Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176094 | ENA |
REPOSITORIES: ENA
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Project description:Recent in vivo studies reported that inhaled carbon nanotube distribute in the alveolar region resulting in an acute inflammation, progressive fibrotic response and particle accumulation at the bronchoalveolar junction with low clearance. With similar biopersistence and shape as asbestos, a known lung carcinogen, growing concern has arisen for elevated risk of carbon nanotube-induced lung carcinogenesis; however few studies have evaluated long-term human health risks associated with chronic pulmonary carbon nanotube exposures compared to asbestos. To address this knowledge gap, we conducted subchronic in vitro exposures of dispersed single walled carbon nanotube, multi-walled carbon nanotube and crocidolite asbestos to human small airway epithelial cells to assess their neoplastic transformation potential. Subchronic single-, multi-walled carbon nanotube and asbestos exposures caused human lung cell neoplastic transformation exhibited by increased proliferation, anchorage-independent growth, invasion and angiogenesis. Whole genome profiling and protein expression analyses showed that carbon nanotube-induced transformation mechanism(s) was largely different from asbestos-related inflammatory signaling, suggesting specific carbon nanotube-induced carcinogenic potential. This study provides novel carbon nanotube and asbestos toxicogenomic information for risk assessment and an in vitro model to evaluate transformation potential of carbon nanotubes and other nanoparticles. Whole genome expression profiling was conducted on human immortalized small airway epithelial cells (SAEC-hTERT) following 6 month in vitro chronic exposure to six separate treatments to assess differences in carbon nanotube (CNT) vs. asbestos potential tumorigenesis signaling. Dispersed single wall CNT (D-SWCNT), multi-wall CNT (D-MWCNT), ultrafine carbon black (D-UFCB), crocidolite asbestos (ASB) and saline (SAL) exposed cells were compared to SurvantaM-BM-. dispersant (DISP) passage control cells. Each treatment possessed 3 biological cDNA replicates. One technical replicate was performed per biological sample.
2013-07-22 | E-GEOD-41178 | biostudies-arrayexpress
Project description:Recent in vivo studies reported that inhaled carbon nanotube distribute in the alveolar region resulting in an acute inflammation, progressive fibrotic response and particle accumulation at the bronchoalveolar junction with low clearance. With similar biopersistence and shape as asbestos, a known lung carcinogen, growing concern has arisen for elevated risk of carbon nanotube-induced lung carcinogenesis; however few studies have evaluated long-term human health risks associated with chronic pulmonary carbon nanotube exposures compared to asbestos. To address this knowledge gap, we conducted subchronic in vitro exposures of dispersed single walled carbon nanotube, multi-walled carbon nanotube and crocidolite asbestos to human small airway epithelial cells to assess their neoplastic transformation potential. Subchronic single-, multi-walled carbon nanotube and asbestos exposures caused human lung cell neoplastic transformation exhibited by increased proliferation, anchorage-independent growth, invasion and angiogenesis. Whole genome profiling and protein expression analyses showed that carbon nanotube-induced transformation mechanism(s) was largely different from asbestos-related inflammatory signaling, suggesting specific carbon nanotube-induced carcinogenic potential. This study provides novel carbon nanotube and asbestos toxicogenomic information for risk assessment and an in vitro model to evaluate transformation potential of carbon nanotubes and other nanoparticles.
