Stimulation of Human and Rat Alveolar Macrophages by Urban Air Particulates: Effects on Oxidant Radical Generation and Cytokine Production

Becker, Susanne; Soukup, Joleen M.; Gilmour, M. Ian; Devlin, Robert B.

doi:10.1006/taap.1996.0330

Cited by 294 publications

(194 citation statements)

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“…Several cell types are involved in allergen sensitization and asthma pathogenesis, including antigenpresenting cells (APC), T-helper 2 (Th2) lymphocytes, IgE-secreting plasma cells, mast cells, eosinophils, neutrophils, mucus-secreting goblet cells, smooth muscle and endothelial cells. DEP can directly impact a number of the cells that play a role in the afferent or efferent immune response [25,[81][82][83][84][85][86][87]. Traditional adjuvants exert their effects on the afferent or early phase of the immune response, which implies possible effects on antigen presenting cells (APC) [88,89].…”

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

809

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

809

529

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“…AM may also produce ROS from mitochondria when exposed to combustion-derived particles, such as ROFA (3). ROS produced by AM may then serve as signaling molecules for downstream events including inflammation, cell growth, and cell death, although previous studies have shown that ROFA-induced ROS production does not predict activation of NF-B or induction of IL-8 (4,39).…”

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confidence: 99%

“…Upon contact with certain environmental particulate pollutants, AM are activated and produce a large quantity of reactive oxygen species (ROS) in the form of chemiluminescence burst. Examples of pollutant particles capable of enhancing the production of ROS by AM include oil fly ash and residual oil fly ash (ROFA) (3,4,30,39) and the Utah Valley dust (48). The exact sources for ROS produced by pollutant-activated AM vary depending on the particles used.…”

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confidence: 99%

Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage

Huang

Soukup

Harder

et al. 2003

American Journal of Physiology-Cell Physiology

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Residual oil fly ash (ROFA) is a pollutant dust that stimulates production of reactive oxygen species (ROS) from mitochondria and apoptosis in alveolar macrophages (AM), but the relationship between these two processes is unclear. In this study, human AM were incubated with ROFA or vanadyl sulfate (VOSO4), the major metal constituent in ROFA, with or without nitro-l-arginine methyl ester (l-NAME), diphenyleneiodonium (DPI), and mitochondrial electron transport inhibitors. Interactions among production of ROS, nitric oxide (NO), and apoptosis of AM were determined. ROFA-stimulated ROS production was attenuated by DPI, rotenone, antimycin, and NaN3, but not by l-NAME, a pattern mimicked by VOSO4. ROFA-induced apoptosis was inhibited byl-NAME and a caspase-3-like protease inhibitor, but not by mitochondrial inhibitors. ROFA enhanced NO-mediated increase in caspase-3-like activity. VOSO4 had minor effects on apoptosis. Thus ROFA-stimulated production of ROS from mitochondria was independent of apoptosis of AM, which was mediated by activation of caspase-3-like proteases and NO. The pro-oxidant effect but not the proapoptotic effect of ROFA was mediated by vanadium.

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“…Macrophages constitute an important target for DEP in the lung (17,18,(21)(22)(23). After phagocytosis of these particles, macrophages respond in a hierarchical fashion to increasing particle load and incremental levels of oxidative stress (24).…”

mentioning

confidence: 99%

Comparison of the Pro-Oxidative and Proinflammatory Effects of Organic Diesel Exhaust Particle Chemicals in Bronchial Epithelial Cells and Macrophages

Wang

Oberley

et al. 2002

The Journal of Immunology

286

231

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Inhaled diesel exhaust particles (DEP) exert proinflammatory effects in the respiratory tract. This effect is related to the particle content of redox cycling chemicals and is involved in the adjuvant effects of DEP in atopic sensitization. We demonstrate that organic chemicals extracted from DEP induce oxidative stress in normal and transformed bronchial epithelial cells, leading to the expression of heme oxygenase 1, activation of the c-Jun N-terminal kinase cascade, IL-8 production, as well as induction of cytotoxicity. Among these effects, heme oxygenase 1 expression is the most sensitive marker for oxidative stress, while c-Jun N-terminal kinase activation and induction of apoptosis-necrosis require incremental amounts of the organic chemicals and increased levels of oxidative stress. While a macrophage cell line (THP-1) responded in similar fashion, epithelial cells produced more superoxide radicals and were more susceptible to cytotoxic effects than macrophages. Cytotoxicity is the result of mitochondrial damage, which manifests as ultramicroscopic changes in organelle morphology, a decrease in the mitochondrial membrane potential, superoxide production, and ATP depletion. Epithelial cells also differ from macrophages in not being protected by a thiol antioxidant, N-acetylcysteine, which effectively protects macrophages against cytotoxic DEP chemicals. These findings show that epithelial cells exhibit a hierarchical oxidative stress response that differs from that of macrophages by more rapid transition from cytoprotective to cytotoxic responses. Moreover, epithelial cells are not able to convert N-acetylcysteine to cytoprotective glutathione.

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Stimulation of Human and Rat Alveolar Macrophages by Urban Air Particulates: Effects on Oxidant Radical Generation and Cytokine Production

Cited by 294 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

Mitochondrial oxidant production by a pollutant dust and NO-mediated apoptosis in human alveolar macrophage

Comparison of the Pro-Oxidative and Proinflammatory Effects of Organic Diesel Exhaust Particle Chemicals in Bronchial Epithelial Cells and Macrophages

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