Impact of tire debris on in vitro and in vivo systems

BACKGROUND: It is estimated that over 80% of respirable particulate matter (PM(10)) in cities comes from road transport and that tire and brake wear are responsible for the 3–7% emission of it. Data on the indicators of environmental impact of tire debris (TD), originated from the tire abrasion on roads, are extremely scarce, even though TD contains chemicals (zinc and organic compounds) which can be released in the environment. METHODS: TD particle morphology was analysed with SEM, TEM and FIB instruments. TD eluates and TD organic extracts were tested at dilution series on human cell lines and Xenopus laevis embryos. 50 and 100 g/L TD were used for the eluates obtained after 24 h at pH 3 and the quantity of zinc present was measured with a ICP-AES. Eluates diluted to 1%, 10%, 50% in culture media and undiluted were used on X. laevis embryos in the FETAX test. HepG2 cells were exposed for 24 h to 0.05 – 50 μg/ml of zinc salt while A549 cells were exposed for 24, 48 and 72 h to 10, 50, 60, or 75 μg/ml of TD extract. X. laevis embryos were exposed to 50, 80, 100, or 120 μg/ml TD extract. RESULTS: The solution of undiluted 50 g/L TD produced 80.2% mortality (p < 0.01) in X. laevis embryos and this toxic effect was three times greater than that produced by 100 g/L TD. Zn accumulation in HepG2 cells was evident after 4 h exposure. A549 cells exposed to TD organic extract for 72 h presented a modified morphology, a decrease in cell proliferation and an increase in DNA damage as shown by comet assay. The dose 80 μg/ml of TD extract produced 14.6% mortality in X. laevis embryos and 15.9% mortality at 120 μg/ml. Treatment with 80, 100, or 120 μg/ml TD organic extract increased from 14.8% to 37.8% malformed larvae percentages compared to 5.6% in the control. CONCLUSION: Since the amount of Zn leached from TD is related to pH, aggregation of particles and elution process, the quantity of TD present in the environment has to be taken into account. Moreover the atmospheric conditions, which may deeply influence the particle properties, have to be considered. The TD organic fraction was toxic for cells and organisms. Thus, because of its chemical components, TD may have a potential environmental impact and has to be further investigated

Transcriptional profiling of human bronchial epithelial cell BEAS-2B exposed to diesel and biomass ultrafine particles

Background: Emissions from diesel vehicles and biomass burning are the principal sources of primary ultrafine particles (UFP). The exposure to UFP has been associated to cardiovascular and pulmonary diseases, including lung cancer. Although many aspects of the toxicology of ambient particulate matter (PM) have been unraveled, the molecular mechanisms activated in human cells by the exposure to UFP are still poorly understood. Here, we present an RNA-seq time-course experiment (five time point after single dose exposure) used to investigate the differential and temporal changes induced in the gene expression of human bronchial epithelial cells (BEAS-2B) by the exposure to UFP generated from diesel and biomass combustion. A combination of different bioinformatics tools (EdgeR, next-maSigPro and reactome FI app-Cytoscape and prioritization strategies) facilitated the analyses the temporal transcriptional pattern, functional gene set enrichment and gene networks related to cellular response to UFP particles.Results: The bioinformatics analysis of transcriptional data reveals that the two different UFP induce, since the earliest time points, different transcriptional dynamics resulting in the activation of specific genes. The functional enrichment of differentially expressed genes indicates that the exposure to diesel UFP induces the activation of genes involved in TNFa signaling via NF-kB and inflammatory response, and hypoxia. Conversely, the exposure to ultrafine particles from biomass determines less distinct modifications of the gene expression profiles. Diesel UFP exposure induces the secretion of biomarkers associated to inflammation (CCXL2, EPGN, GREM1, IL1A, IL1B, IL6, IL24, EREG, VEGF) and transcription factors (as NFE2L2, MAFF, HES1, FOSL1, TGIF1) relevant for cardiovascular and lung disease. By means of network reconstruction, four genes (STAT3, HIF1a, NFKB1, KRAS) have emerged as major regulators of transcriptional response of bronchial epithelial cells exposed to diesel exhaust.Conclusions: Overall, this work highlights modifications of the transcriptional landscape in human bronchial cells exposed to UFP and sheds new lights on possible mechanisms by means of which UFP acts as a carcinogen and harmful factor for human health

