Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells

Boland, Sonja; Bonvallot, Véronique; Fournier, Thierry; Baeza‐Squiban, Armelle; Aubier, Michel; Marano, Francelyne

doi:10.1152/ajplung.2000.278.1.l25

Cited by 92 publications

(80 citation statements)

References 41 publications

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“…This observation is in agreement with previous studies that have shown that peroxynitrite may interfere with surfactant activity (20). Furthermore, we have previously shown that DEPs-induced effects in human airway epithelial cells are partly mediated through the production of reactive oxygen species (9). We hypothesized in the present study that DEPs-induced increase in PC might be mediated by reactive oxygen species of the NO pathway such as peroxynitrite.…”

Section: Discussionsupporting

confidence: 93%

“…This suggests that PAHs, which are adsorbed on DEPs but not on carbon black particles, are responsible for the effects of DEPs. This observation is in agreement with previous reports, which have emphasized the specific PAHs' role in the DEPs activity in bronchial cells (9), macrophages (47), and ATII cells (24). This role of PAHs is corroborated by the observation that the catalysts that reduce the adsorbed organic compounds also reduce the DEPs-induced increase in cytokine secretion by bronchial cells (8).…”

Section: Discussionsupporting

confidence: 93%

“…DEPs treatment was performed as described previously (8,9,24). Stock solutions of particles were prepared by suspension in complete culture medium and sonicated three times for 60 s each at maximal power (8 kilocycles).…”

Section: Methodsmentioning

confidence: 99%

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Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

Juvin

Fournier

Grandsaigne

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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(DEPs) have been shown in vivo as well as in vitro to affect the respiratory function and in particular the immune response to infection and allergens. In the current study, we investigated the effect of DEPs on the production of phosphatidylcholine (PC), a major constituent of surfactant, by rat alveolar type II (ATII) primary cells in vitro. Our results demonstrate that incubation of ATII cells with DEPs lead to a time-and dose-dependent increase in labeled PC release. This effect was mimicked by nitric oxide (NO) donors and cGMP and was abolished by inhibitors of NO synthase (NOS). In addition, a NOS inhibitor inhibits by itself the basal secretion of PC. We next examined the effects of DEPs on NOS gene expression and showed that DEPs increase NO production and upregulate both protein content and mRNA levels of the inducible NOS (NOS II). Together our data demonstrate that DEPs alter the production of surfactant by ATII cells through a NO-dependent signaling pathway. surfactant; nitric oxide MAJOR AIR POLLUTANTS include nitrogen dioxide, ozone sulfur dioxide, and breathable particulate matter of diameter inferior to 10 m (PM10) (12,27). Several studies have particularly implicated diesel exhaust particles (DEPs), a major component of PM10, as contributing to the incidence and severity of respiratory diseases during air pollution episodes. Epidemiological studies have reported that high levels of DEPs are associated with worsening peak flow, inhaler usage, respiratory symptoms, and emergency room visits in asthmatic children and adults (34,38). In a cohort of over half a million adults residing in 151 metropolitan areas in the United States between 1982 and 1989, fine particulate pollution was associated with cardiopulmonary and lung cancer mortality (33). Similarly, a recent work has demonstrated an increased mortality and morbidity rate after DEPs exposure (26).Airway epithelial cells are primary targets for air pollutants. Several studies have investigated the effect of DEPs on nasal, bronchial, and alveolar epithelial cells. In nasal cells, DEPs enhance cytokine expression synergistically with allergens and increase local eosinophil adhesion (15,16,44). In bronchial epithelial cells, DEPs are internalized, inducing airway inflammation (4,8,41) and hyperresponsiveness (43).DEPs also interact with alveolar type II (ATII) cells since their small size (0.1-1 m) allows them to reach the alveolar space (32,46,48). ATII cells regulate the intra-alveolar homeostasis through four main functions. They secrete a large panel of cytokines (5, 13, 31, 39), serve as progenitors to the alveolar type I cells (18), actively transport ions (23), and synthesize and secrete surfactant. We previously demonstrated that one of these functions (i.e., cytokine secretion) was altered by DEPs (24). Synthesis and secretion of surfactant are other very important functions of ATII cells. Surfactant prevents alveolar collapse at end expiration by lowering surface tension at the air/extracellular lining interface in the alveoli and dist...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 93%

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Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

Juvin

Fournier

Grandsaigne

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…For example, activation of NF-B by DEP has been shown to regulate IL-8 and granulocyte-macrophage colony-stimulating factor expression in bronchial epithelial cells (9,57). Similarly, activation of Nrf2 transcription factor, which plays a critical role in the regulation of antioxidant enzyme expression (38), has been correlated with the induction of phase II detoxifying enzymes in bronchial epithelial cells in response to DEP (6).…”

mentioning

confidence: 99%

DEP-inducedfra-1expression correlates with a distinct activation of AP-1-dependent gene transcription in the lung

