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Palmitate induces apoptotic cell death and inflammasome activation in human placental macrophages.

Journal article
Authors Lisa M Rogers
Carlos H Serezani
Alison J Eastman
Alyssa H Hasty
Linda Englund-Ögge
Bo Jacobsson
Kasey C Vickers
David M Aronoff
Published in Placenta
Volume 90
Pages 45-51
ISSN 1532-3102
Publication year 2020
Published at Institute of Clinical Sciences, Department of Obstetrics and Gynecology
Pages 45-51
Language en
Subject categories Obstetrics and gynaecology, Obstetrics and women's diseases


There is an increasing prevalence of non-communicable diseases worldwide. Metabolic diseases such as obesity and gestational diabetes mellitus (GDM) increasingly affect women during pregnancy, which can harm pregnancy outcomes and the long-term health and wellbeing of exposed offspring. Both obesity and GDM have been associated with proinflammatory effects within the placenta, the critical organ governing fetal development.The purpose of these studies was to model, in vitro, the effects of metabolic stress (high levels of glucose, insulin and saturated lipids) on placental macrophage biology, since these cells are the primary innate immune phagocyte within the placenta with roles in governing maternofetal immune tolerance and antimicrobial host defense. Macrophages were isolated from the villous core of term, human placentae delivered through nonlaboring, elective Cesarean sections and exposed to combinations of elevated glucose (30 mM), insulin (10 nM) and the saturated lipid palmitic acid (palmitate, 0.4 mM).We found that palmitate alone induced the activation of the nucleotide-binding oligomerization domain-like receptor (NLR) Family Pyrin Domain Containing 3 (NLRP3) inflammasome in placental macrophages, which was associated with increased interleukin 1 beta release and an increase in apoptotic cell death. Glucose and insulin neither provoked these effects nor augmented the impact of palmitate itself.Our findings confirm an impact of saturated fat on placental macrophage immune activation and could be relevant to the impact of metabolic stress in vivo.

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