Airway Inflammatory Responses to Oxidative Stress Induced by Prolonged Low-Dose Diesel Exhaust Particle Exposure From Birth Differ Between Mouse Balb/C and C57bl/6 Strains

Li, Yingji; Kawada, Tomoyuki; Takizawa, Hajime; Azuma, Arata; Kudoh, Shoji; Sugawara, Isamu; Yamauchi, Yasuhiro; Kohyama, Tadashi

doi:10.1080/01902140701884406

Cited by 14 publications

(14 citation statements)

References 46 publications

(55 reference statements)

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“…It has been reported that exposure of mice to some environmental pollutants such as lead, residual oil fly ash (ROFA), and diesel exhaust particles at the prenatal, perinatal, or postnatal stage increases the level of IgE-or ovalbumin (OVA)-specific IgG1 antibody production (Snyder et al, 2000;Hamada et al, 2007;Li et al, 2008). In contrast to these studies, we found decreased total IgE in the present study.…”

Section: Discussioncontrasting

confidence: 86%

“…We hypothesized that possibly the perinatal exposure to low-level toluene may increase systemic or local Th2-type responses and that the combination with PGN stimulation may suppress the enhanced Th2-type responses in infant mice. Exposure of fetuses or infant mice to some environmental pollutants increased the level of Th2-dependent IgE and IgG1 antibody production (Snyder et al, 2000;Hamada et al 2007;Li et al, 2008). Moreover, in our previous study, it has been demonstrated that interferon (IFN)-, a Th1-type cytokine, in bronchoaleolar lavage (BAL) fluid from adult mice was suppressed by low-level toluene exposure .…”

Section: Introductionmentioning

confidence: 96%

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Suppression of Th1- and Th2-type immune responses in infant mouse spleen after prenatal and postnatal exposure to low-level toluene and peptidoglycan

Yamamoto

Win-Shwe

Yoshida

et al. 2009

Inhalation Toxicology

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The aim of the present study was to investigate the effect of low-level concentrations, under the occupational acceptable limits, of toluene exposure and peptidoglycan (PGN) stimulation on Th1/Th2 immunity in infant mice. Pregnant BALB/c mice and their offspring were exposed to low-level toluene inhalation (0, 5, and 50 ppm) for 4 wk (from the late prenatal stage to early postnatal stage) in a whole-body exposure chamber. Some of the pregnant mice and their offspring were stimulated with PGN during toluene exposure. We measured total immunoglobulins of different subclasses in plasma, and production and expression level of cytokines in the lung and spleen, and transcription factors related to Th1/Th2 immunity in the spleen of infant (3 wk old) mice. Exposure of mice to 5 or 50 ppm toluene resulted in increased immunoglobulin (Ig) G1 and decreased IgG2a and IgE antibodies in the plasma; significantly decreased T-bet, GATA-3, and Foxp3 mRNA in the spleen; and a tendency toward decreased interferon (IFN)-gamma mRNA in spleen. Exposure of mice to low-level toluene together with PGN stimulation resulted in decreased IgG1 as well as IgG2a antibodies in the plasma and Foxp3 mRNA in spleen as compared with control or PGN-treated mice. These findings suggest that low-level toluene exposure and PGN stimulation from the late prenatal to early postnatal stage suppressed the splenic parameter related to Th1/Th2 immunity in infant mice.

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Section: Discussioncontrasting

confidence: 86%

Section: Introductionmentioning

confidence: 96%

Suppression of Th1- and Th2-type immune responses in infant mouse spleen after prenatal and postnatal exposure to low-level toluene and peptidoglycan

Yamamoto

Win-Shwe

Yoshida

et al. 2009

Inhalation Toxicology

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“…Susceptibility to the adverse effects of air pollutants is an intrinsic trait most probably related to genotypes [14]. Animal studies have shown that prolonged low-dose DEP exposure induces airway inflammatory responses that differ remarkably among mouse strains with different genetic backgrounds of oxidative stress response [15]. It has been proposed that host responses to DEP are regulated by a balance between antioxidant defenses and pro-inflammatory responses [16].…”

