Long-Term Exposure to Diesel Exhaust Enhances Antigen-Induced Eosinophilic Inflammation and Epithelial Damage in the Murine Airway

Ichinose, Takamichi; Takano, Hirohisa; Miyabara, Yuichi; Sagai, Masaru

doi:10.1006/toxs.1998.2459

Cited by 30 publications

(29 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…One possible mechanism is nitric oxide generation, as evidenced by the ability of nitric oxide synthase inhibitors to interfere with DEPinduced AHR in mice [60]. Shedding of airway epithelial cells is another possibility, based on the ability of DEP to induce acute epithelial damage in vivo and in vitro [51,[113][114][115].…”

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

821

529

View full text Add to dashboard Cite

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.

show abstract

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

821

529

View full text Add to dashboard Cite

show abstract

“…The degree of eosinophil or neutrophil and mononuclear cell infiltration around the airways and the proliferation of goblet cells in the bronchial epithelium were graded in a blind fashion: 0: not present; 1: very slight; 2: slight; 3: moderate; 4: moderate to marked; 5: marked. An inflammatory reaction affecting ,20% of the airways was defined as ''1'' (,20% goblet cells stained with PAS), ''2'' was defined as 20-40% of the airways were affected, ''3'' 40-60%, ''4'' 60-80% and ''5'': .80% of the airways were affected (n54-5 in each group) [10].…”

Section: Bronchoalveolar Lavagementioning

confidence: 99%

“…Also, DEP have been implicated to modulate allergic reactions [3,4]. DEP enhance the antigen-specific immunoglobulin (Ig)E response [5,6] and aggravate airway inflammation induced by repetitive intratracheal instillation of antigen in vivo [7][8][9][10].…”

mentioning

confidence: 99%

Naphthoquinone enhances antigen-related airway inflammation in mice

Inoue¹,

Takano²,

Hiyoshi³

et al. 2006

Eur Respir J

View full text Add to dashboard Cite

ABSTRACT:The current authors have previously demonstrated that diesel exhaust particles (DEP) enhance antigen-related airway inflammation in mice. Furthermore, a recent study has shown that organic chemicals in DEP, rather than their carbonaceous nuclei, are important contributors to the aggravating effects of airway inflammation. However, the components in DEP responsible for the enhancing effects on the model remain to be identified.The current authors investigated the effects of naphthoquinone (NQ), one of the extractable chemical compounds of DEP, on antigen-related airway inflammation, local expression of cytokine proteins, and antigen-specific immunoglobulin (Ig) production in mice. Pulmonary exposure to NQ dose-dependently aggravated antigen-related airway inflammation, as characterised by infiltration of eosinophils and lymphocytes around the airways and an increase in goblet cells in the bronchial epithelium. Combined exposure to NQ and antigen enhanced the local expression of interleukin (IL)-4, IL-5, eotaxin, macrophage chemoattractant protein-1 and keratinocyte chemoattractant, compared with exposure to antigen or NQ alone. Also, NQ exhibited adjuvant activity for the antigen-specific production of IgG 1 and IgG 2a .These results provide the first experimental evidence that naphthoquinone can enhance antigen-related airway inflammation in vivo, and that naphthoquinone can, to some extent, partly play a role in the pathogenesis of diesel exhaust particle toxicity on the condition. DEP are complicated particles consisting of carbonaceous nuclei and a vast number of organic chemical compounds such as polyaromatic hydrocarbons, aliphatic hydrocarbons, heterocycles, and quinones. Previous studies have indicated that organic chemicals extracted from DEP result in induction of apoptosis [11], increase oxidative stress [12], and induce the production of inflammatory cells [13][14][15] through the release of pro-inflammatory molecules in vitro [15,16]. The current authors have recently demonstrated that extracted organic chemicals from DEP, rather than residual carbonaceous nuclei of DEP after extraction, predominantly enhance antigen-related airway inflammation in mice [17]. However, detailed studies concerning the component(s) of DEP responsible for their effects on the respiratory system and/or pulmonary diseases remain unsatisfied, which is particularly the case for in vivo studies.A variety of quinones have been identified as DEP components [18,19]. Quinones themselves have toxicological properties, serving as alkylating agents and interacting with, for example, flavoproteins to generate reactive oxygen species (ROS) which can induce biological injury [20][21][22][23]. Phenanthraquinone (PQ) is one of the quinones contained in DEP [19,23]. The current authors have recently shown that PQ induces recruitment of inflammatory cells, such as eosinophils and neutrophils, into the lung with the lung expression of pro-inflammatory molecules such as interleukin (IL)-5 and eotaxin in vivo [24]. More recently, it h...

show abstract

“…Diesel exhaust (DE), which contains diesel exhaust particles (DEPs) and diesel exhaust gases such as nitrogen dioxides, carbon oxides, and sulfur dioxide, is an important air pollutant. Lung cancer, 1,2) allergic rhinitis, [3][4][5] and bronchial asthma-like diseases [6][7][8][9][10][11][12] can be caused by exposure to DE or DEP. The effect of DE on the reproductive system has been examined recently along with endocrine-disrupting chemicals.…”

Section: Introductionmentioning

confidence: 99%

Effect of Diesel Exhaust on Development of Fetal Reproductive Function in ICR Female Mice

Tsukue

Yoshida

Sugawara

et al. 2004

JOURNAL OF HEALTH SCIENCE

View full text Add to dashboard Cite

Diesel exhaust (DE) is a serious air pollution problem in big cities. Most suspended particulate matter (SPM) less than 2.5 m in diameter consists of diesel exhaust particles (DEPs), which are reported to cause pulmonary carcinogenesis, allergic rhinitis, and bronchial asthma-like diseases. It has been recently reported that DE also affects the circulatory and reproductive systems. Yoshida et al. reported that mRNA expression of steroidogenic factor-1 (Ad4BP/SF-1) and of Müllerian inhibitory substance (MIS), which are essential for male gonadal differentiation, decreased significantly in male fetuses when maternal mice were exposed to DE at levels of 0.1 or 3.0 mg DEP/m 3 for 8 hr per day between 2 and 13 days postcoitum (dpc). In this study, maternal mice were exposed to DE 0.1 mg DEP /m 3 for 8 hr per day between 2 and 13 dpc. Expression levels of Ad4BP/SF-1 and MIS mRNA in female fetuses were not decreased. However, expression levels of bone morphogenetic protein-15, reported to be related to development of the oocyte, were significantly decreased in comparison with that in the control group. Our data suggest that female fetuses of pregnant mice exposed to DE in utero are less sensitive to the expression levels of mRNAs for Ad4BP/SF-1 and MIS compared with males and that DE may affect development of the oocyte in the female fetus.

show abstract

Long-Term Exposure to Diesel Exhaust Enhances Antigen-Induced Eosinophilic Inflammation and Epithelial Damage in the Murine Airway

Cited by 30 publications

References 40 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

Naphthoquinone enhances antigen-related airway inflammation in mice

Effect of Diesel Exhaust on Development of Fetal Reproductive Function in ICR Female Mice

Contact Info

Product

Resources

About