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Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73063 | GEO | 2015/09/16

SECONDARY ACCESSION(S): PRJNA295992

REPOSITORIES: GEO

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Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-09-16 | E-GEOD-73063 | biostudies-arrayexpress

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory and immune response genes.

Project description:The intensification and concentration of animal production operations expose workers to high levels of organic dusts in the work environment. Exposure to organic dusts is a risk factor for the development of acute and chronic respiratory symptoms and diseases. Lung epithelium plays important roles in the control of immune and inflammatory responses to environmental agents to maintain lung health. To better understand the effects of organic dust on lung inflammatory responses, we characterized the gene expression profiles of A549 alveolar and Beas2B bronchial epithelial and THP-1 monocytic cells influenced by exposure to poultry dust extract by DNA microarray analysis using Illumina Human HT-12 v4 Expression BeadChip. We found that A549 alveolar and Beas2B bronchial epithelial and THP-1 cells responded with unique changes in the gene expression profiles with regulation of genes encoding inflammatory cytokines, chemokines, and other inflammatory proteins being common to all the three cells. Significantly induced genes included IL-8, IL-6, IL-1β, ICAM-1, CCL2, CCL5, TLR4, and PTGS2. Validation by real-time qRT-PCR, ELISA, Western immunoblotting, and immunohistochemical staining of lung sections from mice exposed to dust extract validated DNA microarray results. Pathway analysis indicated that dust extract induced changes in gene expression influenced functions related to cellular growth and proliferation, cell death and survival, and cellular development. These data show that a broad range of inflammatory mediators produced in response to poultry dust exposure can modulate lung immune and inflammatory responses. This is the first report on organic dust induced changes in expression profiles in lung epithelial and THP-1 monocytic cells.

| S-EPMC4824153 | biostudies-literature

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [452 expt: THP-1 vs BEAS 2B]

Project description:The goal of the study was to characterize gene expression profiles of lung epithelial and THP-1 monocytic cells influenzed by exposure to poultry dust extract. Gene expression profiles were determined by DNA microarrayanalysis using Illumina Human HT-12 v4 Expression bead chip, and changes in significantly induced transcripts validated by real time quantitative RT-PCR, ELISA, Western blotting and immunohistochemical staining. Significantly induced genes included IL-8, IL-6, ICAM-1, CCL2, CCL5, TLR4 and PTGS2. Pathway analysis indicated that dust extract treatment induced changes in gene expression influenced functions related to immune and inflammatory responses. Cells were treated with medium alone (control) or dust extract (0.1% or 0.25%) for 1, 3 or 6 h (reference).

2015-09-16 | E-GEOD-73062 | biostudies-arrayexpress

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [452 expt: THP-1 vs BEAS 2B]

2015-09-16 | GSE73062 | GEO

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [391 expt: A549 vs BEAS 2B]

2015-09-16 | E-GEOD-73061 | biostudies-arrayexpress

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators [391 expt: A549 vs BEAS 2B]

2015-09-16 | GSE73061 | GEO

Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators

Project description:Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory mediators

| PRJNA295992 | ENA

Organic dust inhibits surfactant protein expression by reducing thyroid transcription factor-1 levels in human lung epithelial cells.

Project description:Exposure to organic dust is a risk factor for the development of respiratory diseases. Surfactant proteins (SP) reduce alveolar surface tension and modulate innate immune responses to control lung inflammation. Therefore, changes in SP levels could contribute to the development of organic-dust-induced respiratory diseases. Because information on the effects of organic dust on SP levels is lacking, we studied the effects of dust from a poultry farm on SP expression. We found that dust extract reduced SP-A and SP-B mRNA and protein levels in H441 human lung epithelial cells by inhibiting their promoter activities, but did not have any effect on SP-D protein levels. Dust extract also reduced SP-A and SP-C levels in primary human alveolar epithelial cells. The inhibitory effects were not due to LPS or protease activities present in dust extract or mediated via oxidative stress, but were dependent on a heat-labile factor(s). Thyroid transcription factor-1, a key transcriptional activator of SP expression, was reduced in dust-extract-treated cells, indicating that its down-regulation mediates inhibition of SP levels. Our study implies that down-regulation of SP levels by organic dust could contribute to the development of lung inflammation and respiratory diseases in humans.

| S-EPMC6830861 | biostudies-literature

Combined Collagen-Induced Arthritis and Organic Dust-Induced Airway Inflammation to Model Inflammatory Lung Disease in Rheumatoid Arthritis.

