Pulmonary Exposure to Diesel Exhaust Particles Enhances Coagulatory Disturbance with Endothelial Damage and Systemic Inflammation Related to Lung Inflammation

2006 ◽  
Vol 231 (10) ◽  
pp. 1626-1632 ◽  
Author(s):  
Ken-ichiro Inoue ◽  
Hirohisa Takano ◽  
Miho Sakurai ◽  
Toshio Oda ◽  
Hiroshi Tamura ◽  
...  
Keyword(s):  
Systemic Inflammation ◽  
Diesel Exhaust ◽  
Lung Inflammation ◽  
Endothelial Damage ◽  
Diesel Exhaust Particles ◽  
Pulmonary Exposure ◽  
Exhaust Particles

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.

scholarly journals Pulmonary exposure to diesel exhaust particles induces airway inflammation and cytokine expression in NC/Nga mice

2005 ◽  
Vol 79 (10) ◽  
pp. 595-599 ◽  
Author(s):  
Ken-ichiro Inoue ◽  
Hirohisa Takano ◽  
Rie Yanagisawa ◽  
Takamichi Ichinose ◽  
Akinori Shimada ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Diesel Exhaust ◽  
Cytokine Expression ◽  
Diesel Exhaust Particles ◽  
Pulmonary Exposure ◽  
Exhaust Particles

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.

Effects of Volatile Constituents of Rosemary Extract on Lung Inflammation Induced by Diesel Exhaust Particles

2006 ◽  
Vol 99 (1) ◽  
pp. 52-57 ◽  
Author(s):  
Ken-ichiro Inoue ◽  
Hirohisa Takano ◽  
Akira Shiga ◽  
Yoji Fujita ◽  
Hiroaki Makino ◽  
...  
Keyword(s):  
Diesel Exhaust ◽  
Lung Inflammation ◽  
Diesel Exhaust Particles ◽  
Rosemary Extract ◽  
Volatile Constituents ◽  
Exhaust Particles

scholarly journals Differential Roles of Water–Insoluble and –Soluble Fractions of Diesel Exhaust Particles in the Development of Adverse Health Effects due to Chronic Instillation of Diesel Exhaust Particles

2021 ◽  
Author(s):  
Yanyi Xu ◽  
Zhouzhou Li ◽  
Ying Liu ◽  
Bin Pan ◽  
Renzheng Peng ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Gut Microbiota ◽  
Hepatic Steatosis ◽  
Glucose Intolerance ◽  
Systemic Inflammation ◽  
Diesel Exhaust ◽  
Cell Number ◽  
Diesel Exhaust Particles ◽  
Water Soluble ◽  
Exhaust Particles

Abstract Background: Ambient fine particulate matter (PM2.5) has a marked temporospatial variation in chemical composition, but how the composition of PM2.5 influences its toxicity remains elusive. Results: To explore the individual roles of different PM2.5 components in the pathogenesis due to PM2.5 exposure, we prepared water-soluble (WS-DEP) and -insoluble (WIS-DEP) fractions of diesel exhaust particles (DEP) and assessed their effects on pulmonary and systemic inflammation, hepatic steatosis and insulin resistance, systemic glucose homeostasis, and gut microbiota using chronic intratracheal instillation mouse models. Compared to control, instillation of DEP or WIS-DEP, but not WS-DEP, significantly increased pulmonary inflammatory scores and expression of inflammatory markers, bronchoalveolar lavage fluid cell number, and circulating pro-inflammatory cytokines. Consistently, DEP or WIS-DEP-instilled but not WS-DEP-instilled mice versus control had significant hepatic steatosis and insulin resistance and systemic glucose intolerance. In contrast, instillation of WS-DEP versus instillation of WIS-DEP had more similar effects on gut microbiota to that of instillations of DEP. Conclusion: The pulmonary and systemic inflammation, hepatic steatosis and insulin resistance, and systemic glucose intolerance following chronic DEP instillation are all attributable to the water-insoluble fraction of DEP, providing a mechanistic interpretation for the apparent independency of PM2.5 exposure-induced glucose intolerance on PM2.5 composition.

Sign in / Sign up

Export Citation Format

Share Document