Project description:To investigate the role of interleukin-13 (IL-13) and the epidermal growth factor (EGF) receptor pathway in controlling mucus metaplasia, normal human bronchial epithelial (NHBE) cells were cultured on air-liquid interface for 14 days and were treated with IL-13, anti-EGFR antibody or both during the final 48 h of culture. Keywords: Stimulus response
Project description:Normal human bronchial epithelial cells were studied under four different conditions: control, pressure 30 cmH2O, AG1478 (1 microM), and pressure plus AG1478 at 1, 3, and 8 hours, all in the absence of exogenous EGF. Keywords: Normal human bronchial epithelial cells.
Project description:We performed RNA sequencing of gene expression of differentiated primary human bronchial epithelial cells derived from control and asthmatic patients, stimulated with IL-13. The Type 2 Asthma mediator IL-13 was described to induce airway hyperresponsiveness, goblet cell metaplasia, mucus hypersecretion and airway remoddeling including impairment of epithelial barrier integrity. We investigated differential expression of SARS-CoV-2 related host gene expression as well as genes involved in N-linked glycosylation upon IL-13 in bronchial epithelial cells. Top IL-13 affected pathways included ion- and transmembrane transport, lipid metabolic processed and protein glycosylation.
Project description:Normal human bronchial epithelial cells were studied under four different conditions: control, pressure 30 cmH2O, AG1478 (1 microM), and pressure plus AG1478 at 1, 3, and 8 hours, all in the absence of exogenous EGF. Keywords: Normal human bronchial epithelial cells. Time series under 4 different stimuli with no replicate measurements.
Project description:We used ChIP-seq to investigate epigenomic modifications in response to IFN-a, IL-17, and IL-13 in primary human bronchial epithelial cells (HBECs).
Project description:We used bulk cell RNA-seq to investigate transcriptional effects of IFN-a, IL-17, and IL-13 in primary human bronchial epithelial cells (HBECs).
Project description:We used scRNA-seq to investigate cell type-specific transcriptional effects of IFN-a, IL-17, and IL-13 in primary human bronchial epithelial cells (HBECs).
Project description:Cigarette smoking is the major cause of chronic inflammatory diseases such as Chronic Obstructive Pulmonary Disease (COPD). It is paramount to develop pharmacological interventions and delivery strategies against the cigarette smoke (CS) associated oxidative stress in COPD. This study in Wistar rats examined cysteamine in nanoemulsions to counteract the cigarette smoke distressed microenvironment. In vivo, 28 days of cigarette smoke and 15 days of cysteamine nanoemulsions treatment starting on 29th day consisting of oral and inhalation routes were established in Wistar rats. Additionally, we conducted inflammatory and epithelial-to-mesenchymal transition (EMT) studies in vitro in human bronchial epithelial cell lines (BEAS2B) using 5% cigarette smoke extract. Inflammatory and anti-inflammatory markers such as TNF-α, IL-6, IL-1ß, IL-8, IL-10, IL-13, have been quantified in bronchoalveolar lavage fluid (BALF) to evaluate the effects of the cysteamine nanoemulsions in normalizing the diseased condition. Histopathological analysis of the alveoli and the trachea showed the distorted, lung parenchyma and ciliated epithelial barrier, respectively. To obtain mechanistic insights into the cigarette smoke COPD rat model, “shotgun” proteomics of the lung tissues have been carried out using high-resolution mass spectrometry wherein genes such as ABI1, PPP3CA, PSMA2, FBLN5, ACTG1, CSNK2A1, and ECM1 exhibited significant differences across all the groups. Pathway analysis showed autophagy, signaling by receptor tyrosine kinase, cytokine signaling in immune system, extracellular matrix organization, and hemostasis, as the major contributing pathways across all the studied groups. This work offers new preclinical findings on how cysteamine taken orally or inhaled can combat cigarette smoke-induced oxidative stress.
