scholarly journals Fusarium Mycotoxins Disrupt the Barrier and Induce IL-6 Release in a Human Placental Epithelium Cell Line

Toxins ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 665 ◽  
Author(s):  
Negisa Seyed Toutounchi ◽  
Astrid Hogenkamp ◽  
Soheil Varasteh ◽  
Belinda van’t Land ◽  
Johan Garssen ◽  
...  

Deoxynivalenol, T-2 toxin, and zearalenone, major Fusarium mycotoxins, contaminate human food on a global level. Exposure to these mycotoxins during pregnancy can lead to abnormalities in neonatal development. Therefore, the aim of this study was to investigate the effects of Fusarium mycotoxins on human placental epithelial cells. As an in vitro model of placental barrier, BeWo cells were exposed to different concentrations of deoxynivalenol, zearalenone or T-2 toxin. Cytotoxicity, effects on barrier integrity, paracellular permeability along with mRNA and protein expression and localization of junctional proteins after exposure were evaluated. Induction of proinflammatory responses was determined by measuring cytokine production. Increasing mycotoxin concentrations affect BeWo cell viability, and T-2 toxin was more toxic compared to other mycotoxins. Deoxynivalenol and T-2 toxin caused significant barrier disruption, altered protein and mRNA expression of junctional proteins, and induced irregular cellular distribution. Although the effects of zearalenone on barrier integrity were less prominent, all tested mycotoxins were able to induce inflammation as measured by IL-6 release. Overall, Fusarium mycotoxins disrupt the barrier of BeWo cells by altering the expression and structure of junctional proteins and trigger proinflammatory responses. These changes in placental barrier may disturb the maternal–fetal interaction and adversely affect fetal development.

2002 ◽  
Vol 233 (1-2) ◽  
pp. 85-98 ◽  
Author(s):  
Chadarat Ampasavate ◽  
Gurudatt A Chandorkar ◽  
David G Vande Velde ◽  
John F Stobaugh ◽  
Kenneth L Audus

2008 ◽  
Vol 295 (5) ◽  
pp. C1445-C1453 ◽  
Author(s):  
Sarah J. Heaton ◽  
John J. Eady ◽  
Mary L. Parker ◽  
Kathryn L. Gotts ◽  
Jack R. Dainty ◽  
...  

BeWo cells are a placental cell line that has been widely used as an in vitro model for the placenta. The b30 subclone of these cells can be grown on permeable membranes in bicameral chambers to form confluent cell layers, enabling rates of both nutrient uptake into the cells from the apical surface and efflux from the basolateral membrane to be determined. The aim of this study was to evaluate structural and functional properties of confluent b30 BeWo cell layers grown in bicameral chambers, focusing on the potential application for studying receptor-mediated uptake and transport of transferrin (Tf)-bound iron (Fe-Tf). While it proved extremely difficult to establish and maintain an intact BeWo cell monolayer, it was possible to grow the cells to a confluent multilayer. Iron, applied as Fe-Tf, was rapidly transported across this cell layer; 9.3 ± 0.5% of the total dose was transported after 8 h, equivalent to 38.8 ± 2.1 pmol·cm−2·h−1. Transfer of Tf across the cell layer was much more limited; 2.4 ± 0.2% of the total dose was transported after 8 h, equivalent to 5.0 ± 0.4 pmol·cm−2·h−1. Compartmental modeling of these data suggested that iron was transported across the cell layer predominantly, if not exclusively, via a transcellular route, whereas Tf taken up into the cells was predominantly recycled back to the apical compartment. The results suggest that these cells are very efficient at transporting iron and, under carefully controlled conditions, can be a valuable tool for the study of iron transport in the placenta.


Author(s):  
John C. Garancis ◽  
R. A. Pattillo

Growth of cell system (BeWo-cell line) derived from human gestational choriocarcinoma has been established and continuously maintained in-vitro. Furthermore, it is evident from the previous studies that this cell line has retained the physiological function of the placental trophoblasts, namely the synthesis of human chorionic gonadotrophil(HCG).The BeWo cells were relatively small and possessed single nuclei, thus indicating that this cell line consists exclusively of cytotrophoblasts. In some instances cells appeared widely separated and their lateral surfaces were provided with numerous microvilli (Fig.1).


2018 ◽  
Vol 7 (2) ◽  
pp. 1870008 ◽  
Author(s):  
Cassidy Blundell ◽  
Yoon-Suk Yi ◽  
Lin Ma ◽  
Emily R. Tess ◽  
Megan J. Farrell ◽  
...  

