Minerals, fibrosis, and the lung.

Heppleston, A. G.

doi:10.1289/ehp.94-1567953

Cited by 10 publications

(4 citation statements)

References 236 publications

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“…cytokines) and toxic ROIs. Evidence indicates that particle-induced pathomechanisms involve chemotactic, proinflammatory, or fibrogenic cytokines [14,15]. In this study we attempt to determine the role of IL-8 in the migration rates of granulocytes into the lung interstitium [23,34].…”

Section: Discussionmentioning

confidence: 99%

“…Indoor air pollutants such as soot particles from indoor fireplaces and asbestos fibers used in insulating materials induce airway and lung parenchymal injury [8,14,21,25]. In this study we investigated the soot particles FR 101 and Printex 90 (P 90), titanium dioxide (TiO 2 ), and the fiber Chrysotile B to determine their effect on inflammatory mechanisms in the lung.…”

Section: Introductionmentioning

confidence: 99%

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Indoor Air Pollutants Stimulate Interleukin-8-Specific mRNA Expression and Protein Secretion of Alveolar Macrophages

Drumm

Schindler

Buhl

et al. 1999

Lung

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Indoor air pollutants may cause inflammatory changes of the airways and adjacent pulmonary tissue. After phagocytosis of inhaled particles alveolar macrophages (AM) release chemotactic mediators capable of attracting inflammatory cells into the lung tissue. To evaluate these mechanisms further peripheral blood mononuclear cells (PBMNC) and human AM (freshly recovered from the lower respiratory tract) were exposed to the indoor particles Soot FR 101 and Printex 90, the asbestos fiber Chrysotile B, and titanium dioxide (TiO2) at concentrations of 10 or 50 microg/10(6) cells for up to 8 h. The migration of granulocytes into the conditioned supernatants of AM and PBMNC was quantified by chemotaxis assay in a Boyden chamber. Granulocyte migration increased by 42.3 +/- 25.8% (Chrysotile B), 64. 6 +/- 18.3% (FR 101), 74.2 +/- 16.5% (P 90), and 86.7 +/- 25.6% (TiO2) in AM-conditioned supernatants (p < 0.05). Qualitative, Interleukin (IL)-8 specific reverse transcriptase-polymerase chain reaction was performed after exposure of AM or PBMNC to Chrysotile B, FR 101, P 90, and TiO2 at concentrations of 10 and 50 microg/10(6) cells for 90 min. Each of the tested particles caused an increase in IL-8-specific mRNA expression of AM or PBMNC after particle exposure compared with the unexposed control. To find out if IL-8, the most powerful granulocyte chemokine, is involved, supernatants were preincubated with anti-IL-8. Granulocyte migration decreased by up to 35 +/- 15% (50 ng/ml anti-IL-8) and 41.5 +/- 16% (100 ng/ml anti-IL-8) (p < 0.0625) in AM-conditioned supernatants. Pretreatment of the granulocytes with human IL-8 decreased by up to 59 +/- 18% (10 ng/ml) (p < 0.0625) in AM-conditioned supernatants. Similar reaction patterns were observed using anti-IL-8-pretreated supernatants of particle-exposed PBMNC. In conclusion, indoor air pollutants may promote inflammatory changes in the lung via IL-8 release by alveolar macrophages.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Indoor Air Pollutants Stimulate Interleukin-8-Specific mRNA Expression and Protein Secretion of Alveolar Macrophages

Drumm

Schindler

Buhl

et al. 1999

Lung

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“…Peroxidation of cell membrane-associated phospholipids has been implicated in the pathogenesis of various disorders including neurodegenerative diseases, acute lung injury, and lung fibrosis among others (1, 4, 15, 25, 34). Lipid hydroperoxides are the primary products of lipid peroxidation and are the source of highly toxic secondary products such as aldehydes (4).…”

Section: Introductionmentioning

confidence: 99%

Critical role of peroxiredoxin 6 in the repair of peroxidized cell membranes following oxidative stress

