Alveolar macrophage interaction with air pollution particulates.

Goldsmith, Carroll-Ann; Frevert, Charles W.; Imrich, Amy; Sioutas, Constantinos; Kobzik, Lester

doi:10.1289/ehp.97105s51191

Cited by 48 publications

(24 citation statements)

References 15 publications

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“…SOD superoxide dismutase phagocytosis. They may mediate alveolar macrophage binding of certain inert and environmental particulate matter as Fe 2 O 3 , silicates, TiO 2 , quartz, and iron oxide (Arredouani et al 2005;Beamer and Holian 2005;Goldsmith et al 1997;Kobzik 1995;Palecanda et al 1999). Additionally, different types of particles may be ingested by the alveolar macrophage (AM) following activation of diverse surface receptors.…”

Section: Pm-induced Oxidative Stressmentioning

confidence: 99%

“…Additionally, different types of particles may be ingested by the alveolar macrophage (AM) following activation of diverse surface receptors. A dosedependent increase in dichlorofluorescin oxidation (a fluorescent measure of intracellular ROS production) was observed in AM incubated with ROFA and concentrated suspended particles (Goldsmith et al 1997). Additionally, macrophage inflammatory protein-2 (MIP-2) message and tumor necrosis factor-α (TNF-α) production were, respectively, increased in AM and in monocyte-macrophage cell line after ROFA exposure (Goldsmith et al 1998).…”

Section: Pm-induced Oxidative Stressmentioning

confidence: 99%

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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: Pm-induced Oxidative Stressmentioning

confidence: 99%

Section: Pm-induced Oxidative Stressmentioning

confidence: 99%

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

et al. 2010

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“…While one study has demonstrated that epithelial cells can contribute to overall inflammatory response of the lung to inhaled particles (Stringer et al, 1996), a majority of the studies have focused Downloaded by [Stockholm University Library] at 23:58 12 August 2015 on the response of alveolar macrophages to CAPs (Goldsmith et al, 1997(Goldsmith et al, , 1998Imrich et al, 1999Imrich et al, , 2000. The results of these studies have confirmed that most biological effects on alveolar macrophages are mediated by insoluble components of CAPs and certain adsorbed factors such as lipopolysaccharide (LPS).…”

Section: Cell Exposure To Capsmentioning

confidence: 99%

Exposure to Concentrated Ambient Particles (CAPs): A Review

Ghio

Huang

2004

Inhalation Toxicology

100

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Epidemiologic studies support a participation of fine particulate matter (PM) with a diameter of 0.1 to 2.5 microm in the effects of air pollution particles on human health. The ambient fine particle concentrator is a recently developed technology that can enrich the mass of ambient fine particles in real time with little modification. The advantages of concentrators are that the particles produced are "real world" and they allow exposure at pertinent masses. Limitations include variability in both particle mass and composition and some uncertainty over the best statistical approach to analyze the data. Cumulative evidence provided by the body of initial investigation shows that exposures to concentrated ambient particles (CAPs) can be accomplished safely in both humans and animals. Human investigation using the CAPs has shown acute lung inflammation and changes in both blood indices and heart rate variability. Animal studies support a potential pulmonary inflammation, blood changes, alterations of specific cardiac endpoints, and an increased susceptibility of specific models. These studies have helped establish the causal relationship between find particle exposure and adverse health effects in the lung and cardiovascular system. In addition, it appears that specific components in CAPS may differentially affect these tissues.

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“…For example, biological components (i.e., pollen, endotoxins) carried on the PM particles have been shown to activate and stimulate cytokine release and apoptosis in alveolar macrophages (Becker et al, 1996). Lipopolysaccharides, associated with these biologicals, appear to amplify this cytokine release in alveolar macrophages (Goldsmith et al, 1997). Volatile organics (Lies et al, 1986), acids (Chen et al, 1992(Chen et al, , 1995Kimmel et al, 1997), and sulfates (Gwynn et al, 2000) found on PM particles are also inflammatory.…”

Section: Turned To Baseline Upon Washing Of the Cells To Oscillationmentioning

confidence: 99%

Particulate Matter Inflammation and Receptor Sensitivity Are Target Cell Specific

Veronesi

Haar

Roy

et al. 2002

Inhalation Toxicology

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The complexity of primary source particulate matter (PM) and the various cell types encountered by its inhalation raise the possibility that target cells are differentially activated. Since epithelial cells, which line the nasal-tracheal-bronchial airways, and sensory C fibers, which terminate throughout this epithelial layer, are initially targeted by inhaled PM, we compared their relative biological response in vitro to PM originating from volcanic (MSH), anthropogenic (diesel), residential (woodstove), urban ambient (St. Louis, Ottawa), and industrial emission (coal fly ash, CFA; residual oil fly ash, ROFA; oil fly ash, OFA) sources. Increases in intracellular calcium (i.e., [Ca(2+)](i)) are a second-messenger event that indicates cellular activation and signal transduction, in both nerve and epithelial cells. Single-cell calcium imaging recordings were taken of human bronchial epithelial cells (BEAS-2B) exposed to selected PM (50 microg/ml or 30 microg/cm(2)). These cells responded with variable increases in [Ca(2+)](i) ranging from abrupt increases, which returned to baseline upon washing of the cells, to oscillations of the [Ca(2+)](i) that did not wash out. Increases in [Ca(2+)](i) and inflammatory cytokine (i.e., interleukin 6, IL-6) release were measured in populations of BEAS-2B cells exposed to PM (50 microg/ml) and were shown to significantly correlate (r(2) =.80). BEAS-2B cells, stained histochemically with cobalt, displayed a concentration-dependent precipitation in response to acid pH and capsaicin, indicating the presence of acid-sensitive pathways (e.g., VR1 and acid-sensitive receptors). To demonstrate the relevance of these pathways to inflammatory cytokine (i.e., IL-6) release, BEAS-2B cells were pretreated (15 min) with antagonists to the vanilloid (VR1) receptor (i.e., capsazepine, CPZ) or acid-sensitive pathways (i.e., amiloride) before their exposure to the selected PM. A significant reduction of IL-6 release occurred in response to all PM, except for MSH and diesel exhaust. Dorsal root ganglia (DRG), which innervate the tracheal airways, were dissociated from fetal mice and pretreated with CPZ or amiloride before exposure (4 h) to the selected PM (50 microg/ml). Overall, significantly higher release occurred in PM-exposed sensory neurons relative to that of BEAS-2B epithelial cells. Although both CPZ and amiloride significantly reduced IL-6 release for all PM, the degree of inhibition was less for the PM-exposed DRG relative to BEAS-2B cells. These data show that differential increases in [Ca(2+)](i) and IL-6 release occur in BEAS-2B epithelial cells and DRG sensory neurons, when exposed to PM derived from different sources. The degree of this activation, however, depends not only on the source of the PM, but also on its cellular target. This differential sensitivity of target cells may contribute to the organism's overall inflammatory response to PM exposure.

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Alveolar macrophage interaction with air pollution particulates.

Cited by 48 publications

References 15 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

Exposure to Concentrated Ambient Particles (CAPs): A Review

Particulate Matter Inflammation and Receptor Sensitivity Are Target Cell Specific

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