Zhang¹,

Kleeberger²,

Reddy³

2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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. DEP-induced fra-1 expression correlates with a distinct activation of AP-1-dependent gene transcription in the lung. Am J Physiol Lung Cell Mol Physiol 286: L427-L436, 2004. First published October 17, 2003 10.1152/ajplung.00221.2003.-Recent studies indicate a potential role for Fra-1, a heterodimeric partner of activator protein (AP)-1, in toxicant-induced epithelial injury, repair, and cellular transformation. Here we have investigated the effects of diesel exhaust particles (DEP) on fra-1 expression in C10 cells, a murine lung epithelial cell line. DEP markedly upregulated fra-1, but not fra-2, expression. The increase in fra-1 mRNA expression correlated well with its proteinand DNA-binding activity. DNA-binding assays also revealed a predominant presence of Jun-B and Jun-D in the AP-1 complex. Interestingly, DEP did not alter Jun-B and Jun-D protein levels. Transcriptional analysis revealed that fra-1 induction is regulated in part at the transcriptional level. The Ϫ379 to ϩ32 bp 5Ј-flanking region mediated this induction. Furthermore, inhibitors of ERK1/2, JNK1, and p38 mitogen-activated protein kinases (MAPKs) significantly suppressed DEP-stimulated fra-1 transcription, suggesting their involvement in the induction process. Consistent with this finding, DEP stimulated phosphorylation of ERK1/2, JNK1, and p38 MAPKs with a distinct activation pattern. Overexpression of Fra-1 downregulated c-Jun and Nrf2 enhanced AP-1-and ARE-mediated reporter gene expression, respectively. In contrast, Fra-1 had the opposite effect on matrix metalloproteinase (MMP)-9 promoter activity. In particular, it bound to the functional AP-1 site of the MMP-9 promoter after DEP stimulation. Consistent with this result, DEP also markedly upregulated MMP-9 promoter activity. Collectively, these findings suggest that fra-1 induction by DEP may play a role in selectively regulating gene expression involved in alveolar epithelial cell injury and repair. activator protein-1; mitogen-activated protein kinase; diesel exhaust particles; matrix metalloproteinase-9; fos-related antigen-1

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“…Adsorbed organic compounds have been implicated in many of the systemic and molecular responses of respiratory system cells exposed to diesel exhaust particles (3)(4)(5)(6). Studies with residual oil fly ash (ROFA) particles have demonstrated a role for particleassociated metals in inducing inflammatory responses in respiratory cells (7,8).…”

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confidence: 99%

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

Catallo

Kennedy

Henk

et al. 2001

Environ Health Perspect

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Adverse health effects of airborne toxicants, especially small respirable particles and their associated adsorbed chemicals, are of growing concern to health professionals, governmental agencies, and the general public. Areas rich in petrochemical processing facilities (e.g., eastern Texas and southern California) chronically have poor air quality. Atmospheric releases of products of incomplete combustion (e.g., soot) from these facilities are not subject to rigorous regulatory enforcement. Although soot can include respirable particles and carcinogens, the toxicologic and epidemiologic consequences of exposure to environmentally relevant complex soots have not been well investigated. Here we continue our physico-chemical analysis of butadiene soot and report effects of exposure to this soot on putative targets, normal human bronchial epithelial (NHBE) cells. We examined organic extracts of butadiene soot by gas chromatography-mass spectrometry (GC-MS), probe distillation MS, and liquid chromatography (LC)-MS-MS. Hundreds of aromatic hydrocarbons and polycyclic aromatic hydrocarbons with molecular mass as high as 1,000 atomic mass units were detected, including known and suspected human carcinogens (e.g., benzo(a)pyrene). Butadiene soot particles also had strong, solid-state free-radical character in electron spin resonance analysis. Spin-trapping studies indicated that fresh butadiene soot in a buffered aqueous solution containing dimethylsulfoxide (DMSO) oxidized the DMSO, leading to CH(3)* radical formation. Butadiene soot DMSO extract (BSDE)-exposed NHBE cells displayed extranuclear fluorescence within 4 hr of exposure. BSDE was cytotoxic to > 20% of the cells at 72 hr. Morphologic alterations, including cell swelling and membrane blebbing, were apparent within 24 hr of exposure. These alterations are characteristic of oncosis, an ischemia-induced form of cell death. BSDE treatment also produced significant genotoxicity, as indicated by binucleated cell formation. The combination of moderate cytotoxicity and genotoxicity, as occurred here, can be pro-carcinogenic.

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Mechanisms of GM-CSF increase by diesel exhaust particles in human airway epithelial cells

Cited by 92 publications

References 41 publications

Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

Diesel particles increase phosphatidylcholine release through a NO pathway in alveolar type II cells

DEP-inducedfra-1expression correlates with a distinct activation of AP-1-dependent gene transcription in the lung

Combustion products of 1,3-butadiene are cytotoxic and genotoxic to human bronchial epithelial cells.

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