Benipal

Zhou

et al. 2015

Free Radical Biology and Medicine

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Phospholipids are a major structural component of all cell membranes; their peroxidation represents a severe threat to cellular integrity and their repair is important to prevent cell death. Peroxiredoxin 6 (Prdx6), a protein with both GSH peroxidase and phospholipase A2 (PLA2) activities, plays a critical role in antioxidant defense of the lung and other organs. We investigated the role of Prdx6 in the repair of peroxidized cell membranes in pulmonary microvascular endothelial cells (PMVEC) and isolated mouse lungs treated with tert-butylhydroperoxide and lungs from mice exposed to hyperoxia (100% O2). Lipid peroxidation was evaluated by measurement of thiobarbituric acid reactive substances, oxidation of diphenyl-1-pyrenylphosphine, or the ferrous xylenol orange assay. The exposure dose was varied to give a similar degree of lipid peroxidation at the end of exposure in the different models. Values for lipid peroxidation returned to control levels within 2 h after oxidant removal in wild type PMVEC and perfused lungs but were unchanged in Pxdx6 null preparations. An intermediate degree of repair was observed with PMVEC and lungs that express only C47S or D140A mutant Prdx6; the former mutant does not have peroxidase activity while the latter loses its PLA2 activity. Prdx6 null mice showed markedly delayed recovery from lipid peroxidation during a 20 h observation following exposure to hyperoxia. Thus, Prdx6 plays a critical role in the repair of peroxidized phospholipids in cell membranes and the recovery of lung cells from peroxidative stress; the peroxidase and PLA2 activities each contribute to the recovery process.

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“…Soot particles from indoor fireplaces and Chrysotile B fibers (e.g., from insulating materials of buildings) represent indoor air pollutants that are able to induce airway and lung parenchymal injury [13,17,25,27].…”

Section: Introductionmentioning

confidence: 99%

Production of Reactive Oxygen Intermediates by Human Macrophages Exposed to Soot Particles and Asbestos Fibers and Increase in NF-kappa B p50/p105 mRNA

Oettinger¹,

Drumm²,

Knorst³

et al. 1999

Lung

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Alveolar macrophages (AM) play a decisive role in the immunologic defense system of the lung and in inflammatory pulmonary pathomechanisms. AM and blood monocytes (BM) were exposed to chrysotile B, soot FR 101, and Printex 90 (P 90). We evaluated the reactive oxygen intermediate (ROI) release of AM and BM after particle exposure. ROI release was measured by chemiluminescence. Thirty-minute exposure caused a significant (up to 2.5-fold) increase in ROI release of AM (100 micrograms/10(6) cells) compared with control experiments (p < 0.01). Identical exposure conditions for BM resulted in a similar reaction pattern (maximum 2.2-fold increase in ROI release; p < 0.05). After a 90-min particle exposure at concentrations of 10 and 100 micrograms/10(6) cells, we investigated the steady-state level of p50/p105 mRNA encoding for the precursor protein of the p50 subunit of nuclear factor kappa B (NF-kappa B) by semiquantitative reverse transcription-polymerase chain reaction. One hundred micrograms Chrysotile B, FR 101, or P 90 induced a significant maximum 4.0-fold up-regulation of NF-kappa B gene expression in AM and a 3.3-fold up-regulation in BM (p < 0.05). The addition of superoxide dismutase (200 U/ml) to particle- and fiber-exposed macrophages resulted in inhibition of ROI release and a decrease in NF-kappa B mRNA expression (70%). NF-kappa B is an important transcription factor involved in the regulation of numerous genes (e.g., for inflammatory cytokines, and cytokine receptors). These cytokines are supposed to be involved in inflammatory pathomechanisms in bronchial epithelial cells, which result, for example, in chronic obstructive pulmonary disease. Our results suggest that particle-induced ROI release is associated with an increase in NF-kappa B (p50/p105) mRNA steady-state level.

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Minerals, fibrosis, and the lung.

Cited by 10 publications

References 236 publications

Indoor Air Pollutants Stimulate Interleukin-8-Specific mRNA Expression and Protein Secretion of Alveolar Macrophages

Indoor Air Pollutants Stimulate Interleukin-8-Specific mRNA Expression and Protein Secretion of Alveolar Macrophages

Critical role of peroxiredoxin 6 in the repair of peroxidized cell membranes following oxidative stress

Production of Reactive Oxygen Intermediates by Human Macrophages Exposed to Soot Particles and Asbestos Fibers and Increase in NF-kappa B p50/p105 mRNA

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