Real-world outdoor air exposure effects in a model of the human airway epithelium - A comparison of healthy and asthmatic individuals using a mobile laboratory setting.

We developed a mobile laboratory allowing field exposure of lung tissue models to ambient air at localities with various pollution sources (Background, Industrial, Traffic, Urban) in different seasons (summer/fall/winter). In samples originating from healthy and asthmatic individuals, we assessed the parameters of toxicity, lipid peroxidation and immune response; we further performed comprehensive monitoring of air pollutants at sampling sites. We measured lactate dehydrogenase (LDH) and adenylate kinase (AK) production and transepithelial electrical resistance (TEER), analyzed 15-F-isopostane (IsoP) and a panel of 20 cytokines/chemokines/growth factors.

Gene expression profiles and protein-protein interaction networks in THP-1 cells exposed to metal-based nanomaterials.

We analyzed gene expression in THP-1 cells exposed to metal-based nanomaterials (NMs) [TiO (NM-100), ZnO (NM-110), SiO (NM-200), Ag (NM-300 K)]. A functional enrichment analysis of the significant differentially expressed genes (DEGs) identified the key modulated biological processes and pathways. DEGs were used to construct protein-protein interaction networks.

Differential DNA damage response and cell fate in human lung cells after exposure to genotoxic compounds.

DNA damage can impair normal cellular functions and result in various pathophysiological processes including cardiovascular diseases and cancer. We compared the genotoxic potential of diverse DNA damaging agents, and focused on their effects on the DNA damage response (DDR) and cell fate in human lung cells BEAS-2B. Polycyclic aromatic hydrocarbons [PAHs; benzo[a]pyrene (B[a]P), 1-nitropyrene (1-NP)] induced DNA strand breaks and oxidative damage to DNA; anticancer drugs doxorubicin (DOX) and 5-bromo-2'-deoxyuridine (BrdU) were less effective.

Transcription profiles in BEAS-2B cells exposed to organic extracts from particulate emissions produced by a port-fuel injection vehicle, fueled with conventional fossil gasoline and gasoline-ethanol blend.

Emissions from road traffic are among the major contributors to air pollution worldwide and represent a serious environmental health risk. Although traffic-related pollution has been most commonly associated with diesel engines, increasing evidence suggests that gasoline engines also produce a considerable amount of potentially hazardous particulate matter (PM). The primary objective of this study was to compare the intrinsic toxic properties of the organic components of PM, generated by a conventional gasoline engine fueled with neat gasoline (E0), or gasoline-ethanol blend (15 % ethanol, v/v, E15).

Testing Strategies of the In Vitro Micronucleus Assay for the Genotoxicity Assessment of Nanomaterials in BEAS-2B Cells.

The evaluation of the frequency of micronuclei (MN) is a broadly utilised approach in in vitro toxicity testing. Nevertheless, the specific properties of nanomaterials (NMs) give rise to concerns regarding the optimal methodological variants of the MN assay. In bronchial epithelial cells (BEAS-2B), we tested the genotoxicity of five types of NMs (TiO: NM101, NM103; SiO: NM200; Ag: NM300K, NM302) using four variants of MN protocols, differing in the time of exposure and the application of cytochalasin-B combined with the simultaneous and delayed co-treatment with NMs.

Cystinuria in Dogs and Cats: What Do We Know after Almost 200 Years?

The purpose of this review is to summarize current knowledge on canine and feline cystinuria from available scientific reports. Cystinuria is an inherited metabolic defect characterized by abnormal intestinal and renal amino acid transport in which cystine and the dibasic amino acids ornithine, lysine, and arginine are involved (COLA). At a normal urine pH, ornithine, lysine, and arginine are soluble, but cysteine forms a dimer, cystine, which is relatively insoluble, resulting in crystal precipitation.

Markers of lipid oxidation and inflammation in bronchial cells exposed to complete gasoline emissions and their organic extracts.

Road traffic emissions consist of gaseous components, particles of various sizes, and chemical compounds that are bound to them. Exposure to vehicle emissions is implicated in the etiology of inflammatory respiratory disorders. We investigated the inflammation-related markers in human bronchial epithelial cells (BEAS-2B) and a 3D model of the human airways (MucilAir™), after exposure to complete emissions and extractable organic matter (EOM) from particles generated by ordinary gasoline (E5), and a gasoline-ethanol blend (E20; ethanol content 20% v/v).

