Composition of Diesel Particles Influences Acute Pulmonary Toxicity: An Experimental Study in MICE

Laks, Daniel Marinho; Oliveira, Regiani Carvalho de; André, Paulo Afonso de; Macchione, Mariângela; Lemos, Miriam; Faffe, Débora S.; Saldiva, Paulo Hilário Nascimento; Zin, Walter A.

doi:10.1080/08958370802112922

Cited by 39 publications

(45 citation statements)

References 19 publications

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“…Reduced lung function, mainly in children and in the elderly, is also associated with increased suspended particle concentration (Cançado et al 2006;Frye et al 2003;Kan et al 2007;Mccreanor et al 2007). In experimental studies, inhalation and instillation of particles led to decreased lung function and an inflammatory response characterized by polymorphonuclear cell influx and/or cytokine release (Bateson and Schwartz 2008;Clarke et al 1999Clarke et al , 2000Ghio et al 2000;Ghio and Devlin 2001;Kennedy et al 1998;Laks et al 2008;Li et al 1997;Mazzoli-Rocha et al 2008;Oftedal et al 2008;Wegesser and Last 2009). …”

Section: Particulate Matter and Lung Diseasementioning

confidence: 95%

“…However, a fundamental question remains still unanswered: Which components of PM are responsible for phagocyte activation?, as inflammation has been associated with several components as metal content, ultrafine particles (surface area), organic compounds and endotoxins (Brown et al 2001;Goldsmith et al 1998;Mazzoli-Rocha et al 2008). It is noteworthy that even different kinds of diesel can result in more or less pronounced pulmonary inflammation (Laks et al 2008). Exposure to constituents of air particulate matter as its organic fraction may probably contribute to pathological processes.…”

Section: Pm-induced Oxidative Stressmentioning

confidence: 96%

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Roles of oxidative stress in signaling and inflammation induced by particulate matter

et al. 2010

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This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca(2+) influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.

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Section: Particulate Matter and Lung Diseasementioning

confidence: 95%

Section: Pm-induced Oxidative Stressmentioning

confidence: 96%

Roles of oxidative stress in signaling and inflammation induced by particulate matter

et al. 2010

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“…21 First, a 500 lg/mL DEP solution was made by weighing DEP, adding DMEM-F12, and sonicating in an ultrasonic bath (Ultrasonic Cleaner; Testlab, Bernal Oeste, Buenos Aires, Argentina) for 15 minutes. Then, 10, 50, and 100 lg/mL DEP solutions were made from the DEP 500 lg/mL solution and brought to the final volume with DMEM-F12.…”

Section: Diesel Exhaust Particlesmentioning

confidence: 99%

Diesel Exhaust Particles Selectively Induce Both Proinflammatory Cytokines and Mucin Production in Cornea and Conjunctiva Human Cell Lines

Tau

Novaes

Matsuda

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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Citation: Tau J, Novaes P, Matsuda M, Tasat DR, Saldiva PH, Berra A. Diesel exhaust particles selectively induce both proinflammatory cytokines and mucin production in cornea and conjunctiva human cell lines. Invest Ophthalmol Vis Sci. 2013;54:4759-4765. DOI:10.1167/iovs.12-10541 PURPOSE. To evaluate the effect of diesel exhaust particles (DEP) on the viability, proliferation, apoptosis, secretion of cytokines (IL-6, IL-8, and TNF-a), and mucin gene transcription (MUC1, MUC5AC, and MUC16) in human epithelial cells of the cornea (HCLE) and conjunctiva (IOBA-NHC).METHODS. HCLE and IOBA-NHC cells were incubated with DEP (10-500 lg/mL) for 24 hours. Cell proliferation was evaluated by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptotic cells were measured by an annexin V-FITC and propidium iodide kit for flow cytometry. Proinflammatory cytokines were determined by an ELISA kit. Mucin gene transcription was quantified by real-time PCR.RESULTS. DEP significantly decreased the viability, proliferation, and secretion of IL-8, but increased the secretion of IL-6 on both HCLE and IOBA-NHC cell lines in a dose-dependent manner. Neither cornea nor conjunctiva cells incubated with DEP released TNF-a. DEP induced a significant increase in the percentage of apoptotic cells in IOBA-NHC, whereas no changes were observed in HCLE. Finally, DEP significantly decreased the transcription levels of MUC1 and MUC16 in HCLE, but increased the transcription levels of MUC1, MUC5AC, and MUC16 in IOBA-NHC.CONCLUSIONS. These findings suggest that human corneal and conjunctival epithelial cells incubated with DEP showed cytotoxicity and an inflammatory response mediated by IL-6, not by TNF-a or IL-8. Also, the decrease in mucin expression in the cornea cells might leave exposed areas in the cornea for contact with DEP. Finally, the increase in mucin expression in the conjunctiva cells might be involved at least in the clearance of DEP to protect the ocular epithelium.Keywords: diesel, corneal epithelium, conjunctiva OBJETIVO. Evaluar el efecto de las partículas de Diesel (DEP, del Inglés Diesel Exhaust Particles) sobre la viabilidad, la proliferación, la apoptosis, la secreción de citoquinas (IL-6, IL-8 y TNF-a) y la transcripción de genes de mucinas (MUC1, MUC5AC y MUC16) en células epiteliales humanas de córnea (HCLE) y conjuntiva (IOBA-NHC).MÉTODOS. La viabilidad celular se evaluó por el ensayo de exclusión con azul de tripán. La proliferación celular se evaluó por el ensayo de 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT). La cantidad de células apoptóticas se midió por citometría de flujo. La determinación de citoquinas pro-inflamatorias se realizó por ELISA. La transcripción de genes de mucina se cuantificó por PCR en tiempo real.RESULTADOS. DEP disminuyó significativamente la viabilidad, la proliferación y la secreción de IL-8, pero aumentó la secreción de IL-6 en ambas líneas celulares, HCLE y IOBA-NHC, en forma dosis-dependiente. No se detectó liberación de TNF-a ni en las células ...