Section: Introductionmentioning

confidence: 99%

Glutathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells

Wu¹,

Peden²,

McConnell

et al. 2012

Part Fibre Toxicol

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BackgroundDiesel exhaust particles (DEP) contribute substantially to ambient particulate matter (PM) air pollution in urban areas. Inhalation of PM has been associated with increased incidence of lung disease in susceptible populations. We have demonstrated that the glutathione S-transferase M1 (GSTM1) null genotype could aggravate DEP-induced airway inflammation in human subjects. Given the critical role airway epithelial cells play in the pathogenesis of airway inflammation, we established the GSTM1 deficiency condition in primary bronchial epithelial cells from human volunteers with GSTM1 sufficient genotype (GSTM1+) using GSTM1 shRNA to determine whether GSTM1 deficiency could exaggerate DEP-induced expression of interleukin-8 (IL-8) and IL-1β proteins. Furthermore, the mechanisms underlying GSTM1 regulation of DEP-induced IL-8 and IL-1β expression were also investigated.MethodsIL-8 and IL-1β protein levels were measured using enzyme-linked immunosorbent assay. GSTM1 deficiency in primary human bronchial epithelial cells was achieved using lentiviral GSTM1 shRNA particles and verified using real-time polymerase chain reaction and immunoblotting. Intracellular reactive oxygen species (ROS) production was evaluated using flow cytometry. Phosphorylation of protein kinases was detected using immunoblotting.ResultsExposure of primary human bronchial epithelial cells (GSTM1+) to 25-100 μg/ml DEP for 24 h significantly increased IL-8 and IL-1β protein expression. Knockdown of GSTM1 in these cells further elevated DEP-induced IL-8 and IL-1β expression, implying that GSTM1 deficiency aggravated DEP-induced pro-inflammatory response. DEP stimulation induced the phosphorylation of extracellular signal-regulated kinase (ERK) and Akt, the downstream kinase of phosphoinositide 3-kinase (PI3K), in GSTM1+ bronchial epithelial cells. Pharmacological inhibition of ERK kinase and PI3K activity blocked DEP-induced IL-8 and IL-1β expression. DEP-induced ERK and Akt phosphorylation could be increased by GSTM1 knockdown. In addition, pretreatment of HBEC with the antioxidant N-acetyl cysteine significantly inhibited DEP-induced ERK and Akt phosphorylation, and subsequent IL-8 and IL-1β expression.ConclusionGSTM1 regulates DEP-induced IL-8 and IL-1β expression in primary human bronchial epithelial cells by modulation of ROS, ERK and Akt signaling.

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“…This could be mediated by one or more of a number of anti-oxidant enzymes [97,98]. Nrf2 is a redoxsensitive basic leucine zipper transcription factor that is involved in the transcriptional regulation of many anti-oxidant genes [99].…”

Section: Particulate Matter and Allergiesmentioning

confidence: 99%

“…These results strongly suggest that DEPs-induced oxidative stress and host antioxidant responses is regulated by Nrf2. The role played by Nrf2 in an allergic asthma model has been clearly demonstrated [100,101]; indeed, NAC treatment reduced the allergic inflammatory responses caused by DEP exposure [98]. Nrf2-/- mice exposed to low-dose DEPs exhibited significantly increased inflammatory cell numbers and periodic acid-Schiff staining-positive mucus cell hyperplasia.…”

Section: Particulate Matter and Allergiesmentioning

confidence: 99%

Impact of Air Pollution on Allergic Diseases

Takizawa

2011

Korean J Intern Med

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The incidence of allergic diseases in most industrialized countries has increased. Although the exact mechanisms behind this rapid increase in prevalence remain uncertain, a variety of air pollutants have been attracting attention as one causative factor. Epidemiological and toxicological research suggests a causative relationship between air pollution and the increased incidence of asthma, allergic rhinitis, and other allergic disorders. These include ozone, nitrogen dioxide and, especially particulate matter, produced by traffic-related and industrial activities. Strong epidemiological evidence supports a relationship between air pollution and the exacerbation of asthma and other respiratory diseases. Recent studies have suggested that air pollutants play a role in the development of asthma and allergies. Researchers have elucidated the mechanisms whereby these pollutants induce adverse effects; they appear to affect the balance between antioxidant pathways and airway inflammation. Gene polymorphisms involved in antioxidant pathways can modify responses to air pollution exposure. While the characterization and monitoring of pollutant components currently dictates pollution control policies, it will be necessary to identify susceptible subpopulations to target therapy/prevention of pollution-induced respiratory diseases.

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Airway Inflammatory Responses to Oxidative Stress Induced by Prolonged Low-Dose Diesel Exhaust Particle Exposure From Birth Differ Between Mouse Balb/C and C57bl/6 Strains

Cited by 14 publications

References 46 publications

Suppression of Th1- and Th2-type immune responses in infant mouse spleen after prenatal and postnatal exposure to low-level toluene and peptidoglycan

Suppression of Th1- and Th2-type immune responses in infant mouse spleen after prenatal and postnatal exposure to low-level toluene and peptidoglycan

Glutathione-S-transferase M1 regulation of diesel exhaust particle-induced pro-inflammatory mediator expression in normal human bronchial epithelial cells

Impact of Air Pollution on Allergic Diseases

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