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

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 Differential Effect of Carbon Dots on Gene Expression and DNA Methylation of Human Embryonic Lung Fibroblasts as a Function of Surface Charge and Dose.

This study presents a toxicological evaluation of two types of carbon dots (CD), similar in size (<10 nm) but differing in surface charge. Whole-genome mRNA and miRNA expression (RNAseq), as well as gene-specific DNA methylation changes, were analyzed in human embryonic lung fibroblasts (HEL 12469) after 4 h and 24 h exposure to concentrations of 10 and 50 µg/mL (for positive charged CD; pCD) or 10 and 100 µg/mL (for negative charged CD, nCD). The results showed a distinct response for the tested nanomaterials (NMs).

Genotoxicant exposure, activation of the aryl hydrocarbon receptor, and lipid peroxidation in cultured human alveolar type II A549 cells.

The aryl hydrocarbon receptor (AhR) transcription factor is activated by polycyclic aromatic hydrocarbons (PAH) and other ligands. Activated AhR binds to dioxin responsive elements (DRE) and initiates transcription of target genes, including the gene encoding prostaglandin endoperoxide synthase 2 (PTGS-2), which is also activated by the transcription factor NF-ĸB. PTGS-2 catalyzes the conversion of arachidonic acid (AA) into prostaglandins, thromboxanes or isoprostanes.

DNA Methylation Profiles in a Group of Workers Occupationally Exposed to Nanoparticles.

The risk of exposure to nanoparticles (NPs) has rapidly increased during the last decade due to the vast use of nanomaterials (NMs) in many areas of human life. Despite this fact, human biomonitoring studies focused on the effect of NP exposure on DNA alterations are still rare. Furthermore, there are virtually no epigenetic data available.

Gene Expression and Epigenetic Changes in Mice Following Inhalation of Copper(II) Oxide Nanoparticles.

We investigated the transcriptomic response and epigenetic changes in the lungs of mice exposed to inhalation of copper(II) oxide nanoparticles (CuO NPs) (8 × 10 NPs/m) for periods of 3 days, 2 weeks, 6 weeks, and 3 months. A whole genome transcriptome and miRNA analysis was performed using next generation sequencing. Global DNA methylation was assessed by ELISA.

The Biological Effects of Complete Gasoline Engine Emissions Exposure in a 3D Human Airway Model (MucilAir) and in Human Bronchial Epithelial Cells (BEAS-2B).

The biological effects induced by complete engine emissions in a 3D model of the human airway (MucilAir) and in human bronchial epithelial cells (BEAS-2B) grown at the air-liquid interface were compared. The cells were exposed for one or five days to emissions generated by a Euro 5 direct injection spark ignition engine. The general condition of the cells was assessed by the measurement of transepithelial electrical resistance and mucin production.

Toxicity of TiO, ZnO, and SiO Nanoparticles in Human Lung Cells: Safe-by-Design Development of Construction Materials.

Rapid progress in the development of highly efficient nanoparticle-based construction technologies has not always been accompanied by a corresponding understanding of their effects on human health and ecosystems. In this study, we compare the toxicological effects of pristine TiO, ZnO, SiO, and coated SiO nanoparticles, and evaluate their suitability as additives to consolidants of weathered construction materials. First, water soluble tetrazolium 1 (WST-1) and lactate dehydrogenase (LDH) assays were used to determine the viability of human alveolar A549 cells at various nanoparticle concentrations (0-250 μg mL).

Short-term and Long-term Exposure of the MucilAir™ Model to Polycyclic Aromatic Hydrocarbons.

Cells grown in monocultures are widely used to model lung tissue. As a result of these culture conditions, these cells exhibit poor morphological similarity to those present in lung tissue. MucilAir™, a 3-D model comprising human basal, goblet and ciliated cells, represents a fully differentiated respiratory epithelium that can be used as an alternative and a more realistic system.

The repeated cytogenetic analysis of subjects occupationally exposed to nanoparticles: a pilot study.

