Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung

André, Eunice; Stoeger, Tobias; Takenaka, Shinji; Bahnweg, M; Ritter, Baerbel; Karg, Erwin; Lentner, Bernd; Reinhard, Claudia; Schulz, Holger; Wjst, Matthias

doi:10.1183/09031936.06.00071205

Cited by 60 publications

(59 citation statements)

References 45 publications

(50 reference statements)

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“…Carbon black are nanoparticles believed to be inert and harmless to the lungs, although they can induce early and moderate, albeit transient, inflammation [27]. There is a large database in the lung particle toxicology literature supporting significant toxic effects of a variety of nanoparticles [28].…”

Section: Discussionmentioning

confidence: 99%

Bleomycin induces pleural and subpleural fibrosis in the presence of carbon particles

Decologne¹,

Wettstein²,

Kolb³

et al. 2009

European Respiratory Journal

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The pathological changes in idiopathic pulmonary fibrosis (IPF) typically start in subpleural lung regions, a feature that is currently not explained. IPF, as well as bleomycininduced lung fibrosis, are more common in smokers. We hypothesised that carbon particles, which are major components of cigarette smoke that are transported to alveoli and pleural surface, might be involved in the development of subpleural fibrosis through interaction with pleural mesothelial cells.Carbon particles were administered to mice in combination with bleomycin through intratracheal and/or intrapleural injection and fibrosis was assessed using histomorphometry.Carbon administered to the chest cavity caused severe pleural fibrosis in the presence of bleomycin, whereas bleomycin alone had no fibrogenic effect. The pleural response was associated with progressive fibrosis in subpleural regions, similar to IPF in humans. Matrix accumulation within this area evolved through mesothelial-fibroblastoid transformation, where mesothelial cells acquire myofibroblast characteristics. In contrast, carbon did not exaggerate bleomycin-induced pulmonary fibrosis after combined intratracheal administration.This represents a novel approach to induce a robust experimental model of pleural fibrosis. It also suggests that carbon particles might be involved as a cofactor in the initiation and/or progression of (subpleural) pulmonary and pleural fibrosis. Mesothelial cells appear to be critical contributors to this fibrotic process.

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Section: Discussionmentioning

confidence: 99%

Bleomycin induces pleural and subpleural fibrosis in the presence of carbon particles

Decologne¹,

Wettstein²,

Kolb³

et al. 2009

European Respiratory Journal

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“…OPN is generally classified as a pro-inflammatory cytokine [5,13,24,25]. However, emerging evidence supports an antiinflammatory role of OPN in allergic disease.…”

Section: ) T-lymphocytes (Fig 4q-t) and Mast Cells (mentioning

confidence: 99%

Osteopontin expression and relation to disease severity in human asthma

Samitas¹,

Ζervas²,

Vittorakis³

et al. 2010

European Respiratory Journal

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Recent studies have associated osteopontin (OPN) with allergic inflammation; however, its role in human asthma remains unclear. The aim of this study was to measure OPN levels in the serum, bronchoalveolar lavage fluid (BALF) and bronchial tissue of healthy controls and asthmatics, identify cellular sources of OPN and examine possible correlations between OPN expression, disease severity and airway remodelling.Serum samples were obtained from 35 mild-to-moderate asthmatics, 19 severe asthmatics and 17 healthy controls in the steady state and in cases of exacerbation. Of these subjects, 29 asthmatics and nine controls underwent bronchoscopy with endobronchial biopsy and BALF collection. OPN expression was determined by ELISA and immunohistochemistry/immunofluorescence. Reticular basement membrane thickness and goblet cell hyperplasia were also determined.Serum and BALF OPN levels were significantly increased in all asthmatics in the steady state, whereas serum levels decreased during exacerbations. OPN was upregulated in the bronchial tissue of all patients, and expressed by epithelial, airway and vascular smooth muscle cells, myofibroblasts, T-lymphocytes and mast cells. OPN expression correlated with reticular basement membrane thickness and was more prominent in subepithelial inflammatory cells in severe compared to mild-to-moderate asthma.OPN expression is upregulated in human asthma and associated with remodelling changes, and its subepithelial expression correlates with disease severity.

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“…These primary particles typically range in mean diameter from 10 to 50 nm, contain 1 to 20% organic carbon, and have surface areas varying from 40 to 800 m 2 /g. In this context, recent studies exposing mice for 24 h to ultrafine carbon particles affirmed the pro-inflammatory as well as allergy adjuvant properties of these pollutants (Alessandrini et al, 2006;Andre et al, 2006). Proinflammatory effects generally increase with particle surface area.…”

Section: Health Impacts Of Combustion-generated Fine and Ultrafine Pamentioning

confidence: 91%

Report: Combustion Byproducts and Their Health Effects: Summary of the 10th International Congress

Dellinger

D’Alessio

D’Anna

et al. 2008

Environmental Engineering Science

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The 10th International Congress on Combustion Byproducts and their Health Effects was held in Ischia, Italy, from June 17-20, 2007. It is sponsored by the US NIEHS, NSF, Coalition for Responsible Waste Incineration (CRWI), and Electric Power Research Institute (EPRI). The congress focused on: the origin, characterization, and health impacts of combustion-generated fine and ultrafine particles; emissions of mercury and dioxins, and the development/application of novel analytical/diagnostic tools. The consensus of the discussion was that particle-associated organics, metals, and persistent free radicals (PFRs) produced by combustion sources are the likely source of the observed health impacts of airborne PM rather than simple physical irritation of the particles. Ultrafine particle-induced oxidative stress is a likely progenitor of the observed health impacts, but important biological and chemical details and possible catalytic cycles remain unresolved. Other key conclusions were: (1) In urban settings, 70% of airborne fine particles are a result of combustion emissions and 50% are due to primary emissions from combustion sources, (2) In addition to soot, combustion produces one, possibly two, classes of nanoparticles with mean diameters of ϳ10 nm and ϳ1 nm. (3) The most common metrics used to describe particle toxicity, viz. surface area, sulfate concentration, total carbon, and organic carbon, cannot fully explain observed health impacts, (4) Metals contained in combustion-generated ultrafine and fine particles mediate formation of toxic air pollutants such as PCDD/F and PFRs. (5) The combination of metal-containing nanoparticles, organic carbon compounds, and PFRs can lead to a cycle generating oxidative stress in exposed organisms.

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Inhalation of ultrafine carbon particles triggers biphasic pro-inflammatory response in the mouse lung

Cited by 60 publications

References 45 publications

Bleomycin induces pleural and subpleural fibrosis in the presence of carbon particles

Bleomycin induces pleural and subpleural fibrosis in the presence of carbon particles

Osteopontin expression and relation to disease severity in human asthma

Report: Combustion Byproducts and Their Health Effects: Summary of the 10th International Congress

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