Cardiovascular and lung inflammatory effects induced by systemically administered diesel exhaust particles in rats

2007 ◽  
Vol 292 (3) ◽  
pp. L664-L670 ◽  
Author(s):  
Abderrahim Nemmar ◽  
Sultan Al-Maskari ◽  
Badreldin H. Ali ◽  
Issa S. Al-Amri
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Diesel Exhaust ◽  
Ultrafine Particles ◽  
Blood Platelet ◽  
Diesel Exhaust Particles ◽  
Lung Edema ◽  
Dependent Manner ◽  
Exhaust Particles

Pollution by particulates has consistently been associated with increased cardiorespiratory morbidity and mortality. It has been suggested that ultrafine particles, of which diesel exhaust particles (DEP) are significant contributors, are able to translocate from the airways into the bloodstream in vivo. In the present study, we assessed the effect of systemic administration of DEP on cardiovascular and respiratory parameters. DEP were administered into the tail vein of rats, and heart rate, blood pressure, blood platelet activation, and lung inflammation were studied 24 h later. Doses of 0.02, 0.1, or 0.5 mg DEP/kg (8, 42, or 212 μg DEP/rat) induced a significant decrease of heart rate and blood pressure compared with saline-treated rats. Although the number of platelets was not affected, all the doses of DEP caused a shortening of the bleeding time. Similarly, in addition to triggering lung edema, the bronchoalveolar lavage analysis revealed the presence of neutrophil influx in DEP-treated rats in a dose-dependent manner. We conclude that the presence of DEP in the systemic circulation leads not only to cardiovascular and haemostatic changes but it also triggers pulmonary inflammation.

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

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 Combined Inhaled Diesel Exhaust Particles and Allergen Exposure Alter Methylation of T Helper Genes and IgE Production In Vivo

2007 ◽  
Vol 102 (1) ◽  
pp. 76-81 ◽  
Author(s):  
Jinming Liu ◽  
Manisha Ballaney ◽  
Umaima Al-alem ◽  
Chunli Quan ◽  
Ximei Jin ◽  
...  
Keyword(s):  
Diesel Exhaust ◽  
Allergen Exposure ◽  
Diesel Exhaust Particles ◽  
T Helper ◽  
Exhaust Particles
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