Brominated flame retardants, hexabromocyclododecane and tetrabromobisphenol A, affect proinflammatory protein expression in human bronchial epithelial cells via disruption of intracellular signaling

Koike, E; Yanagisawa, R; Takano, H

HERO ID

3350501

Reference Type

Journal Article

Year

2016

Language

English

PMID

26718265

HERO ID 3350501
In Press No
Year 2016
Title Brominated flame retardants, hexabromocyclododecane and tetrabromobisphenol A, affect proinflammatory protein expression in human bronchial epithelial cells via disruption of intracellular signaling
Authors Koike, E; Yanagisawa, R; Takano, H
Journal Toxicology In Vitro
Volume 32
Page Numbers 212-219
Abstract Hexabromocyclododecane (HBCD) and tetrabromobisphenol A (TBBPA) are widely used as brominated flame retardants (BFRs) in consumer products. Because humans can be exposed to BFRs mainly through air or dust, the effects of the BFRs on the respiratory system and the underlying mechanisms were investigated. HBCD exposure significantly increased the expression of intercellular adhesion molecule (ICAM)-1 and the production of interleukin (IL)-6 and -8 in human bronchial epithelial cells (BEAS-2B). TBBPA exposure significantly increased the expression of ICAM-1 and IL-6, but not IL-8. HBCD and TBBPA stimulated epidermal growth factor (EGF) production and EGF receptor (EGFR) phosphorylation. Inhibitors of EGFR-selective tyrosine kinase and the subsequent mitogen-activated protein kinase effectively blocked the increase in the expression of proinflammatory proteins. The activation of nuclear factor-kappa B (p50, p65) and activator protein 1 (c-Jun) was also observed following HBCD exposure. Furthermore, the modulation for nuclear receptors was investigated. TBBPA but not HBCD showed ligand activity for thyroid hormone receptor (TR) and TR antagonist significantly suppressed the TBBPA-induced increase of the expression of ICAM-1 and IL-6. In conclusion, HBCD and TBBPA can disrupt the expression of proinflammatory proteins in bronchial epithelial cells, possibly via the modulation of EGFR-related pathways and/or nuclear receptors.
Doi 10.1016/j.tiv.2015.12.013
Pmid 26718265
Wosid WOS:000372760900024
Url https://search.proquest.com/docview/1770888799?accountid=171501
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English
Keyword Hexabromocyclododecane; Tetrabromobisphenol a; Bronchial epithelial cells; Proinflammatory proteins; Epidermal growth factor receptor; Nuclear receptor
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