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• W2149776807 abstract "ObjectiveAir pollution is implicated in causing inflammatory-mediated respiratory and cardiovascular disease, and may contribute to pregnancy disorders. Inhaling small particles from diesel fuel emissions, among other sources, stimulates local inflammatory responses in the lung and has been associated with a systemic proinflammatory state. Particulate matter may cause placental inflammation and increase the risk of preterm birth. The purpose of this study is to demonstrate that particulate matter induces NF-kB activation in human JEG3 trophoblast cells and murine placental fibroblasts.Study designJEG3 human trophoblast cells and primary murine placental fibroblast cells were transfected with NF-kB luciferase and beta-galactosidase expression vectors using Fugene 6 (Boehringer Manheim, Indianapolis, IN) overnight. The cells were then stimulated with commercially prepared LPS- free particles measuring 0.1 micron (ultrafine) or measuring 0.98 micron (fine) overnight. Control groups were treated with serum-free medium alone or with lipopolysaccharide (LPS). NF-kB luciferase activity was assessed by luciferase assay and use of a luminometer. Calorimetric beta-galactosidase assay was performed to correct for transfection efficiency. The NF-kB activation in the experimental groups was compared to the activity of the media-treated or LPS-stimulated cells. Statistical significance was calculated using ANOVA and student t-test.ResultsData analysis suggested that exposure to particulate matter induced NF-kB activation in JEG3 trophoblasts after a twenty-four hour stimulation (p=0.02), with a trend toward NF-kB activation in cells exposed to ultrafine particles (0.1 micron) (p=0.14). Data from placental fibroblasts suggest a trend toward activation of NF-kB by ultrafine particles as well (p=0.079). Fine particles (0.98 micron) did not induce NF-kB activation in either cell type.ConclusionUltrafine particles may activate NF-kB in human trophoblast cells and murine placental fibroblasts, and may contribute to local and systemic inflammation in pregnancy. ObjectiveAir pollution is implicated in causing inflammatory-mediated respiratory and cardiovascular disease, and may contribute to pregnancy disorders. Inhaling small particles from diesel fuel emissions, among other sources, stimulates local inflammatory responses in the lung and has been associated with a systemic proinflammatory state. Particulate matter may cause placental inflammation and increase the risk of preterm birth. The purpose of this study is to demonstrate that particulate matter induces NF-kB activation in human JEG3 trophoblast cells and murine placental fibroblasts. Air pollution is implicated in causing inflammatory-mediated respiratory and cardiovascular disease, and may contribute to pregnancy disorders. Inhaling small particles from diesel fuel emissions, among other sources, stimulates local inflammatory responses in the lung and has been associated with a systemic proinflammatory state. Particulate matter may cause placental inflammation and increase the risk of preterm birth. The purpose of this study is to demonstrate that particulate matter induces NF-kB activation in human JEG3 trophoblast cells and murine placental fibroblasts. Study designJEG3 human trophoblast cells and primary murine placental fibroblast cells were transfected with NF-kB luciferase and beta-galactosidase expression vectors using Fugene 6 (Boehringer Manheim, Indianapolis, IN) overnight. The cells were then stimulated with commercially prepared LPS- free particles measuring 0.1 micron (ultrafine) or measuring 0.98 micron (fine) overnight. Control groups were treated with serum-free medium alone or with lipopolysaccharide (LPS). NF-kB luciferase activity was assessed by luciferase assay and use of a luminometer. Calorimetric beta-galactosidase assay was performed to correct for transfection efficiency. The NF-kB activation in the experimental groups was compared to the activity of the media-treated or LPS-stimulated cells. Statistical significance was calculated using ANOVA and student t-test. JEG3 human trophoblast cells and primary murine placental fibroblast cells were transfected with NF-kB luciferase and beta-galactosidase expression vectors using Fugene 6 (Boehringer Manheim, Indianapolis, IN) overnight. The cells were then stimulated with commercially prepared LPS- free particles measuring 0.1 micron (ultrafine) or measuring 0.98 micron (fine) overnight. Control groups were treated with serum-free medium alone or with lipopolysaccharide (LPS). NF-kB luciferase activity was assessed by luciferase assay and use of a luminometer. Calorimetric beta-galactosidase assay was performed to correct for transfection efficiency. The NF-kB activation in the experimental groups was compared to the activity of the media-treated or LPS-stimulated cells. Statistical significance was calculated using ANOVA and student t-test. ResultsData analysis suggested that exposure to particulate matter induced NF-kB activation in JEG3 trophoblasts after a twenty-four hour stimulation (p=0.02), with a trend toward NF-kB activation in cells exposed to ultrafine particles (0.1 micron) (p=0.14). Data from placental fibroblasts suggest a trend toward activation of NF-kB by ultrafine particles as well (p=0.079). Fine particles (0.98 micron) did not induce NF-kB activation in either cell type. Data analysis suggested that exposure to particulate matter induced NF-kB activation in JEG3 trophoblasts after a twenty-four hour stimulation (p=0.02), with a trend toward NF-kB activation in cells exposed to ultrafine particles (0.1 micron) (p=0.14). Data from placental fibroblasts suggest a trend toward activation of NF-kB by ultrafine particles as well (p=0.079). Fine particles (0.98 micron) did not induce NF-kB activation in either cell type. ConclusionUltrafine particles may activate NF-kB in human trophoblast cells and murine placental fibroblasts, and may contribute to local and systemic inflammation in pregnancy. Ultrafine particles may activate NF-kB in human trophoblast cells and murine placental fibroblasts, and may contribute to local and systemic inflammation in pregnancy." @default.
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• W2149776807 title "NF-kB activation in human JEG3 trophoblast cells and murine placental fibroblasts after exposure to ultrafine particulate matter" @default.
• W2149776807 doi "https://doi.org/10.1016/j.ajog.2005.10.740" @default.
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