Lipopolysaccharide Priming Amplifies Lung Macrophage Tumor Necrosis Factor Production in Response to Air Particles

Imrich, Amy; Ning, Yao; Koziel, Henry; Coull, Brent A.; Kobzik, Lester

doi:10.1006/taap.1999.8731

Cited by 71 publications

(49 citation statements)

References 25 publications

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“…Our hypothesis is that in the inflammatory milieu of diseased lungs, AMs may be primed for enhanced responses to inhaled air particles. In vitro, lipopolysaccharide priming substantially enhances particle-mediated TNF release by AMs from both rat and human sources (26). Moreover, we have observed that CAPs cause decreased bacterial clearance and increased pneumonic inflammation in mice in vivo, and that IFN-␥ priming of mice before CAPs administration substantially enhances this effect (unpublished data).…”

Section: Discussionmentioning

confidence: 67%

Effect of Concentrated Ambient Particles on Macrophage Phagocytosis and Killing of Streptococcus pneumoniae

Zhou

Kobzik

2007

Am J Respir Cell Mol Biol

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109

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Particulate air pollution is linked to increased pneumonia epidemiologically and diminished lung bacterial clearance experimentally. We investigated the effect of concentrated ambient particles (CAPs, р PM 2.5 ) on the interaction of murine primary alveolar macrophages (AMs) and the murine macrophage cell line, J774 A.1, with Streptococcus pneumoniae. We found that CAPs increased binding of bacteria by both primary AMs and J774 cells (66.7 Ϯ 10.6% and 58.9 Ϯ 4.0%, respectively, n ϭ 4). In contrast to bacterial binding, CAPs decreased internalization in both AMs and J774 (55.4 Ϯ 8.5% and 54.7 Ϯ 5.1%, respectively, n ϭ 4). The rate of killing of internalized bacteria was similar, but CAPs caused a decrease in the absolute number of bacteria killed by macrophages, mainly due to decreased internalization. Additional analyses showed that soluble components of CAPs mediated the enhanced binding and decreased internalization of S. pneumoniae. Chelation of iron in soluble CAPs substantially reversed, while addition of iron as ferric ammonium citrate restored inhibition of phagocytosis of S. pneumoniae in vitro. The results identify phagocytic internalization as a specific target for toxic effects of air pollution particles on AMs.

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Section: Discussionmentioning

confidence: 67%

Effect of Concentrated Ambient Particles on Macrophage Phagocytosis and Killing of Streptococcus pneumoniae

Zhou

Kobzik

2007

Am J Respir Cell Mol Biol

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109

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“…Endotoxin content is unlikely because the extracted endotoxin levels were well below that considered to be proinflammatory in healthy CD rats (7), interactions between endotoxin and metal exposure notwithstanding (20,21). In light of the brownish discoloration of the 1986 and 1988 suspensions, the influence of as yet unidentified soluble organics (i.e., acid organics) cannot be discounted at this time.…”

Section: Discussionmentioning

confidence: 99%

Acute pulmonary toxicity of particulate matter filter extracts in rats: coherence with epidemiologic studies in Utah Valley residents.

Dye

Lehmann

McGee

et al. 2001

Environ Health Perspect

130

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Epidemiologic reports by C.A. Pope III et. al. demonstrated that in the Utah Valley, closure of an open-hearth steel mill over the winter of 1987 was associated with reductions in respiratory disease and related hospital admissions in valley residents. To better examine the relationship between plant-associated changes in ambient particulate matter (PM) and respiratory health effects, we obtained total suspended particulate filters originally collected near the steel mill during the winter of 1986 (before closure), 1987 (during closure), and 1988 (after plant reopening). PM subcomponents were water-extracted from these filters and Sprague-Dawley rats were intratracheally instilled with equivalent masses of extract. Data indicated that 24 hr later, rats exposed to 1986 or 1988 extracts developed significant pulmonary injury and neutrophilic inflammation. Additionally, 50% of rats exposed to 1986 or 1988 extracts had increased airway responsiveness to acetylcholine, compared to 17 and 25% of rats exposed to saline or the 1987 extract, respectively. By 96 hr, these effects were largely resolved except for increases in lung lavage fluid neutrophils and lymphocytes in 1986 extract-exposed rats. Analogous effects were observed with lung histologic assessment. Extract analysis using inductively coupled plasma-mass spectroscopy demonstrated in all three extracts nearly 70% of the mass appeared to be sodium-based salts derived from the glass filter matrix. Interestingly, relative to the 1987 extract, the 1986/1988 extracts contained more sulfate, cationic salts (i.e., calcium, potassium, magnesium), and certain metals (i.e., copper, zinc, iron, lead, strontium, arsenic, manganese, nickel). Although total metal content was (3/4) 1% of the extracts by mass, the greater quantity detected in the 1986 and 1988 extracts suggests metals may be important determinants of the pulmonary toxicity observed. In conclusion, the pulmonary effects induced by exposure of rats to water-based extracts of local ambient PM filters were in good accord with the cross-sectional epidemiologic reports of adverse respiratory health effects in Utah Valley residents.

