Abstract P312: Tracheal Instillation of Diesel Exhaust Particles Exacerbates Myocardial Ischaemia and Reperfusion Injury in Rats

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Sarah Robertson ◽  
Ashleigh L Thomson ◽  
Catherine A Shaw ◽  
Mark R Miller ◽  
David E Newby ◽  
...  
Keyword(s):  
Air Pollution ◽  
Infarct Size ◽  
Systemic Inflammation ◽  
Myocardial Ischaemia ◽  
Diesel Exhaust ◽  
Ex Vivo ◽  
Diesel Exhaust Particles ◽  
Autonomic Activation ◽  
Exhaust Particles

Episodes of increased air pollution are associated with higher cardiovascular mortality. The adverse effects of air pollution have been attributed to particulate matter, especially ultrafine particles. This study addresses the hypothesis that ultrafine diesel exhaust particles (DEP) exacerbate myocardial ischaemia reperfusion (I/R) injury secondary to induction of a systemic inflammatory response. Wistar rats (n=5–6/group) received DEP (0.5 mg) or saline vehicle by intratracheal instillation. 6h later I/R was induced either in vivo or ex vivo in isolated buffer perfused hearts. Lung inflammation was confirmed 6h after DEP instillation by increased levels of neutrophils, total protein and IL-6 in bronchoalveolar lavage fluid. However, there was no evidence for systemic inflammation as assessed by plasma cytokine levels (IL-6, TNF-α, and CRP) or by neutrophil priming (CD11b expression) or activation (CD62L expression). In vivo , systolic blood pressure was significantly higher in DEP-instilled rats (129 ± 7 mmHg) than in saline controls (92 ± 3 mmHg, P<0.01), consistent with increased autonomic activation. Arrhythmias occurred intermittently after induction of ischaemia (in total 8.2±1.2 s in the saline group) and were more prevalent in DEP-instilled rats (32.9±5.0s, P<0.001). Fatal arrhythmias occurred in 60% of rats receiving DEP but not at all in saline controls. Following reperfusion, infarct size (extent of triphenyltetrazolium chloride staining) was significantly increased after DEP (34.7 ± 1.2% left ventricle) vs saline-instilled (10.3 ± 1.2%, P<0.001). Infarct size was similarly potentiated in hearts isolated from DEP instilled rats and perfused ex-vivo . Histological examination confirmed the absence of inflammatory infiltrate in hearts prior to I/R. Prior exposure to pollution in vivo thus renders the heart more vulnerable to I/R injury, either in situ in the body or ex vivo when the heart is isolated from systemic mediators and cells. Systemic inflammation does not appear to be necessary for this ‘priming’ effect of DEP. The role of autonomic activation in promoting cardiac arrythmia in vivo after DEP instillation and in determining the ability of the heart to withstand subsequent I/R injury merits further investigation.

scholarly journals Prolonged Pulmonary Exposure to Diesel Exhaust Particles Exacerbates Renal Oxidative Stress, Inflammation and DNA Damage in Mice with Adenine-Induced Chronic Renal Failure

2016 ◽  
Vol 38 (5) ◽  
pp. 1703-1713 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Turan Karaca ◽  
Sumaya Beegam ◽  
Priya Yuvaraju ◽  
Javed Yasin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Dna Damage ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Diesel Exhaust ◽  
Diesel Exhaust Particles ◽  
Kidney Weight ◽  
Pulmonary Exposure ◽  
Exhaust Particles

