Effect of Tetrabromobisphenol A on expression of biomarkers for inflammation and neurodevelopment by the placenta

Yuko Arita, Matthew Pressman, Darios Getahun, Ramkumar Menon, Morgan R. Peltier

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Objective: Polybrominated diphenyl ethers (PBDEs) enhance basal and bacteria-stimulated production of proinflammatory cytokines by the placenta and may also increase the risk of preterm birth and neurodevelopmental disorders. Whether or not other brominated flame retardants such as Tetrabromobisphenol A (TBBPA) have similar properties is unclear. Therefore, we evaluated the effects of TBBPA on the production of steroids, as well as biomarkers for inflammation, oxidative stress, and neurodevelopment by the placenta. Methods: Placental explant cultures were established from women undergoing elective Cesarean sections at term and treated with 5–50,000 nM TBBPA in the presence and absence of 107 CFU/ml heat-killed E. coli. Concentrations of P4, E2, testosterone (T), IL-1β, TNF-α, IL-10, HO-1, IL-6, 8-IsoP and BDNF were quantified in the conditioned medium. Results: In the absence of bacteria, TBBPA tended to increase P4 and T as well as IL-6 and 8-IsoP. For bacteria-treated cultures, TBBPA generally inhibited P4, IL-1β, and HO-1 production but enhanced TNF-α and IL-6 production. Conclusions: TBBPA alters placental steroidogenesis to favor T production and increases oxidative stress and placental inflammation as suggested by its promotion of 8-IsoP and IL-6 production. TBBPA may also function as a risk modifier where it enhances bacteria-stimulated production TNF-α and IL-6 but reduces HO-1 production, however, this was balanced by reductions in IL-1β. Further studies are warranted to determine if TBBPA increases the risk of adverse pregnancy outcomes such as preterm birth, pPROM and neurodevelopmental disorders such as autism that have been associated with increased production of proinflammatory cytokines, oxidative stress and/or T.

Original languageEnglish (US)
Pages (from-to)33-39
Number of pages7
JournalPlacenta
Volume68
DOIs
StatePublished - Aug 1 2018

Fingerprint

Placenta
Biomarkers
Inflammation
Interleukin-6
Interleukin-1
Bacteria
Oxidative Stress
Premature Birth
Interleukin-8
Halogenated Diphenyl Ethers
Flame Retardants
Cytokines
tetrabromobisphenol A
Brain-Derived Neurotrophic Factor
Pregnancy Outcome
Autistic Disorder
Conditioned Culture Medium
Cesarean Section
Interleukin-10
Testosterone

Keywords

  • Flame retardant
  • Infection
  • Inflammation
  • Neurodevelopmental disorder
  • Placenta
  • Preterm birth

ASJC Scopus subject areas

  • Reproductive Medicine
  • Obstetrics and Gynecology
  • Developmental Biology

Cite this

Effect of Tetrabromobisphenol A on expression of biomarkers for inflammation and neurodevelopment by the placenta. / Arita, Yuko; Pressman, Matthew; Getahun, Darios; Menon, Ramkumar; Peltier, Morgan R.

In: Placenta, Vol. 68, 01.08.2018, p. 33-39.

Research output: Contribution to journalArticle

Arita, Yuko ; Pressman, Matthew ; Getahun, Darios ; Menon, Ramkumar ; Peltier, Morgan R. / Effect of Tetrabromobisphenol A on expression of biomarkers for inflammation and neurodevelopment by the placenta. In: Placenta. 2018 ; Vol. 68. pp. 33-39.
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AU - Arita, Yuko

AU - Pressman, Matthew

AU - Getahun, Darios

AU - Menon, Ramkumar

AU - Peltier, Morgan R.

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AB - Objective: Polybrominated diphenyl ethers (PBDEs) enhance basal and bacteria-stimulated production of proinflammatory cytokines by the placenta and may also increase the risk of preterm birth and neurodevelopmental disorders. Whether or not other brominated flame retardants such as Tetrabromobisphenol A (TBBPA) have similar properties is unclear. Therefore, we evaluated the effects of TBBPA on the production of steroids, as well as biomarkers for inflammation, oxidative stress, and neurodevelopment by the placenta. Methods: Placental explant cultures were established from women undergoing elective Cesarean sections at term and treated with 5–50,000 nM TBBPA in the presence and absence of 107 CFU/ml heat-killed E. coli. Concentrations of P4, E2, testosterone (T), IL-1β, TNF-α, IL-10, HO-1, IL-6, 8-IsoP and BDNF were quantified in the conditioned medium. Results: In the absence of bacteria, TBBPA tended to increase P4 and T as well as IL-6 and 8-IsoP. For bacteria-treated cultures, TBBPA generally inhibited P4, IL-1β, and HO-1 production but enhanced TNF-α and IL-6 production. Conclusions: TBBPA alters placental steroidogenesis to favor T production and increases oxidative stress and placental inflammation as suggested by its promotion of 8-IsoP and IL-6 production. TBBPA may also function as a risk modifier where it enhances bacteria-stimulated production TNF-α and IL-6 but reduces HO-1 production, however, this was balanced by reductions in IL-1β. Further studies are warranted to determine if TBBPA increases the risk of adverse pregnancy outcomes such as preterm birth, pPROM and neurodevelopmental disorders such as autism that have been associated with increased production of proinflammatory cytokines, oxidative stress and/or T.

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KW - Infection

KW - Inflammation

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KW - Placenta

KW - Preterm birth

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