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Role of NOD2 in antiphospholipid antibody-induced and bacterial MDP amplification of trophoblast inflammation.

Abstract：

:Women with antiphospholipid antibodies (aPL) are at high risk for pregnancy complications, such as preeclampsia. We previously demonstrated that aPL recognizing β2GPI promote an extravillous trophoblast pro-inflammatory, anti-migratory and anti-angiogenic profile similar to that seen in preeclampsia. Since preeclampsia in the absence of aPL may have an underlying infectious element, women with aPL may be at increased risk for preeclampsia or other adverse outcomes if an infection is present. Our objective was to determine the impact the common bacterial component, muramyl dipeptide (MDP), has on trophoblast responses to aPL. Herein, we report that bacterial MDP amplifies trophoblast IL-1β expression, processing, and secretion in the presence of aPL through activation of NOD2. In the absence of MDP, NOD2 also mediates anti- β2GPI antibody-induced trophoblast IL-1β and VEGF secretion. Additionally, we report a role for extravillous trophoblast vimentin as a novel danger signal that contributes to the aPL-induced trophoblast IL-1β production. Together our data indicate that NOD2 mediates trophoblast inflammatory and angiogenic responses to aPL alone, and mediates trophoblast inflammation in the presence of bacterial MDP. These findings suggest that a bacterial infection at the maternal-fetal interface may exacerbate the impact aPL have on trophoblast inflammation and, thus, on pregnancy outcome.

journal_name

J Autoimmun

journal_title

Journal of autoimmunity

authors

Mulla MJ,Pasternak MC,Salmon JE,Chamley LW,Abrahams VM

doi

10.1016/j.jaut.2018.12.003

subject

Has Abstract

pub_date

2019-03-01 00:00:00

pages

103-112

eissn

0896-8411

issn

1095-9157

pii

S0896-8411(18)30478-5

journal_volume

98

pub_type

杂志文章

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