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JEG-3 placental cells in toxicology studies: a promising tool to reveal pregnancy disorders
Elodie Olivier,Anaïs Wakx,Sophie Fouyet,Mélody Dutot,Patrice Rat 대한해부학회 2021 Anatomy & Cell Biology Vol.54 No.1
Placental alterations are responsible for adverse pregnancy outcomes like preeclampsia and intrauterine growth restriction. And yet, placenta toxicology has not become a fully-f ledged toxicology field. Because placenta is very often seen only as a barrier between the mother and the fetus, there is a lack and therefore a need for an experimental human model with technical recommendations to study placenta toxicology. In vitro approaches are recommended in experimental toxicology as they focus on a specific biological process and yield high-throughput screening methods. In the present study, we first established incubation conditions to preserve signatures of the human JEG-3 cell line identity while enabling toxicity detection. JEG-3 cells prepared in our incubation conditions were renamed JEG-Tox cells. As placental alterations are mainly triggered by uncontrolled apoptosis, we second used known apoptotic agents pregnant women are exposed to, to check that JEG-Tox cells can trigger apoptosis. Ethanol, bisphenol F, quinalphos, 4,4’-DDT, benzalkonium chloride, phenoxyethanol, propylparaben, and perfluorooctanic acid all induced chromatin condensation in JEG-Tox cells. Our incubation conditions allow JEG-Tox cells to keep placental cell identity and to respond to toxic chemicals. JEG-Tox cells are a pertinent model for placenta toxicology and could be used to better understand pregnancy alterations.
( Elodie Descloux ),( Maguy Daures ),( Cecile Balter Veysseyre ),( Olivier Simon ),( Yann Barguil ),( Isabelle Missotte ),( Ann Claire Gourinat ),( Michele John ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: Invasive Meningococcal Disease (IMD) is three fold more common in New Caledonia (NC) than in metropolitan France. Many IMD cases (35. 7%) are due to serogroups Y and W135. The purpose of our study was to identify IMD risk factors in NC. Methods: A retrospective study of all IMD cases that occurred in NC between 2005 and 2011 was conducted. Socio-environmental and clinico-biological data were collected. A search for immune defi ciency was proposed to all cases. IMD presentation and outcome were compared according to meningoccal serogroups and the presence of complement defi ciency (C-defi ciency). Results: 66 sporadic IMD cases (29 B serogroup, 20 Y or W135, 6 C, 1 A, 10 unknown) occurred in 64 patients often <19 years-old and of Melanesian origin. five patients died (7. 8%). No socioenvironmental risk factors were identifi ed. No asplenia, HIV infection or immunoglobulin defi ciency were found. Two patients had diabetes and 28 of 53 (52. 8%) patients had a C-defi ciency including 20 (71. 4%) cases of late complement component defi ciency. Patients with C-defi ciency were mainly Melanesian (92. 8%) originating from Loyalty Islands (62. 1%). They were mostly infected with serogroup Y/W135 (42. 9%) or B (32. 1%). They often developed later and more severe disease than patients without C-defi ciency (need for intensive cares in 62% versus 28% of cases, p = 0. 01). Conclusions: A high prevalence of C-defi ciency in the Melanesian population may explain clinico-epidemiological features of IMD in NC. Our data are consistent with previous studies confi rming a higher age at fi rst infection, a risk of IMD recurrence and a high frequency of Y/W135 serogroups in C-defi cient patients. However our results do not match previous fi ndings regarding disease severity. Our fi ndings imply an adaptation of C-defi ciency screening and meningococcal vaccine strategies in NC.