Effects of Diesel Exhaust Particles on the Release of Interleukin-1 and Tumor Necrosis Factor-Alpha from Rat Alveolar Macrophages

Yang, Huimin; Jane, Y. C.; Castranova, Vincent; Joseph, K. H.

doi:10.3109/01902149709087372

Cited by 92 publications

(81 citation statements)

References 38 publications

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“…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: 82%

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: 82%

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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“…Increases in IL-8 secretion by alveolar macrophages have also been noted after in vitro exposure to a dichloromethane extract of (standard) DEP; however, the intact DEP themselves (as well as carbon black) had no effect (Mundandhara et al, 2006). When cells were exposed to the particles or organic extract prior to LPS stimulation, levels of IL-1β, IL-8, and TNFα secretion were all seen to be decreased (Yang et al, 1997;Saito et al, 2002;Mundandhara et al, 2006). Similarly, LPS-induced stimulation of IL-10 formation was reduced by exposure to DEP (Inoue et al, 2007).…”

Section: Discussionmentioning

confidence: 92%

“…Indeed, the production of IL-1β by alveolar macrophages was increased when these types of cells were exposed to DEP or the extracts. Interestingly, this effect was not observed for tumor necrosis factor-α (TNFα) secretion (Yang et al, 1997;Saito et al, 2002). Increases in IL-8 secretion by alveolar macrophages have also been noted after in vitro exposure to a dichloromethane extract of (standard) DEP; however, the intact DEP themselves (as well as carbon black) had no effect (Mundandhara et al, 2006).…”

Section: Discussionmentioning

confidence: 95%

Effect of Polycyclic Aromatic Hydrocarbons and Carbon Black Particles on Pro-Inflammatory Cytokine Secretion: Impact of PAH Coating Onto Particles

Goulaouic¹,

Foucaud²,

Bennasroune³

et al. 2008

Journal of Immunotoxicology

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It has been suggested that the organic fraction of particulate matter in air pollution has a major role in the toxicity of this pollutant, notably via its effects on inflammation. The major organic compounds adsorbed onto these particles are polycyclic aromatic hydrocarbons (PAH), among which benzo In general, coating the CB with PAH did not modify the effect of the CB alone; the exception was that LPS-induced IL-1β secretion was reduced. In contrast, ultrafine CB (14 nm diameter: ufCB) caused a decrease in cytokine secretion; this effect was modified by PAH coating. For example, PAH coating on ufCB amplified the inhibitory effect of ufCB against IL-1β secretion but did not modify IL-8 formation. Moreover, PAH coating on ufCB tended to minimize the effect of LPS stimulation; this included (i) inhibition of the decrease in IL-12 secretion induced by uncoated ufCB and (ii) stimulation of IL-10 production. It was concluded that adsorption of PAH onto these particles could decrease their bioavailability and so their abilities to affect cell cytokine production. The results also showed that when PAH were adsorbed onto the fine particles, any observed increases in cytokine secretion consistently appeared to be due to the particles themselves. In contrast, while ufCB alone almost uniformly led to decreases in cytokine formation by the

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“…Several cell types are involved in allergen sensitization and asthma pathogenesis, including antigenpresenting cells (APC), T-helper 2 (Th2) lymphocytes, IgE-secreting plasma cells, mast cells, eosinophils, neutrophils, mucus-secreting goblet cells, smooth muscle and endothelial cells. DEP can directly impact a number of the cells that play a role in the afferent or efferent immune response [25,[81][82][83][84][85][86][87]. Traditional adjuvants exert their effects on the afferent or early phase of the immune response, which implies possible effects on antigen presenting cells (APC) [88,89].…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

820

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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Effects of Diesel Exhaust Particles on the Release of Interleukin-1 and Tumor Necrosis Factor-Alpha from Rat Alveolar Macrophages

Cited by 92 publications

References 38 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

Effect of Polycyclic Aromatic Hydrocarbons and Carbon Black Particles on Pro-Inflammatory Cytokine Secretion: Impact of PAH Coating Onto Particles

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

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