Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta

M. R. Peltier, N. G. Klimova, Y. Arita, E. M. Gurzenda, A. Murthy, K. Chawala, Veronica T. Lerner, J. Richardson, N. Hanna

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Polybrominated diphenyl ether(s) (PBDE) are ubiquitous environmental contaminants that bind and cross the placenta but their effects on pregnancy outcome are unclear. It is possible that environmental contaminants increase the risk of inflammation-mediated pregnancy complications such as preterm birth by promoting a proinflammatory environment at the maternal-fetal interface. We hypothesized that PBDE would reduce IL-10 production and enhance the production of proinflammatory cytokines associated with preterm labor/birth by placental explants. Second-trimester placental explants were cultured in either vehicle (control) or 2 μM PBDE mixture of congers 47, 99 and 100 for 72 h. Cultures were then stimulated with 106 CFU/ml heat-killed Escherichia coli for a final 24 h incubation and conditioned medium was harvested for quantification of cytokines and PGE2. COX-2 content and viability of the treated tissues were then quantified by tissue ELISA and MTT reduction activity, respectively. PBDE pre-treatment reduced E. coli-stimulated IL-10 production and significantly increased E. coli-stimulated IL-1β secretion. PBDE exposure also increased basal and bacteria-stimulated COX-2 expression. Basal, but not bacteria-stimulated PGE2, was also enhanced by PBDE exposure. No effect of PBDE on viability of the explants cultures was detected. In summary, pre-exposure of placental explants to congers 47, 99, and 100 enhanced the placental proinflammatory response to infection. This may increase the risk of infection-mediated preterm birth by lowering the threshold for bacteria to stimulate a proinflammatory response(s). Crown

Original languageEnglish (US)
Pages (from-to)745-749
Number of pages5
JournalPlacenta
Volume33
Issue number9
DOIs
StatePublished - Sep 1 2012
Externally publishedYes

Fingerprint

Halogenated Diphenyl Ethers
Placenta
Cytokines
Premature Birth
Escherichia coli
Bacteria
Dinoprostone
Interleukin-10
Tissue Survival
Pregnancy Complications
Premature Obstetric Labor
Second Pregnancy Trimester
Pregnancy Outcome
Conditioned Culture Medium
Infection
Crowns
Interleukin-1
Hot Temperature
Enzyme-Linked Immunosorbent Assay
Mothers

Keywords

  • Environment
  • Inflammation
  • PBDE
  • Placenta

ASJC Scopus subject areas

  • Obstetrics and Gynecology
  • Reproductive Medicine
  • Developmental Biology

Cite this

Peltier, M. R., Klimova, N. G., Arita, Y., Gurzenda, E. M., Murthy, A., Chawala, K., ... Hanna, N. (2012). Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta. Placenta, 33(9), 745-749. https://doi.org/10.1016/j.placenta.2012.06.005

Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta. / Peltier, M. R.; Klimova, N. G.; Arita, Y.; Gurzenda, E. M.; Murthy, A.; Chawala, K.; Lerner, Veronica T.; Richardson, J.; Hanna, N.

In: Placenta, Vol. 33, No. 9, 01.09.2012, p. 745-749.

Research output: Contribution to journalArticle

Peltier, MR, Klimova, NG, Arita, Y, Gurzenda, EM, Murthy, A, Chawala, K, Lerner, VT, Richardson, J & Hanna, N 2012, 'Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta', Placenta, vol. 33, no. 9, pp. 745-749. https://doi.org/10.1016/j.placenta.2012.06.005
Peltier MR, Klimova NG, Arita Y, Gurzenda EM, Murthy A, Chawala K et al. Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta. Placenta. 2012 Sep 1;33(9):745-749. https://doi.org/10.1016/j.placenta.2012.06.005
Peltier, M. R. ; Klimova, N. G. ; Arita, Y. ; Gurzenda, E. M. ; Murthy, A. ; Chawala, K. ; Lerner, Veronica T. ; Richardson, J. ; Hanna, N. / Polybrominated diphenyl ethers enhance the production of proinflammatory cytokines by the placenta. In: Placenta. 2012 ; Vol. 33, No. 9. pp. 745-749.
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