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: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:In this analysis we have used gene expression measurements form human bronchial epithelial cells following exposure to whole cigarette smoke.
Project description:Chronic obstructive pulmonary disease (COPD) is a serious global health problem characterized by chronic airway inflammation, progressive airflow limitation and destruction of lung parenchyma. Remodeling of the bronchial airways in COPD includes changes in both the bronchial epithelium and the subepithelial extracellular matrix (ECM). To explore the impact of an aberrant ECM on epithelial cell phenotype in COPD we developed a new ex vivo model, in which normal human bronchial epithelial (NHBE) cells repopulate and differentiate on decellularized human bronchial scaffolds derived from COPD patients and healthy individuals. By using transcriptomics, we show that bronchial ECM from COPD patients induces differential gene expression in primary NHBE cells when compared to normal bronchial ECM. The gene expression profile indicated altered activity of upstream mediators associated with COPD pathophysiology, including hepatocyte growth factor, transforming growth factor beta 1 and platelet-derived growth factor B, which suggests that COPD-related changes in the bronchial ECM contribute to the defective regenerative ability in the airways of COPD patients.
Project description:We have characterized the effect of the CEACAM5 targeting monoclonal antibody labetuzumab (2 µg/mL) on the transcriptional response to interleukin-13 (IL-13) treatment (10ng/mL) of air-liquid interface (ALI) cultures generated from primary human bronchial epithelial cells. ALI cultures were treated with IL-13 and labetuzumab during the last 7 days of ALI development and the transcriptomes analyzed by RNA-seq.
Project description:Microarray analysis was performed to identify transcriptional changes that occur during mucociliary differentiation of human primary bronchial epithelial cells cultured at an air-liquid interface (ALI). Keywords: time course