Background/Aims: Epidemiological evidence indicates that patients with chronic kidney diseases have increased susceptibility to adverse outcomes related to long-term exposure to particulate air pollution. However, mechanisms underlying these effects are not fully understood. Methods: Presently, we assessed the effect of prolonged exposure to diesel exhaust particles (DEP) on chronic renal failure induced by adenine (0.25% w/w in feed for 4 weeks), which is known to involve inflammation and oxidative stress. DEP (0.5m/kg) was intratracheally (i.t.) instilled every 4th day for 4 weeks (7 i.t. instillation). Four days following the last exposure to either DEP or saline (control), various renal endpoints were measured. Results: While body weight was decreased, kidney weight increased in DEP+adenine versus saline+adenine or DEP. Water intake, urine volume, relative kidney weight were significantly increased in adenine+DEP versus DEP and adenine+saline versus saline. Plasma creatinine and urea increased and creatinine clearance decreased in adenine+DEP versus DEP and adenine+saline versus saline. Tumor necrosis factor α, lipid peroxidation and reactive oxygen species were significantly increased in adenine+DEP compared with either DEP or adenine+saline. The antioxidant calase was significantly decreased in adenine+DEP compared with either adenine+saline or DEP. Notably, renal DNA damage was significantly potentiated in adenine+DEP compared with either adenine+saline or DEP. Similarly, systolic blood pressure was increased in adenine+DEP versus adenine+saline or DEP, and in DEP versus saline. Histological evaluation revealed more collagen deposition, higher number of necrotic cell counts and dilated tubules, cast formation and collapsing glomeruli in adenine+DEP versus adenine+saline or DEP. Conclusion: Prolonged pulmonary exposure to diesel exhaust particles worsen renal oxidative stress, inflammation and DNA damage in mice with adenine-induced chronic renal failure. Our data provide biological plausibility that air pollution aggravates chronic renal failure.

Gene Expression Analysis to Investigate Biological Networks Underlying Nasal Inflammatory Dysfunctions Induced by Diesel Exhaust Particles Using an In Vivo System

2019 ◽  
Vol 129 (3) ◽  
pp. 245-255 ◽  
Author(s):  
Hyun Soo Kim ◽  
Byeong-Gon Kim ◽  
Sohyeon Park ◽  
Nahyun Kim ◽  
An-Soo Jang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Signaling Pathways ◽  
Diesel Exhaust ◽  
Expression Profiles ◽  
Complex Mixture ◽  
Diesel Exhaust Particles ◽  
The Body ◽  
Exhaust Particles

Objectives: Diesel exhaust particles (DEP)s are notorious ambient pollutants composed of a complex mixture of a carbon core and diverse chemical irritants. Several studies have demonstrated significant relationships between DEP exposure and serious nasal inflammatory response in vitro, but available information regarding underlying networks in terms of gene expression changes has not sufficiently explained potential mechanisms of DEP-induced nasal damage, especially in vivo. Methods: In the present study, we identified DEP-induced gene expression profiles under short-term and long-term exposure, and identified signaling pathways based on microarray data for understanding effects of DEP exposure in the mouse nasal cavity. Results: Alteration in gene expression due to DEP exposure provokes an imbalance of the immune system via dysregulated inflammatory markers, predicted to disrupt protective responses against harmful exogenous substances in the body. Several candidate markers were identified after validation using qRT-PCR, including S100A9, CAMP, IL20, and S100A8. Conclusions: Although further mechanistic studies are required for verifying the utility of the potential biomarkers suggested by the present study, our in vivo results may provide meaningful suggestions for understanding the complex cellular signaling pathways involved in DEP-induced nasal damages.

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

2022 ◽  
Vol 25 ◽  
Author(s):  
Rituraj Niranjan ◽  
Muthukumaravel Subramanian ◽  
Devaraju Panneer ◽  
Sanjay Kumar Ojha
Keyword(s):  
Cell Proliferation ◽  
Statistical Analysis ◽  
Diesel Exhaust ◽  
A549 Cells ◽  
Diesel Exhaust Particles ◽  
Tissue Remodelling ◽  
Interleukin 13 ◽  
Exhaust Particles

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.

scholarly journals Diesel Exhaust Particles Suppress In Vivo IFN-γ Production by Inhibiting Cytokine Effects on NK and NKT Cells

