Storme L.,EA4489 |
Luton D.,Hopitaux Universitaires Paris Nord Val Of Seine |
Abdennebi-Najar L.,Polytechnic Institute of LaSalle Beauvais |
Le Huerou-Luron I.,UR1341
Medecine/Sciences | Year: 2016
The first epidemiological studies showing a link between low birth weight and chronic diseases in adults did not distinguish the origins of low birth weight. A low birth weight may be the result of a premature birth. It can also be caused by an intrauterine growth restriction (IUGR). A child can be both preterm and IUGR. It is clear now that prematurity is an independent risk factor for programming chronic adult diseases. However, unlike adults born IUGR, adults born prematurely do not have an increased risk to develop metabolic syndrome (dyslipidemia or obesity). An increased risk of neurodevelopmental and psychiatric morbidity and hypertension is found after a premature birth. Mechanisms of chronic diseases programming are multiple: they involve both the cause of prematurity and IUGR such as infection/inflammation or placental insufficiency, but also consequences for therapeutic or nutritional strategies needed to support these children. This chapter describes the possible prevention of perinatal programming of noncommunicable diseases. © 2016 médecine/sciences-Inserm.
Sisino G.,EA4489 |
Sisino G.,University of Lille Nord de France |
Bouckenooghe T.,EA4489 |
Bouckenooghe T.,University of Lille Nord de France |
And 9 more authors.
Biochimica et Biophysica Acta - Molecular Basis of Disease | Year: 2013
Growing evidence indicates that maternal pathophysiological conditions, such as diabetes, influence fetal growth and could program metabolic disease in adulthood. Placental cells, particularly Hofbauer cells (HBCs), which are placental macrophages characterized by an anti-inflammatory profile (M2), can sense the modified maternal environment. The goal of this study was to investigate the direct effect of hyperglycemia on HBCs. We studied, at mRNA and protein levels, some markers of M2 and M1 (pro-inflammatory) macrophages in placentae from control and diabetic patients to assess the balance between pro- and anti-inflammatory macrophages: an imbalance of M2 to M1 macrophages has been observed in humans. We used pregnant rats, receiving a single injection of streptozotocin (STZ), as a model of maternal diabetes. We noticed a M2-to-M1 macrophage unbalance as we observed in human. An in vitro model of isolated rat HBCs was used to identify the direct effects of high glucose. We found that high glucose stimulation activated genes belonging to TLR (Toll-Like Receptor)-dependent inflammatory pathways. Moreover, the HBCs stimulated by high glucose switched their M2 profile towards M1, with increased expression of pro-inflammatory cytokines and markers. We also noticed that the oxidative-stress pathway was activated in response to high glucose driven by Hif-1α. In this study, we demonstrated that diabetes/hyperglycemia affect the anti-inflammatory profile of HBCs, by stimulating these cells to acquire an inflammatory profile leading to adverse consequences for the fetal-placental-maternal axis. © 2013 Elsevier B.V.