Evidence map›Paper›PMID 22069639›Full record

ReviewToxins2010

Deoxynivalenol-induced proinflammatory gene expression: mechanisms and pathological sequelae.

James J Pestka

Open access · goldAbstract readReview
In one paragraph

Review in Toxins, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
8.7field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 187 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Occurrence and Co-Occurrence of Regulated and Emerging Mycotoxins in Foods Marketed to U.S. Toddlers.International journal of environmental research and public health · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Combined exposure to emergingFrontiers in toxicology · 2026
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

29 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

1 author at 1 institution in 1 country.

James J PestkaDepartment of Microbiology and Molecular Genetics, Michigan State University, East Lansing, MI 48824, USA. Pestka@msu.edu
Michigan State University · US

Funding

Trichothecene Toxicity and the Ribotoxic Stress ResponseR01ES003358 · NIEHS · MICHIGAN STATE UNIVERSITY · PI PESTKA, JAMES J · 1985 to 2012
$3.3M
Mechanisms of Trichothecene ToxicityR56ES003358 · NIEHS · MICHIGAN STATE UNIVERSITY · PI PESTKA, JAMES J · 2005 to 2005
$113k
NIEHS NIH HHS ES 3358NIEHS NIH HHS R01 ES003358NIEHS NIH HHS R56 ES003358
6 · The paper itself

Abstract

The trichothecene mycotoxin deoxynivalenol (DON) is commonly encountered in human cereal foods throughout the world as a result of infestation of grains in the field and in storage by the fungus Fusarium. Significant questions remain regarding the risks posed to humans from acute and chronic DON ingestion, and how to manage these risks without imperiling access to nutritionally important food commodities. Modulation of the innate immune system appears particularly critical to DON's toxic effects. Specifically, DON induces activation of mitogen-activated protein kinases (MAPKs) in macrophages and monocytes, which mediate robust induction of proinflammatory gene expression-effects that can be recapitulated in intact animals. The initiating mechanisms for DON-induced ribotoxic stress response appear to involve the (1) activation of constitutive protein kinases on the damaged ribosome and (2) autophagy of the chaperone GRP78 with consequent activation of the ER stress response. Pathological sequelae resulting from chronic low dose exposure include anorexia, impaired weight gain, growth hormone dysregulation and aberrant IgA production whereas acute high dose exposure evokes gastroenteritis, emesis and a shock-like syndrome. Taken together, the capacity of DON to evoke ribotoxic stress in mononuclear phagocytes contributes significantly to its acute and chronic toxic effects in vivo. It is anticipated that these investigations will enable the identification of robust biomarkers of effect that will be applicable to epidemiological studies of the human health effects of this common mycotoxin.

Indexed as

AnimalsEndoplasmic Reticulum Chaperone BiPGene Expression RegulationHumansImmunity, InnateInflammationLeukocytesRibosomesTrichothecenesdeoxynivalenolEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanTrichothecenescytokinedeoxynivalenol (DON)ER stressmacrophagemonocyteribosometranslation inhibition

Identifiers

PMID22069639
PMCPMC3153246
OpenAlexW2061169138

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.