2013-07-22 | GSE41178 | GEO
Project description:Whole genome expression signature of SWCNT and MWCNT vs. asbestos subchronic exposures to human pleural mesothelial cells
| PRJNA212005 | ENA
Project description:Pulmonary exposure to multiwalled carbon nanotubes (MWCNT) induces an inflammatory and rapid fibrotic response, although the long-term signaling mechanisms are unknown. The aim of this study was to examine the effects of 1, 10, 40, or 80 µg MWCNT administered by pharyngeal aspiration on bronchoalveolar lavage (BAL) fluid for polymorphonuclear cell (PMN) infiltration, lactate dehydrogenase (LDH) activity, and lung histopathology for inflammatory and fibrotic responses in mouse lungs 1 mo, 6 mo, and 1 yr postexposure. Further, a 120-µg crocidolite asbestos group was incorporated as a positive control for comparative purposes. Results showed that MWCNT increased BAL fluid LDH activity and PMN infiltration in a dose-dependent manner at all three postexposure times. Asbestos exposure elevated LDH activity at all 3 postexposure times and PMN infiltration at 1 mo and 6 mo postexposure. Pathological changes in the lung, the presence of MWCNT or asbestos, and fibrosis were noted at 40 and 80 µg MWCNT and in asbestos-exposed mice at 1 yr postexposure. To determine potential signaling pathways involved with MWCNT-associated pathological changes in comparison to asbestos, up- and down-regulated gene expression was determined in lung tissue at 1 yr postexposure. Exposure to MWCNT tended to favor those pathways involved in immune responses, specifically T-cell responses, whereas exposure to asbestos tended to favor pathways involved in oxygen species production, electron transport, and cancer. Data indicate that MWCNT are biopersistent in the lung and induce inflammatory and fibrotic pathological alterations similar to those of crocidolite asbestos, but may reach these endpoints by different mechanisms.
2018-04-06 | GSE112780 | GEO
Project description:Pulmonary exposure to multiwalled carbon nanotubes (MWCNT) induces an inflammatory and rapid fibrotic response, although the long-term signaling mechanisms are unknown. The aim of this study was to examine the effects of 1, 10, 40, or 80 μg MWCNT administered by pharyngeal aspiration on bronchoalveolar lavage (BAL) fluid for polymorphonuclear cell (PMN) infiltration, lactate dehydrogenase (LDH) activity, and lung histopathology for inflammatory and fibrotic responses in mouse lungs 1 mo, 6 mo, and 1 yr postexposure. Further, a 120-μg crocidolite asbestos group was incorporated as a positive control for comparative purposes. Results showed that MWCNT increased BAL fluid LDH activity and PMN infiltration in a dose-dependent manner at all three postexposure times. Asbestos exposure elevated LDH activity at all 3 postexposure times and PMN infiltration at 1 mo and 6 mo postexposure. Pathological changes in the lung, the presence of MWCNT or asbestos, and fibrosis were noted at 40 and 80 μg MWCNT and in asbestos-exposed mice at 1 yr postexposure. To identify non-invasive miRNA biomarkers, miRNA profiling was performed in blood samples collected from MWCNT exposed mice.
2019-07-26 | GSE130109 | GEO
Project description:Accessible in vitro models recapitulating the human airway that are amenable to study whole cannabis smoke exposure are needed for immunological and toxicological studies that inform public health policy and recreational cannabis use. In the present study, we developed and validated a novel 3D printed In Vitro Exposure System (IVES) that can be directly applied to study the effect of cannabis smoke exposure on primary human bronchial epithelial cells. Using commercially available design software and a 3D printer, we designed a four-chamber Transwell® insert holder for exposures to whole smoke. Software was used to model gas distribution, concentration gradients, velocity profile and shear stress within IVES. Following simulations, primary human bronchial epithelial cells cultured at air-liquid interface on Transwell® inserts were exposed to whole cannabis smoke. IVES represents an accessible, open-source, exposure system that can be used to model varying types of cannabis smoke exposures with human airway epithelial cells grown under air-liquid interface culture conditions.
2021-10-22 | GSE161139 | GEO
Project description:As the application of carbon nanotubes (CNT) in consumer products continues to rise, studies have expanded to determine the associated risks of exposure on human and environmental health. In particular, several lines of evidence indicate that exposure to multi-walled carbon nanotubes (MWCNT) could pose a carcinogenic risk similar to asbestos fibers. However, to date the potential markers of MWCNT exposure are not yet explored in humans. Global mRNA and lncRNA expression profiles in the whole blood of exposed workers, having direct contact with MWCNT aerosols for atleast 6 months (n=8), were compared with expression profiles of non-exposed (n=7) workers (e.g., proffessional and/or technical staff) from the same manufacturing facility.
