Project description:The goal was to assess global gene expression changes in primary human bronchial epithelial cells exposed to environmental tobacco smoke (ETS) condensate. ETS-C was standardized by HPLC analysis and two timepoints of exposure in two different donor bronchial epithelial cell populations were assessed. These findings demonstrate that even short exposure (4.5 h) to ETS is sufficient to induce a stress response, as reflected by decreased antioxidant levels, induced HSP family members, and modulation of the family of glutathione metabolism enzymes in primary human lung cells. Upon longer exposures (48 h) with ETS-condensate, bronchial epithelial cells arrest at the G2/M phase of the cell cycle. Taken together, these data support a stress-induced state in primary human bronchial epithelial cells that culminates in cell cycle arrest. Keywords: time course, comparative, stress response
Project description:In this analysis we have used gene expression measurements form human bronchial epithelial cells following exposure to whole cigarette smoke.
Project description:Δ8-tetrahydrocannabinol (Δ8-THC) vaping products rapidly expanded following the 2018 Farm Bill, yet remain largely unregulated despite high cannabinoid concentrations, additives and contaminants, and growing links to adverse respiratory outcomes. Here we show that the reactive electrophile Δ8-THC quinone (Δ8-THCQ, HU-336) is present in significant quantities in commercial Δ8-THC distillate and disposable products and increases after vaping. Across high concentration products, Δ8-THCQ rose an average of 3.67-fold, reaching millimolar levels. While Δ8-THC itself produced no measurable transcriptomic response in a bronchial epithelial cell line, Δ8-THCQ markedly altered gene expression, prominently upregulating cilia and stress related programs alongside xenobiotic metabolism and inflammatory pathways. Using primary differentiated human bronchial epithelial cells exposed with the UNC Vaping Product Exposure System (VaPES), we demonstrate that vaped commercial Δ8-THC mixtures induce immediate early stress genes, suppress ribosome and mitochondrial pathways, and trigger fibrosis associated signaling, while juices caused comparatively modest effects, primarily limited to upregulation of cell-cycle and proliferation-associated genes. Computational analysis further mechanistically linked coordinated chemical features of Δ8-THC aerosols to the airway transcriptional programs they induced, identifying clusters of chemicals that drive specific biological responses. Functionally, distillate and disposable aerosols rapidly impaired motile cilia activity. Together, these data identify Δ8-THCQ as a major vaping-generated reactive product in Δ8-THC aerosols and suggest that repeated inhalation may disrupt mucociliary defense and promote chronic airway injury.
Project description:Purpose: To understand the molecular mechanisms underlying Cd exposure-induced diseases. Methods: Immortalized human bronchial epithelial cells (BEAS-2B) were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM, Cellgro) supplemented with 1% Penicillin Streptomycin and 10% Fetal Bovine Serum (FBS, Atlanta Biologicals) at 37 degree C and 5 % CO2. For Cd exposure, 0, 2.5, 5 and 10 µM of CdCl2 was added to the media and the cells were cultured for 72h. Results: This study shows that cadmium exposure induces SNAIL1 expression via miR-30e downregulation and the cells undergo epithelial-mesenchymal transition.
Project description:We carry out a comparative proteomic analysis of human bronchial epithelial cells from patients clinically treated or not with inhaled budesonide and stimulated or not with the viral mimic Poly(I:C).We also wanted to investigate the potential anti-viral effects of imiquimod, a TLR7 agonist, on the bronchial epithelial cells proteome in vitro.
Project description:This study aims to identify the proteomic targets of THC in the early postnatal hippocampus of developing mice. Therefore, early postnatal C57Bl/6 mice (P5) were exposed daily and for 30 days to plant extracted THC (either 1 mg/kg or 5 mg/kg) or vehicle solution (saline with 3% Tween® 80) for the control group. All animals stayed with their mothers until P25 and after the initial drug exposure time (until P35) animals were given a drug-free resting period. The animals were sacrificed, and their hippocampus was dissected and prepared for the following proteomic analysis at either P48 or after an extended resting period at P120. We found 31 proteins to be changed after THC exposure compared to vehicle at P48 and 186 proteins showing modifications at P120. Gene ontology classification of protein targets revealed a substantial amount of proteins involved in metabolic processes of neurons after THC exposure. The results highlight the vulnerability of the developing hippocampus towards THC exposure and identify the mitochondrial as well as other cell metabolic processes as potential drug targets.
Project description:This SuperSeries is composed of the following subset Series:; GSE14383: Effects of chronic exposure of human bronchial epithelial cells to low doses of cigarette smoke condensate; GSE14385: Response of bronchial epithelial cells to low doses of cigarette smoke condensate and subsequent demethylation agent Experiment Overall Design: Refer to individual Series