Project description:Rheumatoid arthritis (RA) is characterized by extra-articular involvement including lung disease, yet the mechanisms linking the two conditions are poorly understood. The collagen-induced arthritis (CIA) model was combined with the organic dust extract (ODE) airway inflammatory model to assess bone/joint-lung inflammatory outcomes. DBA/1J mice were intranasally treated with saline or ODE daily for 5 weeks. CIA was induced on days 1 and 21. Treatment groups included sham (saline injection/saline inhalation), CIA (CIA/saline), ODE (saline/ODE), and CIA + ODE (CIA/ODE). Arthritis inflammatory scores, bones, bronchoalveolar lavage fluid, lung tissues, and serum were assessed. In DBA/1J male mice, arthritis was increased in CIA + ODE > CIA > ODE versus sham. Micro-computed tomography (µCT) demonstrated that loss of BMD and volume and deterioration of bone microarchitecture was greatest in CIA + ODE. However, ODE-induced airway neutrophil influx and inflammatory cytokine/chemokine levels in lavage fluids were increased in ODE > CIA + ODE versus sham. Activated lung CD11c+ CD11b+ macrophages were increased in ODE > CIA + ODE > CIA pattern, whereas lung hyaluronan, fibronectin, and amphiregulin levels were greatest in CIA + ODE. Serum autoantibody and inflammatory marker concentrations varied among experimental groups. Compared with male mice, female mice showed less articular and pulmonary disease. The interaction of inhalation-induced airway inflammation and arthritis induction resulted in compartmentalized responses with the greatest degree of arthritis and bone loss in male mice with combined exposures. Data also support suppression of the lung inflammatory response, but increases in extracellular matrix protein deposition/interstitial disease in the setting of arthritis. This coexposure model could be exploited to better understand and treat RA-lung disease. © 2019 American Society for Bone and Mineral Research.

| S-EPMC6744331 | biostudies-literature

Oxidative Stress, Cytotoxic and Inflammatory Effects of Urban Ultrafine Road-Deposited Dust from the UK and Mexico in Human Epithelial Lung (Calu-3) Cells.

Project description:Road-deposited dust (RD) is a pervasive form of particulate pollution identified (typically via epidemiological or mathematical modelling) as hazardous to human health. Finer RD particle sizes, the most abundant (by number, not mass), may pose greater risk as they can access all major organs. Here, the first in vitro exposure of human lung epithelial (Calu-3) cells to 0-300 µg/mL of the ultrafine (<220 nm) fraction of road dust (UF-RDPs) from three contrasting cities (Lancaster and Birmingham, UK, and Mexico City, Mexico) resulted in differential oxidative, cytotoxic, and inflammatory responses. Except for Cd, Na, and Pb, analysed metals were most abundant in Mexico City UF-RDPs, which were most cytotoxic. Birmingham UF-RDPs provoked greatest ROS release (only at 300 µg/mL) and greatest increase in pro-inflammatory cytokine release. Lancaster UF-RDPs increased cell viability. All three UF-RDP samples stimulated ROS production and pro-inflammatory cytokine release. Mass-based PM limits seem inappropriate given the location-specific PM compositions and health impacts evidenced here. A combination of new, biologically relevant metrics and localised regulations appears critical to mitigating the global pandemic of health impacts of particulate air pollution and road-deposited dust.

| S-EPMC9495992 | biostudies-literature

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