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Primary normal human bronchial epithelial cells (NHBE) cultured at air liquid interface with or without macrophage cells (+/- Mac) derived from primary peripheral blood mononuclear cells

ABSTRACT: The purpose is to obtain samples for mRNA analysis in primary normal human bronchial epithelial cells cultured with or without macrophage cells (+/- Mac) derived from primary peripheral blood monnumclear cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE156727 | GEO | 2020/09/02

REPOSITORIES: GEO

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Primary normal human bronchial epithelial cells (NHBE) cultured at air liquid interface with or without macrophage cells (+/- Mac) derived from primary peripheral blood mononuclear cells

Project description:Primary normal human bronchial epithelial cells (NHBE) cultured at air liquid interface with or without macrophage cells (+/- Mac) derived from primary peripheral blood mononuclear cells

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miRNA expression in differentiating primary human bronchial epithelial cells cultured at air-liquid-interface

Project description:We performed microarray analysis of miRNA expression in differentiating primary human bronchial epithelial cells. The goal was to identify miRNAs that are dynamically expressed under airway epithelial development. Cells were cultured at air-liquid-interface and were harvested day 4, 6, 8, 11, 13, 15, 18, 20 and 22 for analysis.

2021-01-09 | GSE164448 | GEO

Mac-1 cells with SATB1 silencing vs control Mac-1 cells

Project description:Transcriptional profiling of primary cutaneous anaplastic large cell lymphoma cell line Mac-1 cells transduced with lenti-virus vector harboring shRNA against SATB1 gene comparing control untreated Mac-1 cells and Mac-1 cells transduced with scrambled shRNA, in which SATB1 expression is not affected. Two condition experiment, SATB1 silenced Mac-1 cells vs control Mac-1 cells. Biological replicates: 2 transduced replicates, 2 control replicates

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Mac-1 cells with SATB1 silencing vs control Mac-1 cells

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Cigarette smoke alters primary human bronchial epithelial cell differentiation at the air-liquid interface.

Project description:The differentiated human airway epithelium consists of different cell types forming a polarized and pseudostratified epithelium. This is dramatically altered in chronic obstructive pulmonary disease (COPD), characterized by basal and goblet cell hyperplasia, and squamous cell metaplasia. The effect of cigarette smoke on human bronchial epithelial cell (HBEC) differentiation remains to be elucidated. We analysed whether cigarette smoke extract (CSE) affected primary (p)HBEC differentiation and function. pHBEC were differentiated at the air-liquid interface (ALI) and differentiation was quantified after 7, 14, 21, or 28 days by assessing acetylated tubulin, CC10, or MUC5AC for ciliated, Clara, or goblet cells, respectively. Exposure of differentiating pHBEC to CSE impaired epithelial barrier formation, as assessed by resistance measurements (TEER). Importantly, CSE exposure significantly reduced the number of ciliated cells, while it increased the number of Clara and goblet cells. CSE-dependent cell number changes were reflected by a reduction of acetylated tubulin levels, an increased expression of the basal cell marker KRT14, and increased secretion of CC10, but not by changes in transcript levels of CC10, MUC5AC, or FOXJ1. Our data demonstrate that cigarette smoke specifically alters the cellular composition of the airway epithelium by affecting basal cell differentiation in a post-transcriptional manner.

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Exposure of Air-Liquid-Interface bronchial epithelial cells to whole birch pollen

Project description:Human BEAS-2B were exposed to whole birch pollen using a Pollen Sedimentation Chamber. The chamber was designed to be able to dose cells to dry whole pollen. The goal was to understand the reaction of human epithelial cells to a human real life pollen exposure.

2021-11-03 | GSE179942 | GEO

Liquid Application Dosing Alters the Physiology of Air-Liquid Interface Primary Bronchial Epithelial Cell/Lung Fibroblast Co-Cultures and In Vitro Testing Relevant Endpoints

Project description:Liquid Application Dosing Alters the Physiology of Air-Liquid Interface Primary Bronchial Epithelial Cell/Lung Fibroblast Co-Cultures and In Vitro Testing Relevant Endpoints

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miRNA expression in differentiating primary human bronchial epithelial cells cultured at air-liquid-interface

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Liquid Application Dosing Alters the Physiology of Air-Liquid Interface Primary Bronchial Epithelial Cultures and In vitro Testing Relevant Endpoints.

Project description:Differentiated Primary human bronchial epithelial cell (dpHBEC) cultures grown under air-liquid interface (ALI) conditions exhibit key features of the human respiratory tract and are thus critical for respiratory research as well as efficacy and toxicity testing of inhaled substances (e.g., consumer products, industrial chemicals, and pharmaceuticals). Many inhalable substances (e.g., particles, aerosols, hydrophobic substances, reactive substances) have physiochemical properties that challenge their evaluation under ALI conditions in vitro. Evaluation of the effects of these methodologically challenging chemicals (MCCs) in vitro is typically conducted by "liquid application," involving the direct application of a solution containing the test substance to the apical, air-exposed surface of dpHBEC-ALI cultures. We report that the application of liquid to the apical surface of a dpHBEC-ALI co-culture model results in significant reprogramming of the dpHBEC transcriptome and biological pathway activity, alternative regulation of cellular signaling pathways, increased secretion of pro-inflammatory cytokines and growth factors, and decreased epithelial barrier integrity. Given the prevalence of liquid application in the delivery of test substances to ALI systems, understanding its effects provides critical infrastructure for the use of in vitro systems in respiratory research as well as in the safety and efficacy testing of inhalable substances.

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Ordinary Gasoline Emissions Induce a Toxic Response in Bronchial Cells Grown at Air-Liquid Interface.

Project description:Gasoline engine emissions have been classified as possibly carcinogenic to humans and represent a significant health risk. In this study, we used MucilAir™, a three-dimensional (3D) model of the human airway, and BEAS-2B, cells originating from the human bronchial epithelium, grown at the air-liquid interface to assess the toxicity of ordinary gasoline exhaust produced by a direct injection spark ignition engine. The transepithelial electrical resistance (TEER), production of mucin, and lactate dehydrogenase (LDH) and adenylate kinase (AK) activities were analyzed after one day and five days of exposure. The induction of double-stranded DNA breaks was measured by the detection of histone H2AX phosphorylation. Next-generation sequencing was used to analyze the modulation of expression of the relevant 370 genes. The exposure to gasoline emissions affected the integrity, as well as LDH and AK leakage in the 3D model, particularly after longer exposure periods. Mucin production was mostly decreased with the exception of longer BEAS-2B treatment, for which a significant increase was detected. DNA damage was detected after five days of exposure in the 3D model, but not in BEAS-2B cells. The expression of CYP1A1 and GSTA3 was modulated in MucilAir™ tissues after 5 days of treatment. In BEAS-2B cells, the expression of 39 mRNAs was affected after short exposure, most of them were upregulated. The five days of exposure modulated the expression of 11 genes in this cell line. In conclusion, the ordinary gasoline emissions induced a toxic response in MucilAir™. In BEAS-2B cells, the biological response was less pronounced, mostly limited to gene expression changes.

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