The application of nanomaterials has been rapidly increasing during recent years. Inhalation exposure to nanoparticles (NP) may result in negative toxic effects but there is a critical lack of human studies, especially those related to possible DNA alterations. We analyzed pre-shift and post-shift a group of nanocomposite researchers with a long-term working background (17.

Molecular Responses in THP-1 Macrophage-Like Cells Exposed to Diverse Nanoparticles.

In the body, engineered nanoparticles (NPs) may be recognized and processed by immune cells, among which macrophages play a crucial role. We evaluated the effects of selected NPs [NM-100 (TiO), NM-110 (ZnO), NM-200 (SiO), and NM-300 K (Ag)] on THP-1 macrophage-like cells. The cells were exposed to subcytotoxic concentrations of NPs (1-25 µg/mL) and the expression of immunologically relevant genes (VCAM1, TNFA, CXCL8, ICAM1, CD86, CD192, and IL1B) was analyzed by RT-qPCR.

A murine model of the effects of inhaled CuO nanoparticles on cells of innate and adaptive immunity - a kinetic study of a continuous three-month exposure.

The inhalation or application of nanoparticles (NPs) has serious impacts on immunological reactivity. However, the effects of NPs on the immune system are influenced by numerous factors, which cause a high variability in the results. Here, mice were exposed to a three month continuous inhalation of copper oxide (CuO) NPs, and at different time intervals (3, 14, 42 and 93 days), the composition of cell populations of innate and adaptive immunity was evaluated in the spleen by flow cytometry.

The processes associated with lipid peroxidation in human embryonic lung fibroblasts, treated with polycyclic aromatic hydrocarbons and organic extract from particulate matter.

Polycyclic aromatic hydrocarbons (PAHs) may cause lipid peroxidation via reactive oxygen species generation. 15-F2t-isoprostane (IsoP), an oxidative stress marker, is formed from arachidonic acid (AA) by a free-radical induced oxidation. AA may also be converted to prostaglandins (PG) by prostaglandin-endoperoxide synthase (PTGS) induced by NF-κB.

Quality of life, self-stigma, and coping strategies in patients with neurotic spectrum disorders: a cross-sectional study.

Background: Modern psychiatry focuses on self-stigma, coping strategies, and quality of life (QoL). This study looked at relationships among severity of symptoms, self-stigma, demographics, coping strategies, and QoL in patients with neurotic spectrum disorders.

Methods: A total of 153 clinically stable participants who met criteria for generalized anxiety disorder, social phobia, panic disorder, agoraphobia, mixed anxiety-depressive disorder, adjustment disorders, somatoform disorders, or obsessive-compulsive disorder were included in a cross-sectional study.

Bulky DNA adducts, microRNA profiles, and lipid biomarkers in Norwegian tunnel finishing workers occupationally exposed to diesel exhaust.

Objectives: This study aimed to assess the biological impact of occupational exposure to diesel exhaust (DE) including DE particles (DEP) from heavy-duty diesel-powered equipment in Norwegian tunnel finishing workers (TFW).

Methods: TFW (n=69) and referents (n=69) were investigated for bulky DNA adducts (by P-postlabelling) and expression of microRNAs (miRNAs) (by small RNA sequencing) in peripheral blood mononuclear cells (PBMC), as well as circulating free arachidonic acid (AA) and eicosanoid profiles in plasma (by liquid chromatography-tandem mass spectrometry).

Results: PBMC from TFW showed significantly higher levels of DNA adducts compared with referents.

Nano-TiO stability in medium and size as important factors of toxicity in macrophage-like cells.

TiO along with nano-TiO are commonly found in consumer products. In vivo studies have observed an accumulation of nano-TiO in macrophages. However, characteristics of nano-TiO determining toxicity remain unclear.

In Vitro Transformation of Human Bronchial Epithelial Cells by Diesel Exhaust Particles: Gene Expression Profiling and Early Toxic Responses.

Occupational exposure to diesel exhaust may cause lung cancer in humans. Mechanisms include DNA-damage and inflammatory responses. Here, the potential of NIST SRM2975 diesel exhaust particles (DEP) to transform human bronchial epithelial cells (HBEC3) in vitro was investigated.