Eosinophils Restrict Diesel Exhaust Particles Induced Cell Proliferation of Lung Epithelial A549 Cells, Vial Interleukin-13 Mediated Mechanisms: Implications for Tissue Remodelling And Fibrosis

Background: Diesel exhaust particulates (DEPs) affect lung physiology and cause serious damage to the lungs. A number of studies demonstrated that, eosinophils play a very important role in the development of tissue remodelling and fibrosis of lungs. However, the exact mechanism of pathogenesis of tissue remodelling and fibrosis is not known. Methods: Both in vitro and in vivo models were used in the study. HL-60 and A549 cells were used in the study. Balb/C mice of 8 to 12 weeks old were used for in vivo study. Cell viability by MTT assay, RNA isolation by tri reagent was accomplished. mRNA expression of inflammatory genes were accomplished by real time PCR or qPCR. Immunohistochemistry was done to asses the localization and expressions of proteins. One way ANOVA followed by post hoc test were done for the statistical analysis. Graph-Pad Prism software was used for statistical analysis. Results: We for the first time demonstrate that, Interleukin-13 plays a very important role in the development of tissue remodelling and fibrosis. We report that, diesel exhaust particles significantly induce eosinophils cell proliferation and interleukin-13 release in in vitro culture conditions. Supernatant collected from DEP-induced eosinophils cells significantly restrict cell proliferation of epithelial cells in response to exposure of diesel exhast particles. Furthermore, purified interleukin-13 decreases the proliferation of A549 cells, highliting the involvement of IL-13 in tissue remodeling. Notably, Etoricoxib (selective COX-2 inhibitor) did not inhibit DEP-triggered release of interleukin-13, suggesting another cell signalling pathway. The in vivo exposer of DEP to the lungs of mice, resulted in high level of eosinophils degranulation as depicted by the EPX-1 immunostaining and altered level of mRNA expressions of inflammatory genes. We also found that, a-SMA, fibroblast specific protein (FSP-1) has been changed in response to DEP in the mice lungs along with the mediators of inflammation. Conclusion: Altogether, we elucidated, the mechanistic role of eosinophils and IL-13 in the DEP-triggered proliferation of lungs cells thus providing an inside in the pathophysiology of tissue remodelling and fibrosis of lungs.

The Salutary Effects of Catalpol on Diesel Exhaust Particles-Induced Thrombogenic Changes and Cardiac Oxidative Stress, Inflammation and Apoptosis

Inhaled particulate air pollution exerts pulmonary inflammation and cardiovascular toxicity through secondary systemic effects due to oxidative stress and inflammation. Catalpol, an iridiod glucoside, extracted from the roots of Rehmannia glutinosa Libosch, has been reported to possess anti-inflammatory and antioxidant properties. Yet, the potential ameliorative effects of catalpol on particulate air pollution—induced cardiovascular toxicity, has not been studied so far. Hence, we evaluated the possible mitigating mechanism of catalpol (5 mg/kg) which was administered to mice by intraperitoneal injection one hour before the intratracheal (i.t.) administration of a relevant type of pollutant particle, viz. diesel exhaust particles (DEPs, 30 µg/mouse). Twenty-four hours after the lung deposition of DEPs, several cardiovascular endpoints were evaluated. DEPs caused a significant shortening of the thrombotic occlusion time in pial microvessels in vivo, induced platelet aggregation in vitro, and reduced the prothrombin time and the activated partial thromboplastin time. All these actions were effectively mitigated by catalpol pretreatment. Likewise, catalpol inhibited the increase of the plasma concentration of C-reactive proteins, fibrinogen, plasminogen activator inhibitor-1 and P- and E-selectins, induced by DEPs. Moreover, in heart tissue, catalpol inhibited the increase of markers of oxidative (lipid peroxidation and superoxide dismutase) and nitrosative (nitric oxide) stress, and inflammation (tumor necrosis factor α, interleukin (IL)-6 and IL-1β) triggered by lung exposure to DEPs. Exposure to DEPs also caused heart DNA damage and increased the levels of cytochrome C and cleaved caspase, and these effects were significantly diminished by the catalpol pretreatment. Moreover, catalpol significantly reduced the DEPs-induced increase of the nuclear factor κB (NFκB) in the heart. In conclusion, catalpol significantly ameliorated DEPs–induced procoagulant events and heart oxidative and nitrosative stress, inflammation, DNA damage and apoptosis, at least partly, through the inhibition of NFκB activation.

Particles formation due to the wear of tires and measures for the wear reduction: A review

Tires are a very important part of a vehicle, necessary for the vehicle driving. During the vehicle exploitation, due to the friction which appears in the contact between the tire and the road, it comes to the formation of so called non-exhaust particles. The particles formed during the vehicle exploitation can be composed of heavy metals and they are harmful for people’s health and for the environment. Several factors influence the size of the wear of tires. The investigations about the tires behavior as well as the size of the wear can be conducted on the road, in the laboratory, as well as by application of modern software. The paper shows the applied methodologies applied by other researchers during the investigation of tires particles formation, the applied materials for the tires manufacturing, influential parameters on the wear of tires, as well as methods for the wear of tires reduction. After analyzing other researches in the subject field, the authors have come to the conclusions related to the factors which can reduce the wear of tires and these factors should be given proper attention in further studies.

Environmental Risk Assessment of Vehicle Exhaust Particles on Aquatic Organisms of Different Trophic Levels

Vehicle emission particles (VEPs) represent a significant part of air pollution in urban areas. However, the toxicity of this category of particles in different aquatic organisms is still unexplored. This work aimed to extend the understanding of the toxicity of the vehicle exhaust particles in two species of marine diatomic microalgae, the planktonic crustacean Artemia salina, and the sea urchin Strongylocentrotus intermedius. These aquatic species were applied for the first time in the risk assessment of VEPs. Our results demonstrated that the samples obtained from diesel-powered vehicles completely prevented egg fertilization of the sea urchin S. intermedius and caused pronounced membrane depolarization in the cells of both tested microalgae species at concentrations between 10 and 100 mg/L. The sample with the highest proportion of submicron particles and the highest content of polycyclic aromatic hydrocarbons (PAHs) had the highest growth rate inhibition in both microalgae species and caused high toxicity to the crustacean. The toxicity level of the other samples varied among the species. We can conclude that metal content and the difference in the concentrations of PAHs by itself did not directly reflect the toxic level of VEPs, but the combination of both a high number of submicron particles and high PAH concentrations had the highest toxic effect on all the tested species.