Evidence map›Paper›PMID 35405286›Full record

ArticleToxicology2022

Toll-like receptors in the mechanism of tributyltin-induced production of pro-inflammatory cytokines, IL-1β and IL-6.

Aliyah Alcala, Brooke Osborne, Blake Allen, Aleshia Seaton-Terry, Toran Kirkland, Margaret Whalen

Open access · greenAbstract read
In one paragraph

Article in Toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Targeted lungScience advances · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. 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

6 authors at 1 institution in 1 country.

Aliyah AlcalaDepartments of Biology and Chemistry, Tennessee State University, Nashville, TN 37209, USA.
Brooke OsborneDepartments of Biology and Chemistry, Tennessee State University, Nashville, TN 37209, USA.
Blake AllenDepartments of Biology and Chemistry, Tennessee State University, Nashville, TN 37209, USA.
Aleshia Seaton-TerryDepartments of Biology and Chemistry, Tennessee State University, Nashville, TN 37209, USA.
Toran KirklandDepartments of Biology and Chemistry, Tennessee State University, Nashville, TN 37209, USA.
Margaret WhalenDepartments of Biology and Chemistry, Tennessee State University, Nashville, TN 37209, USA. Electronic address: mwhalen@tnstate.edu.
Tennessee State University · US

Funding

TRAININGU54CA163066 · NCI · TENNESSEE STATE UNIVERSITY · PI MARGARET M WHALEN · 2011 to 2026
$12.8M
MARC U*STAR Program at Tennessee State UniversityT34GM007663 · NIGMS · TENNESSEE STATE UNIVERSITY · PI WHALEN, MARGARET M · 1985 to 2021
$6.3M
U-RISE at Tennessee State UniversityT34GM145334 · NIGMS · TENNESSEE STATE UNIVERSITY · PI WHALEN, MARGARET M · 2022 to 2024
$625k
NCI NIH HHS U54 CA163066NIGMS NIH HHS T34 GM007663NIGMS NIH HHS T34 GM145334
6 · The paper itself

Abstract

Tributyltin (TBT) is an environmental contaminant due to its use in a variety of applications as a biocide, including in marine anti-fouling paints. It has been detected in a number of human tissues including blood. Previous studies have shown that exposure to TBT increases the cellular production (secretion plus intracellular levels) of the pro-inflammatory cytokines IL-1β and IL-6 by peripheral blood mononuclear cells (PMBCs) and this increase requires MAPK activation. Toll-like receptors (TLR) activate immune cells to produce pro-inflammatory cytokines in response to pathogen associated molecular patterns (PAMPs) and damage associated molecular patterns (DAMPs) leading to activation of MAPKs as well as other intracellular components that regulate cytokine production. The current study shows that selective inhibition of TLRs 4,1/2, and 8 diminishes the ability of TBT to stimulate IL-1β and IL-6 production. However, selective inhibition of TLR3 enhanced the TBT-induced production of IL-1β. This indicates that TBT may be either directly or indirectly interacting with certain TLR receptors as part of its mechanism of stimulating pro-inflammatory cytokine production. These results provide an important advance in understanding TBT stimulation of IL-1β and IL-6, which has the potential to cause chronic inflammation and its attendant pathologies.

Indexed as

CytokinesInterleukin-6HumansInterleukin-1betaLeukocytes, MononuclearToll-Like ReceptorsTrialkyltin CompoundsCytokinesInterleukin-1betaInterleukin-6Toll-Like ReceptorsTrialkyltin CompoundstributyltinPro-inflammatory cytokinesTLRTributyltin

Identifiers

PMID35405286
PMCPMC9081264
OpenAlexW4223638006

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.