Optical scattering (TAOS) by tire debris particles: preliminary results

Tire debris particles from low severity laboratory wear tests have been investigated by the TAOS optical scattering facility at Yale University. The incident wavelength is 532 nm. After the TAOS event some particle samples have been imaged by a scanning electron microscope and microanalyzed. The TAOS intensity patterns recorded within a solid angle in the backward sector have been processed by cluster analysis and compared with the patterns computed by a T-matrix code. Preliminary agreement has been found between TAOS data and the particle models (size, shape, refractive index). The purpose of the investigation is to obtain signatures of the material, based on its TAOS pattern. © 2001 Optical Society of America

Effect of Nanoparticles and Environmental Particles on a Cocultures Model of the Air-Blood Barrier

Exposure to engineered nanoparticles (NPs) and to ambient particles (PM) has increased significantly. During the last decades the application of nano-objects to daily-life goods and the emissions produced in highly urbanized cities have considerably augmented. As a consequence, the understanding of the possible effects of NPs and PM on human respiratory system and particularly on the air-blood barrier (ABB) has become of primary interest. The crosstalk between lung epithelial cells and underlying endothelial cells is indeed essential in determining the effects of inhaled particles. Here we report the effects of metal oxides NPs (CuO and TiO2) and of PM on an in vitro model of the ABB constituted by the type II epithelial cell line (NCI-H441) and the endothelial one (HPMEC-ST1.6R). The results demonstrate that apical exposure of alveolar cells induces significant modulation of proinflammatory proteins also in endothelial cells

Carta mecanografiada de Maria Camatini a Cristina Vicente

Per tal d'organitzar el 4th International Congress of Myriapodology i fer el programa d'aquest, demana la seva intenció en certs temes que volen tractar

Characterization of actin isoforms in ejaculated boar spermatozoa

Actin was localized in boar ejaculated spermatozoa by using specific antisera against cytoplasmic isoforms of actin [Otey et al., J Cell Biol, 102:1726–1737, 1986; Skalli et al., J Cell Biol, 103:2787–2796, 1986; Miller et al., Biochemistry, 26:6064–6070, 1987]. Indirect immunofluorescence and immunoelectron microscopy showed that γ and β actins were codistributed in the acrosomal and postacrosomal regions. Sperm actin was also identified on two‐dimensional gel as two spots in the isoelectric point and molecular weight corresponding to β and γ actins. Coelectrophoresis of sperm actin and chicken gizzard actin and immunoblots stained with the specific antibodies confirmed the presence of these two isoforms of actin. Copyright © 1988 Alan R. Liss, Inc

Release of IL-1β Triggered by Milan Summer PM10: Molecular Pathways Involved in the Cytokine Release

Particulate matter (PM) exposure is related to pulmonary and cardiovascular diseases, with increased inflammatory status. The release of the proinflammatory interleukin- (IL-) 1β, is controlled by a dual pathway, the formation of inactive pro-IL-1β, through Toll-like receptors (TLRs) activation, and its cleavage by NLRP3 inflammasome. THP-1-derived macrophages were exposed for 6 h to 2.5 μg/cm2 of Milan PM10, and the potential to promote IL-1β release by binding TLRs and activating NLRP3 has been examined. Summer PM10, induced a marked IL-1β response in the absence of LPS priming (50-fold increase compared to unexposed cells), which was reduced by caspase-1 inhibition (91% of inhibition respect summer PM10-treated cells) and by TLR-2 and TLR-4 inhibitors (66% and 53% of inhibition, resp.). Furthermore, summer PM10 increased the number of early endosomes, and oxidative stress inhibition nearly abolished PM10-induced IL-1β response (90% of inhibition). These findings suggest that summer PM10 contains constituents both related to the activation of membrane TLRs and activation of the inflammasome NLPR3 and that TLRs activation is of pivotal importance for the magnitude of the response. ROS formation seems important for PM10-induced IL-1β response, but further investigations are needed to elucidate the molecular pathway by which this effect is mediated

BASE: a sustainable path for the University of Milano-Bicocca

Since its foundation, in 1998, the University of Milano-Bicocca has been pursuing the objective to make its structures sustainable from an environmental, social and economic point of view. To this end, in 2015 the University of Milano-Bicocca created BASE (Bicocca Ambiente Società Economia - Bicocca Environment Society Economy), an internal office aimed at promoting the interaction between research and training and at stimulating sustainability both within the University and outside. BASE proposes a holistic approach to sustainability including energy efficiency, waste reduction, sustainable mobility, climate change attention and water and food supply. The report will focus on the interventions recently carried out in the various fields, paying particular attention to the issues of waste management and of mobility