2004 ◽  
Vol 172 (6) ◽  
pp. 3808-3813 ◽  
Author(s):  
Fred D. Finkelman ◽  
Mingyan Yang ◽  
Tatyana Orekhova ◽  
Erin Clyne ◽  
Jonathan Bernstein ◽  
...  
Keyword(s):  
Diesel Exhaust ◽  
Nkt Cells ◽  
Diesel Exhaust Particles ◽  
Exhaust Particles ◽  
Ifn Γ

scholarly journals Label-free detection of uptake, accumulation, and translocation of diesel exhaust particles in ex vivo perfused human placenta

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Eva Bongaerts ◽  
Leonie Aengenheister ◽  
Battuja B. Dugershaw ◽  
Pius Manser ◽  
Maarten B. J. Roeffaers ◽  
...  
Keyword(s):  
Pregnant Women ◽  
Human Placenta ◽  
Diesel Exhaust ◽  
Ex Vivo ◽  
Developmental Toxicity ◽  
Placental Tissue ◽  
Diesel Exhaust Particles ◽  
Label Free ◽  
Label Free Detection ◽  
Exhaust Particles

Abstract Background Pregnant women and developing fetuses comprise a particularly vulnerable population as multiple studies have shown associations between prenatal air pollution exposure and adverse pregnancy outcomes. However, the mechanisms underlying the observed developmental toxicity are mostly unknown, in particular, if pollution particles can cross the human placenta to reach the fetal circulation. Results Here, we investigated the accumulation and translocation of diesel exhaust particles (DEPs), as a model particle for combustion-derived pollution, in human perfused placentae using label-free detection by femtosecond pulsed laser illumination. The results do not reveal a significant particle transfer across term placentae within 6 h of perfusion. However, DEPs accumulate in placental tissue, especially in the syncytiotrophoblast layer that mediates a wealth of essential functions to support and maintain a successful pregnancy. Furthermore, DEPs are found in placental macrophages and fetal endothelial cells, showing that some particles can overcome the syncytiotrophoblasts to reach the fetal capillaries. Few particles are also observed inside fetal microvessels. Conclusions Overall, we show that DEPs accumulate in key cell types of the placental tissue and can cross the human placenta, although in limited amounts. These findings are crucial for risk assessment and protection of pregnant women and highlight the urgent need for further research on the direct and indirect placenta-mediated developmental toxicity of ambient particulates.

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

Biomedicines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 99
Author(s):  
Abderrahim Nemmar ◽  
Sumaya Beegam ◽  
Nur Elena Zaaba ◽  
Salem Alblooshi ◽  
Saleh Alseiari ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Dna Damage ◽  
Diesel Exhaust ◽  
Nitrosative Stress ◽  
Antioxidant Properties ◽  
Diesel Exhaust Particles ◽  
Cardiovascular Toxicity ◽  
Particulate Air Pollution ◽  
Exhaust Particles

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.

The Use of Standardized Diesel Exhaust Particles in Alzheimer’s Disease Research

2021 ◽  
pp. 1-2
Author(s):  
Michelle L. Block ◽  
Urmila P. Kodavanti
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Air Pollution ◽  
Particulate Matter ◽  
Diesel Exhaust ◽  
Disease Risk ◽  
Urban Air Pollution ◽  
Diesel Exhaust Particles ◽  
Urban Air ◽  
Exhaust Particles

The mechanisms underlying how urban air pollution exposure conveys Alzheimer’s disease risk and affects plaque pathology is largely unknown. Because particulate matter, the particle component of urban air pollution, varies across location, pollution source, and time, a single model representative of all ambient particulate matter is unfeasible for research investigating the role of ar pollution in central nervous system diseases. More specifically, the investigation of several models of particulate matter with enrichment of source-specific components are essential to employ, in order to more fully understand what characteristics of particulate matter affects Alzheimer’s disease, including standardized diesel exhaust particles.

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