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Original Articles

Interleukin 10 Deficiency Exacerbates Toll-Like Receptor 3–Induced Preeclampsia-Like Symptoms in Mice

Piyali Chatterjee, Valorie L. Chiasson, Shelley E. Kopriva, Kristina J. Young, Victor Chatterjee, Kathleen A. Jones, Brett M. Mitchell
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https://doi.org/10.1161/HYPERTENSIONAHA.111.172114
Hypertension. 2011;HYPERTENSIONAHA.111.172114
Originally published July 18, 2011
Piyali Chatterjee
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Valorie L. Chiasson
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Shelley E. Kopriva
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Kristina J. Young
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Victor Chatterjee
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Kathleen A. Jones
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Brett M. Mitchell
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Abstract

Preeclampsia may result from overactivation of the maternal immune system and is characterized by endothelial dysfunction and excessive inflammation. Given the importance of maternal immune system regulation and anti-inflammatory cytokines in normotensive pregnancies, we hypothesized that maternal immune system activation via Toll-like receptor 3 during pregnancy would cause preeclampsia-like symptoms in mice, which would be made worse by deficiency of the anti-inflammatory cytokine interleukin 10. The Toll-like receptor 3 agonist polyinosine-polycytidylic acid (poly I:C) caused hypertension, endothelial dysfunction, and proteinuria in mice only when pregnant. In the absence of poly I:C, pregnant interleukin 10 knockout mice exhibited a significant increase in systolic blood pressure, endothelial dysfunction, and serum proinflammatory cytokines, as well as aortic and placental platelet-endothelial cell adhesion molecule expression compared with pregnant wild-type mice. Deficiency of interleukin 10 further augmented these measures in poly I:C–treated pregnant mice. In addition, sera from poly I:C-treated pregnant wild-type mice significantly decreased relaxation responses and increased platelet-endothelial cell adhesion molecule expression in isolated aortas from nonpregnant wild-type mice, and these effects were augmented by sera from poly I:C-treated interleukin 10 knockout mice. Coincubation with recombinant interleukin 10 normalized relaxation responses and platelet-endothelial cell adhesion molecule expression in all of the groups. Collectively, Toll-like receptor 3 activation during pregnancy causes preeclampsia-like symptoms, which are exacerbated by the absence of interleukin 10. Exogenous interleukin 10 treatment had beneficial effects on endothelial function and may be beneficial in women with preeclampsia.

  • interleukin 10
  • endothelium
  • hypertension
  • pregnancy-induced
  • inflammation
  • pregnancy
  • preeclampsia
  • Received February 22, 2011.
  • Revision received March 9, 2011.
  • Accepted June 20, 2011.
  • © 2011 American Heart Association, Inc.
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    Interleukin 10 Deficiency Exacerbates Toll-Like Receptor 3–Induced Preeclampsia-Like Symptoms in Mice
    Piyali Chatterjee, Valorie L. Chiasson, Shelley E. Kopriva, Kristina J. Young, Victor Chatterjee, Kathleen A. Jones and Brett M. Mitchell
    Hypertension. 2011;HYPERTENSIONAHA.111.172114, originally published July 18, 2011
    https://doi.org/10.1161/HYPERTENSIONAHA.111.172114

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    Interleukin 10 Deficiency Exacerbates Toll-Like Receptor 3–Induced Preeclampsia-Like Symptoms in Mice
    Piyali Chatterjee, Valorie L. Chiasson, Shelley E. Kopriva, Kristina J. Young, Victor Chatterjee, Kathleen A. Jones and Brett M. Mitchell
    Hypertension. 2011;HYPERTENSIONAHA.111.172114, originally published July 18, 2011
    https://doi.org/10.1161/HYPERTENSIONAHA.111.172114
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