2016-03-09 | E-GEOD-73830 | biostudies-arrayexpress
Project description:As the application of carbon nanotubes (CNT) in consumer products continues to rise, studies have expanded to determine the associated risks of exposure on human and environmental health. In particular, several lines of evidence indicate that exposure to multi-walled carbon nanotubes (MWCNT) could pose a carcinogenic risk similar to asbestos fibers. However, to date the potential markers of MWCNT exposure are not yet explored in humans.
2016-03-09 | GSE73830 | GEO
Project description:Multi-walled carbon nanotubes (MWCNT) present a wide variety of exciting application opportunities. As MWCNT are produced in large quantities, occupational exposure and human health is of particular concern. However, there is no consensus regarding their potential harmful effects. In particular, chronic exposure to MWCNT and mechanisms of their action at protein and lipid levels are unknown. In this study, we aimed to investigate effects of long-term chronic exposure to MWCNT on cellular proteome and lipidome. Since the lung is the major target organ, an in vitro normal bronchial epithelial cell model was used. To better mimic exposure at occupational settings, cells were chronically exposed for 13 weeks to low-doses of MWCNT. MWCNT-treatment increased ROS levels in cells without increasing DNA damage and resulted in differential expression of multiple apoptotic proteins. A shotgun proteomic and lipidomic analysis of the MWCNT-exposed cells showed that of amongst the >5000 identified protein s,groups; more than 200 were altered in treated cells. Functional analysis revealed association of these differentially regulated proteins in various cellular processes such as cell death and survival, cellular assembly and organization. Similarly, the lipid profile of the MWCNT treated cells showed accumulation of multiple lipid classes. This is first study to present results indicating that long-term MWCNT-exposure of human normal lung cells at occupationally relevant low-dose may alter both the proteome and the lipidome profile of target epithelial cells in the lung.
2020-05-06 | PXD005970 | Pride
Project description:Multi-walled carbon nanotubes (MWCNT) cause lung fibrosis in rodents and exacerbate airway fibrosis in the mouse ovalbumin model of allergic asthma. Interleukin 13 (IL-13) is a key cytokine secreted by T helper type 2 (Th2) cells. IL-13 is up-regulated in human asthma and animal models that activate pro-fibrotic and pro-proliferative cell signaling cascades in human lung fibroblasts (HLF). This study tested the hypothesis that IL-13 alters the gene expression profile of HLF exposed to MWCNT. Carbon black nanoparticles (CBNP) were also compared to MWCNT as they are relatively inert nanoparticles that do not cause fibrosis. Confluent, quiescent cultures of HLF were treated with 10 ng/ml IL-13 or serum-free defined medium (vehicle) for 24 hours prior to treatment with 10 µg/cm2 MWCNT or CBNP. At 4, 24, or 48 hours following nanoparticle exposure, total RNA was isolated and gene expression was measured using the Affymetrix Human Genome U133A2.0 Array. The data were analyzed using the JMP Genomics statistical platform. IL-13 and MWCNT each caused changes in the expression of distinct gene subsets over the time-course investigated. The combination of IL-13 and MWCNT resulted in a gene expression profile that was distinct from patterns induced or suppressed by either IL-13 or MWCNT alone. CBNP caused changes in gene expression that were distinct from IL-13 or MWCNT. Interestingly, the combination of IL-13 and MWCNT increased the expression of IL-17A and increased collagen (Col1A1), while MWCNT alone increased interferon-inducible protein-27 (IFI27), suggesting that Th2 microenvironment containing IL-13 shifts MWCNT-induced gene expression from a Th1 to a Th17 gene expression profile. These data provide insight into the mechanisms by which MWCNT alter the biology of fibroblasts during normal and allergic inflammatory conditions.
2013-05-29 | GSE43515 | GEO