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“…In vitro studies have also showed a variety of biologic responses to concentrated ambient particles (CAPs), including redox regulation and proliferation (Jimenez et al 2000;Timblin et al 1998), increased production of proinflammatory cytokines (Imrich et al 1999;Monn and Becker 1999), increased oxidation of redox-sensitive fluorescent dyes (Baeza-Squiban et al 1999;Goldsmith et al 1998;Prahalad et al 1999;Shukla et al 2000), and transcriptional activation of redox-sensitive genes (Shukla et al 2000). Although the in vitro findings support the hypothesis that ROSs are mediators of PM biologic effects, we have no direct evidence to date of a particle-driven increased production of oxidants in vivo.…”

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confidence: 99%

Rapid increases in the steady-state concentration of reactive oxygen species in the lungs and heart after particulate air pollution inhalation.

Gurgueira¹,

Lawrence²,

Coull³

et al. 2002

Environ Health Perspect

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497

301

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In vitro studies suggest that reactive oxygen species contribute to the cardiopulmonary toxicity of particulate air pollution. To evaluate the ability of particulate air pollution to promote oxidative stress and tissue damage in vivo, we studied a rat model of short-term exposure to concentrated ambient particles (CAPs). We exposed adult Sprague-Dawley rats to either CAPs aerosols (group 1; average CAPs mass concentration, 300 +/- 60 micro g/m3) or filtered air (sham controls) for periods of 1-5 hr. Rats breathing CAPs aerosols for 5 hr showed significant oxidative stress, determined as in situ chemiluminescence in the lung [group 1, 41 +/- 4; sham, 24 +/- 1 counts per second (cps)/cm2] and heart (group 1, 45 +/- 4; sham, 24 +/- 2 cps/cm2) but not liver (group 1, 10 +/- 3; sham, 13 +/- 3 cps/cm2). Increases in oxidant levels were also triggered by highly toxic residual oil fly ash particles (lung chemiluminescence, 90 +/- 10 cps/cm2; heart chemiluminescence, 50 +/- 3 cps/cm2) but not by particle-free air or by inert carbon black aerosols (control particles). Increases in chemiluminescence showed strong associations with the CAPs content of iron, manganese, copper, and zinc in the lung and with Fe, aluminum, silicon, and titanium in the heart. The oxidant stress imposed by 5-hr exposure to CAPs was associated with slight but significant increases in the lung and heart water content (approximately 5% in both tissues, p < 0.05) and with increased serum levels of lactate dehydrogenase (approximately 80%), indicating mild damage to both tissues. Strikingly, CAPs inhalation also led to tissue-specific increases in the activities of the antioxidant enzymes superoxide dismutase and catalase, suggesting that episodes of increased particulate air pollution not only have potential for oxidant injurious effects but may also trigger adaptive responses.

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Lipopolysaccharide Priming Amplifies Lung Macrophage Tumor Necrosis Factor Production in Response to Air Particles

Cited by 71 publications

References 25 publications

Effect of Concentrated Ambient Particles on Macrophage Phagocytosis and Killing of Streptococcus pneumoniae

Effect of Concentrated Ambient Particles on Macrophage Phagocytosis and Killing of Streptococcus pneumoniae

Acute pulmonary toxicity of particulate matter filter extracts in rats: coherence with epidemiologic studies in Utah Valley residents.

Rapid increases in the steady-state concentration of reactive oxygen species in the lungs and heart after particulate air pollution inhalation.

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