Diesel exhaust particles enhance antigen-induced airway inflammation and local cytokine expression in mice.

Takano, Hirohisa

doi:10.2492/jsir1981.19.9

Cited by 95 publications

(188 citation statements)

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“…Additional evidence supporting the role of oxidative stress in PM-induced airway inflammation comes from animal studies [56][57][58]. For example, intratracheal instillation of DEP leads to increased PMN infiltration, increased mucus, nitric oxide production, and increased airway hyperreactivity (AHR) in mice, all of which play important role in the pathogenesis of asthma [59][60][61][62][63][64][65]. These effects can be suppressed by pre-treating the animals with SOD or with the nitric oxide synthase inhibitors [60,63,64].…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

820

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

820

529

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“…Diesel particles have been found to stimulate IgE production, eosinophilic degranulation and augmentation of cytokine and chemokine production F all effects related to a permanent atopic/asthmatic predisposition, arguing for a causal effect (Casilas et al, 1999;Sagai et al, 1993). Diesel exhaust particles is also indicated as an adjuvant with environmental allergens, inducing and/or increasing atopic individuals' allergic reactions (Takano et al, 1997;Ishizaki et al, 1987), an important effect that remains to be studied for biomass smoke. There may be a link between the ''hygiene hypothesis'' (Strachan, 1989) and particle pollution, as diesel exhaust particles appear to enhance the differentiation of CD4 þ T lymphocytes into the IgE producing Th2 phenotype associated with atopy (Pandya et al, 2002).…”

Section: Biomass-smoke Exposurementioning

confidence: 99%

Childhood asthma and indoor woodsmoke from cooking in Guatemala

Schei

Hessen

Smith

et al. 2004

J Expo Sci Environ Epidemiol

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We estimated the prevalence and severity of asthma, and the association with cooking on open wood fires, as preparation for a large-scale randomized field trial on effects of indoor air pollution and child health. This is one of the first systematic studies of asthma and indoor wood-smoke pollution and to our knowledge the first asthma study in a purely indigeneous population in Latin America. The mothers of 1058 children aged 4-6 years were interviewed, using the standardized ISAAC (International Study of Asthma and Allergies in Childhood) procedures and questionnaire. The study population is a Mam-speaking (Maya), indigenous group living at relatively high altitude (2000 m) in Western Guatemalan Highlands. We found that asthma prevalence is low among indigenous children in Gautemala, compared to other populations in Latin America. Only 3.3% of the children reported wheezing symptoms in the last 12 months, and 72% wheezing symptoms ever. The majority of the current wheezers had at least one of the criteria for severe asthma. The prevalence of all the symptoms of asthma was higher in children from households that used open fires compared to improved stoves with chimneys. In a logistic regression model, use of open fire for cooking was a significant risk factor for a number of asthma symptoms, with odds ratios varying from 2.0 to 3.5. Among the different cooking technologies (1Fimproved stove with chimney, 2Fmixture of gas and open fire, 3Fopen fire) trends of higher prevalence with more pollution was found for some of the symptoms. Hence use of open fire for cooking, may be an important risk factor for asthma symptoms and severity.

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“…It has been demonstrated previously, by extensive epidemiological studies, that particulate air pollutants, such as DEP, are related to allergic diseases including asthma and allergic rhinitis (Diaz-Sanchez et al, 2003). Although a number of animal and human studies have demonstrated that DEP act as an adjuvant during allergen exposure, and affect acute asthma exacerbations (Sagai et al, 1996;Takano et al, 1997Takano et al, , 1998Lim et al, 1998;Miyabara et al, 1998;Nel et al, 1998;Ohta et al, 1999;Walters et al, 2001;Ichinose et al, 2002), questions remain concerning the ability of DEP to induce asthma in the absence of an allergen.…”

Section: Discussionmentioning

confidence: 99%

“…Many studies (Sagai et al, 1996;Takano et al, 1997Takano et al, , 1998Lim et al, 1998;Miyabara et al, 1998;Nel et al, 1998;Ohta et al, 1999;Walters et al, 2001;Ichinose et al, 2002) have demonstrated that long-term exposure to DEP affects AHR and airway inflammation, depending on dose, frequency, and time of DEP treatment. Such chronic exposure protocols require diesel engines, which are costly and not widely available, to investigate the effect of DEP on asthma phenotypes such as airway inflammation and AHR.…”

Section: Discussionmentioning

confidence: 99%

Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

Song

Jang

Ahn

et al. 2008

Environmental Toxicology

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Background: Chitinase may play a role in regulating allergic diseases. Objective: We studied the role of chitinase in a mouse model exposed to diesel exhaust particles (DEP). Mice were exposed to intranasal DEP (0.6 mg/mL) for 5 days and challenged with aerosolized DEP (6 mg/m 3 ) on days 6-8. Enhanced pause (Penh), as an airway obstruction marker, was measured on day 9, and bronchoalveolar lavage (BAL) fluid and lung tissues were collected on day 10. The expression of Ym1 and Ym2 mRNA was assessed in lung tissue extracts by reverse transcription-polymerase chain reaction. Results: DEP induced significant increases in methacholine-induced Penh and IL-4 levels in BAL fluid relative to the control group. Peribronchial and perivascular inflammatory cell infiltrates were prominent in the DEP group. DEP induced Ym1 and Ym2 mRNA expression in lung tissue extracts relative to the control group.-Conclusion: These results demonstrate that DEP induced airway hyperresponsiveness and Ym mRNA expression via a Th2 cell-biased response, suggesting that chitinase may play an important role in airway inflammation and responsiveness upon exposure to DEP in a mouse model, and may therefore be involved in regulating allergic diseases. #

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Diesel exhaust particles enhance antigen-induced airway inflammation and local cytokine expression in mice.

Cited by 95 publications

References 0 publications

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Childhood asthma and indoor woodsmoke from cooking in Guatemala

Ym1 and Ym2 expression in a mouse model exposed to diesel exhaust particles

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