010
$2.2M
NIAID NIH HHS 2R01 AI34530NIAID NIH HHS R01 AI034530
6 · The paper itself

Abstract

Infection with Shiga toxin (Stx)-producing bacteria and the subsequent release of Stxs and endotoxins into the bloodstream may damage blood vessels in the colon, kidneys, and central nervous system, leading to bloody diarrhea, acute renal failure, and neurological complications. The proinflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin-1beta (IL-1beta) may contribute to the pathogenesis of Stx-induced vascular lesions by up-regulating toxin receptor expression on endothelial cells. We previously showed that macrophages treated with purified Shiga toxin 1 (Stx1) or lipopolysaccharides (LPS) secrete TNF-alpha and IL-1beta. Northern blot analysis revealed that treatment of the human monocytic cell line THP-1 with LPS induced a rapid and transient increase in steady-state TNF-alpha and IL-1beta transcripts. In contrast, Stx1 induced slower but prolonged elevations in cytokine transcripts. The presence of both stimulants resulted in optimal cytokine mRNA induction in terms of kinetics and prolonged expression. Compared to LPS, Stx1 was a poor inducer of IL-1beta protein expression, although levels of soluble IL-1beta induced by all treatments continually increased over 72 h. IL-1beta transcripts were not induced by Stx1 B-subunits. Using the transcriptional inhibitor actinomycin D, we determined that treatment with Stx1 or Stx1 plus LPS induced cytokine transcripts with increased stability compared to transcripts induced by LPS alone. For all treatments, IL-1beta mRNA decay was slower than TNF-alpha. Collectively, our data suggest that Stxs affect cytokine expression, in part, at the posttranscriptional level by stabilizing mRNAs. Optimal TNF-alpha expression occurs when both Stxs and LPS are present.

Indexed as

Cell LineCytokinesEscherichia coliGene Expression RegulationHumansInflammation MediatorsInterleukin-1KineticsLipopolysaccharidesMonocytesRNA, MessengerRNA StabilityShiga Toxin 1Shigella dysenteriaeTumor Necrosis Factor-alphaCytokinesInflammation MediatorsInterleukin-1LipopolysaccharidesRNA, MessengerShiga Toxin 1Tumor Necrosis Factor-alpha

Identifiers

PMID15102770
PMCPMC387879
OpenAlexW2024355918

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.