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“…We focused our measurements on the acute response elicited by particle exposure, allowing 24 h for the development of an inflammatory response. In addition, some air pollution studies indicate that a 24-h lag occurs between exposure and respiratory adverse effects (Arbex et al, 2000;Braga et al, 2001;Braga et al, 2002;Cançado et al, 2006;Arbex et al, 2007;Laks et al, 2008;Mazzoli-Rocha et al, 2008).…”

Section: Ctrl Alummentioning

confidence: 98%

Pulmonary function and histological impairment in mice after acute exposure to aluminum dust

Mazzoli‐Rocha¹,

Santos²,

Fernandes³

et al. 2010

Inhalation Toxicology

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Along the aluminum refining process, alumina (Al2O3) constitutes the main source of dust. Although aluminum refinery workers present respiratory symptoms with lung functional changes, no conclusive data about lung function impairment after alumina exposure has been so far reported. We examined the pulmonary alterations of exposure to material collected in an aluminum refinery in Brazil. BALB/c mice were exposed in a whole-body chamber for 1 h to either saline (CTRL, n = 11) or to a suspension (in saline) of 8 mg/m(3) of the dust (ALUM, n = 11) both delivered by an ultrasonic nebulizer. Twenty-four hours after exposure lung mechanics were measured by the end-inflation method. Lungs were prepared for histology. ALUM showed significantly higher static elastance (34.61 +/- 5.76 cmH2O/mL), elastic component of viscoelasticity (8.16 +/- 1.20 cmH2O/mL), pressure used to overcome the resistive component of viscoelasticity (1.62 +/- 0.24 cmH2O), and total resistive pressure (2.21 +/- 0.49 cmH2O) than CTRL (27.95 +/- 3.63 cmH2O/mL, 6.12 +/- 0.99 cmH2O/mL, 1.23 +/- 0.19 cmH2O, and 1.68 +/- 0.23 cmH2O, respectively). ALUM also presented significantly higher fraction area of alveolar collapse (69.7 +/- 1.2%) and influx of polymorphonuclear cells (27.5 +/- 1.1%) in lung parenchyma than CTRL (27.2 +/- 1.1% and 14.6 +/- 0.7%, respectively). The composition analysis of the particulate matter showed high concentrations of aluminum. For the first time it was demonstrated in an experimental model that an acute exposure to dust collected in an aluminum producing facility impaired lung mechanics that could be associated with inflammation.

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Composition of Diesel Particles Influences Acute Pulmonary Toxicity: An Experimental Study in MICE

Cited by 39 publications

References 19 publications

Roles of oxidative stress in signaling and inflammation induced by particulate matter

Roles of oxidative stress in signaling and inflammation induced by particulate matter

Diesel Exhaust Particles Selectively Induce Both Proinflammatory Cytokines and Mucin Production in Cornea and Conjunctiva Human Cell Lines

Pulmonary function and histological impairment in mice after acute exposure to aluminum dust

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