Toll-like receptors in the mechanism of tributyltin-induced production of pro-inflammatory cytokines, IL-1β and IL-6.
Pro-inflammatory cytokines
TLR
Tributyltin
Journal
Toxicology
ISSN: 1879-3185
Titre abrégé: Toxicology
Pays: Ireland
ID NLM: 0361055
Informations de publication
Date de publication:
30 04 2022
30 04 2022
Historique:
received:
15
02
2022
revised:
24
03
2022
accepted:
05
04
2022
pubmed:
12
4
2022
medline:
11
5
2022
entrez:
11
4
2022
Statut:
ppublish
Résumé
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.
Identifiants
pubmed: 35405286
pii: S0300-483X(22)00089-0
doi: 10.1016/j.tox.2022.153177
pmc: PMC9081264
mid: NIHMS1796906
pii:
doi:
Substances chimiques
Cytokines
0
Interleukin-1beta
0
Interleukin-6
0
Toll-Like Receptors
0
Trialkyltin Compounds
0
tributyltin
4XDX163P3D
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
153177Subventions
Organisme : NIGMS NIH HHS
ID : T34 GM007663
Pays : United States
Organisme : NCI NIH HHS
ID : U54 CA163066
Pays : United States
Informations de copyright
Copyright © 2022 Elsevier B.V. All rights reserved.
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