The role of IL-6 released from pulmonary epithelial cells in diesel UFP-induced endothelial activation

Diesel exhaust particles (DEP) and their ultrafine fraction (UFP) are known to induce cardiovascular effects in exposed subjects. The mechanisms leading to these outcomes are still under investigation, but the activation of respiratory endothelium is likely to be involved. Particles translocation through the air-blood barrier and the release of mediators from the exposed epithelium have been suggested to participate in the process. Here we used a conditioned media in vitro model to investigate the role of epithelial-released mediators in the endothelial cells activation. Diesel UFP were sampled from a Euro 4 vehicle run over a chassis dyno and lung epithelial BEAS-2B cells were exposed for 20 h (dose 5 microg/cm2). The exposure media were collected and used for endothelial HPMEC-ST1.6R cells treatment for 24 h. The processes related to oxidative stress and inflammation were investigated in the epithelial cells, accordingly to the present knowledge on DEP toxicity. The release of IL-6 and VEGF was significantly augmented in diesel exposed cells. In endothelial cells, VCAM-1 and ICAM-1 adhesion molecules levels were increased after exposure to the conditioned media. By interfering with IL-6 binding to its endothelial receptor, we demonstrate the role of this interleukin in inducing the endothelial response. DEP modulates oxidative stress, MAPK activation and IL-6 release in lung cells. Treatments with endothelial supernatants induce endothelial activation which is down-regulated by IL-6 suppression

Graphite particles induce ROS formation in cell free systems and human cells

It is commonly accepted that the toxicity of carbonaceous particulate matter (PM) is due to the production of reactive oxygen species (ROS) which induce biological damages in the exposed cells. It is also known that PM produced during the combustion processes consists of a carbonaceous core \u201cdressed\u201d with other organic and/or inorganic materials. In spite of this knowledge, the role of these materials in the production of ROS is not yet clear. This work aims at understanding whether \u201cnaked\u201d carbonaceous particles are capable to form ROS either in cell-free or in-cell systems. The problem has been treated based on the data collected on pure graphite samples of different size obtained by ball\u2013milling pure graphite for various time lengths. The experimental approach considered Raman, ESR (spin trapping), cell viability and fluorescence spectroscopy measurements. These techniques allowed to carry out measurements both in cell and cell-free systems and the results consistently indicate that also pure naked carbonaceous particles can catalyze the electron transfer that produces superoxide ions. The process depends on the particle size and enlightens the role of the edges of the graphitic platelets. Evidence has been collected that even \u201cnaked\u201d graphitic nanoparticles are capable to produce ROS and decrease the cell viability thus representing a potential danger to human health

INCLUSIVE PROPERTIES OF D MESONS PRODUCED IN 360-GeV pi- p INTERACTIONS

The inclusive cross sections for forward D meson production at √s = 26 Gev in π-p interactions have been measured to be: σ(π̅p→D<SUP>0</SUP>/D<SUP>−0</SUP>)X<SUB>F</SUB>&gt;0 = (10.1±2.2) μb, σ(π̅p→D<SUP>±</SUP> + X)X<SUB>F</SUB>&gt;0 = (5.7±1.6) μb . The distribution in X<SUB>F</SUB>for all D and for X<SUB>F</SUB> &gt; 0 has the form dσ/dX<SUB>F</SUB> = 107<SUP>+39</SUP><SUB>-37</SUB>(1-X<SUB>F</SUB>)7.5<SUP>+2.5</SUP><SUB>-1.7</SUB> + 5.4<SUP>+6.0</SUP><SUB>-3.8</SUB>(1-X<SUB>F</SUB>)0.7<SUP>1.0</SUP><SUB>-0.7</SUB>μb, with evidence for leading D production. The P<SUP>2</SUP><SUB>T</SUB> distribution is exponential with slope parameter [−1.18<SUP>+0.18</SUP><SUB>−0.16</SUB>](GeV/c)<SUP>−2</SUP>. The data are compared with predictions from first-order quark/gluon fusion calculations