2004 ◽  
Vol 82 (2) ◽  
pp. 84-93 ◽  
Author(s):  
I Dublineau ◽  
F Lebrun ◽  
S Grison ◽  
N M Griffiths

Irradiation of the digestive system leads to alterations of the small intestine. We have characterized the disruption of the barrier integrity in rat ileum from 1 to 14 days following irradiation ranging from 6 to 12 Gy. The intestinal permeability to 14C-mannitol and 3H-dextran 70 000 was measured in vitro in Ussing chambers. In parallel to these functional studies, immunohistochemical analyses of junctional proteins (ZO-1 and β-catenin) of ileal epithelium were performed by confocal microscopy. Irradiation with 10 Gy induced a marked decrease in epithelial tissue resistance at three days and a fivefold increase in mannitol permeability, without modifications of dextran permeability. A disorganization of the localization for ZO-1 and β-catenin was also observed. At 7 days after irradiation, we observed a recovery of the organization of junctional proteins in parallel to a return of intestinal permeability to control value. In addition to these time-dependent effects, a gradual effect on epithelial integrity of the radiation doses was observed 3 days after irradiation. This study shows a disruption of the integrity of the intestinal barrier in rat ileum following abdominal X-irradiation, depending on the time postirradiation and on the delivered dose. The loss of barrier integrity was characterized by a disorganization of proteins of tight and adherent junctions, leading to increased intestinal permeability to mannitol.Key words: intestinal permeability, ZO-1, β-catenin, tight and adherent junctions.


2015 ◽  
Vol 17 (5) ◽  
pp. 1193-1199 ◽  
Author(s):  
Amal A. Akour ◽  
Mary Jayne Kennedy ◽  
Phillip M. Gerk

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Veronica H.L. Leinster ◽  
Thomas J. Phillips ◽  
Nicola Jones ◽  
Sharon Sanderson ◽  
Katja Simon ◽  
...  

Abstract Episodes of hypoxia and hypoxia/reoxygenation during foetal development have been associated with increased risk of neurodevelopmental conditions presenting in later life. The mechanism for this is not understood; however, several authors have suggested that the placenta plays an important role. Previously we found both placentas from a maternal hypoxia model and pre-eclamptic placentas from patients release factors lead to a loss of dendrite complexity in rodent neurons. Here to further explore the nature and origin of these secretions we exposed a simple in vitro model of the placental barrier, consisting of a barrier of human cytotrophoblasts, to hypoxia or hypoxia/reoxygenation. We then exposed cortical cultures from embryonic rat brains to the conditioned media (CM) from below these exposed barriers and examined changes in cell morphology, number, and receptor presentation. The barriers released factors that reduced dendrite and astrocyte process lengths, decreased GABAB1 staining, and increased astrocyte number. The changes in astrocytes required the presence of neurons and were prevented by inhibition of the SMAD pathway and by neutralising Bone Morphogenetic Proteins (BMPs) 2/4. Barriers exposed to hypoxia/reoxygenation also released factors that reduced dendrite lengths but increased GABAB1 staining. Both oxygen changes caused barriers to release factors that decreased GluN1, GABAAα1 staining and increased GluN3a staining. We find that hypoxia in particular will elicit the release of factors that increase astrocyte number and decrease process length as well as causing changes in the intensity of glutamate and GABA receptor staining. There is some evidence that BMPs are released and contribute to these changes.


2019 ◽  
Vol 87 (2) ◽  
pp. 13 ◽  
Author(s):  
Dai-Hung Ngo ◽  
Dai-Nghiep Ngo ◽  
Thi Thanh Nhan Vo ◽  
Thanh Sang Vo

Diabetes is a major metabolic disorder whose prevalence is increasing daily. Medicinal plants have played an important role in the prevention and treatment of type 2 diabetes via prophylactic and therapeutic management. In this study, Mangifera Indica leaf (MIL) extract was investigated for its promising anti-diabetic activity via an in vitro model. It was found that MIL extract possessed significant inhibition on alpha-amylase activity up to (51.4 ± 2.7)% at a concentration of 200 µg/mL. Moreover, glucose adsorption capacity of MIL was identified at (2.7 ± 0.19) mM glucose/g extract. Furthermore, the extract caused a significant increase in glucose uptake up to (143 ± 9.3)% in LO-2 liver cells. Notably, MIL extract was effective in scavenging (63.3 ± 2.1)% 1,1-diphenyl-2-picryl-hydrazyl (DPPH) and (71.6 ± 4.3)% 2,2-azinobis-3-ethyl benzothiazoline-6-sulfonic acid (ABTS)+ radicals and inhibiting (66 ± 4.9)% NO production from RAW264.7 cells without any cytotoxicity effects. Accordingly, M. indica leaves are suggested as a promising material for development of hypoglycemic products.


2009 ◽  
Vol 189 ◽  
pp. S195
Author(s):  
Sara Correia Carreira ◽  
Laura Cartwright ◽  
Margaret Saunders ◽  
Susan Thawley

Sign in / Sign up

Export Citation Format

Share Document