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BackgroundEmissions 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.ResultsThe 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 TNFα 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.ConclusionsOverall, 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.Electronic supplementary materialThe online version of this article (10.1186/s12864-018-4679-9) contains supplementary material, which is available to authorized users.

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Background: Reef-building corals regularly experience changes in intra and extracellular H+ concentration ([H+]) due to physiological and environmental processes. Stringent control of [H+] is required for the maintenance of homeostatic acid-base balance in coral cells and is achieved through the regulation of intracellular pH (pHi). This task is especially challenging for reef-building corals that share an endosymbiotic relationship with photosynthetic dinoflagellates (family Symbiodinaceae), which exert a significant effect on the pHi of coral cells. Despite their importance, the pH regulatory proteins involved in the homeostatic acid-base balance have been scarcely investigated in corals. Here, we reported the full characterisation in terms of genomic structure, domain topology and phylogeny of three majors H+ transporter families implicated in pHi regulation; we investigated their tissue-specific expression and we assessed the effect of seawater acidification on their level of expression.Results: We identified members of the Na+/H+ exchanger (SLC9), vacuolar-type electrogenic H+-ATP hydrolases (V-ATPase) and voltage-gated proton channels (HvCN) families in the genome and transcriptome of S. pistillata. In addition, we identified a novel member of the HvCN gene family in the cnidarian subclass Hexacorallia, which has never been described in any species to date. We also reported key residues that participate to the H+ transporters substrate specificity, protein function and regulation. Lastly, we demonstrated that some of these have different tissue expression patterns and are mostly unaffected by exposure to seawater acidification.Conclusions: In this study, we provide the first characterization of the H+ transporters genes that contribute to homeostatic acid-base balance in coral cells. This work will enrich knowledge about basic aspects of coral biology, bearing important implications for our understanding of how corals regulate their intracellular environment.

Despite the well-established link between particulate vehicle emissions and adverse health effects, the biological effects produced by ultrafine particles generated from fuel combustion need to be investigated. The biological impact of nano-sized organic carbon particles in the size range 3-7 nm, obtained from an engine fuelled with a standard diesel and four diesel fuels doped with additives of commercial interest is reported. Our data showed that the number of particles < 10 nm is to a very small extent reduced by diesel particle filters, despite its ability to trap micrometric and submicrometric particulates, and that there is a correlation between the additives used and the chemical characteristics of the nanoparticles sampled. The results show that the different nano-sized organic carbon particles induce cytotoxic and proinflammatory effects on the in vitro systems A549 (epithelial cells) and BEAS-2B (bronchial cells). All the fuels tested are able to induce the release of proinflammatory interleukins 8 and 6; moreover, the IC50 values show that the additives can increase the toxic potential of particles 10 times. Further analyses are therefore needed to better define the potential impact of organic ultrafine particles on human health.