A new approach to evaluate toxicity of gases on mobile cells in culture

Laval-Gilly, Philippe; Falla, Jaı̈ro; Klestadt, Deborah; Henryon, Michel

doi:10.1016/s1056-8719(01)00114-9

Cited by 12 publications

(8 citation statements)

References 18 publications

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“…Velocity alterations of a motile human macrophage cell line have been used to evaluate toxicity of atmospheric pollutants [57]. Likewise, potential modifications of mussel hemocyte motility might constitute a valuable tool for marine ecotoxicology.…”

Section: Resultsmentioning

confidence: 99%

Characterisation of Mytilus edulis hemocyte subpopulations by single cell time-lapse motility imaging

Foll

Rioult

Boussa

et al. 2010

Fish & Shellfish Immunology

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Section: Resultsmentioning

confidence: 99%

Characterisation of Mytilus edulis hemocyte subpopulations by single cell time-lapse motility imaging

Foll

Rioult

Boussa

et al. 2010

Fish & Shellfish Immunology

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“…One hundred thousand THP-1 cells in 0.2 ml of RPMI 1640 medium were incubated with 25, 50, and 100 mg/ml PM at 37 8 …”

Section: Cytotoxicitymentioning

confidence: 99%

“…THP-1 cells have been well characterized and are a low-cost, highthroughput system relevant to the response of airway monocytes and macrophages (6). Along with epithelial cells, these are the initial cells that encounter inhaled particulates (7,8). Inhaled PM can activate airway macrophages via interaction with cell surface receptors and induction of wellknown signaling pathways, including extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) pathways (9)(10)(11).…”

mentioning

confidence: 99%

Inflammatory Response of Monocytes to Ambient Particles Varies by Highway Proximity

Muller

Berhane

et al. 2014

Am J Respir Cell Mol Biol

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Epidemiological studies have demonstrated associations of chronic respiratory disease with near-roadway pollutant exposure, effects that were independent of those of regional air pollutants. However, there has been limited study of the potential mechanisms for nearroadway effects. Therefore, we examined the in vitro effect of respirable particulate matter (PM) collected adjacent to a major Los Angeles freeway and at an urban background location. PM was collected on filters during two consecutive 15-day periods. Oxidative stress and inflammatory response (intracellular reactive oxygen species [ROS], IL-1b, IL-6, IL-8, and TNF-a) to PM aqueous extract was assessed in THP-1 cells, a model for evaluating monocyte/ macrophage lineage cell responses. The near-roadway PM induced statistically significantly higher levels of IL-6, IL-8, and TNF-a (P , 0.01) and a near significant increase in IL-1b (P = 0.06) but did not induce ROS activity (P = 0.17). The contrast between urban background and near-roadway PM-induced inflammatory cytokines was similar in magnitude to that corresponding to temporal differences between the two collection periods. PM-induced proinflammatory protein expression was attenuated by antioxidant pretreatment, and PM stimulation enhanced the activity of protein kinases, including extracellular signal-regulated kinase and c-Jun N-terminal kinase. Pretreatment of THP-1 cells with kinase inhibitors reduced PM-induced proinflammatory mediator expression. The proinflammatory response was also reduced by pretreatment with polymyxin B, suggesting a role for endotoxin. However, the patterns of PM-induced protein kinase response and the attenuation of inflammatory responses by antioxidant or polymyxin B pretreatment did not vary between near-roadway and urban background locations. We conclude that near-roadway PM produced greater inflammatory response than urban background PM, a finding consistent with emerging epidemiologic findings, but these differences were not explained by PM endotoxin content or by MAPK pathways. Nevertheless, THP-1 cells may be a model for the development of biologically relevant metrics of long-term spatial variation in exposure for study of chronic disease.

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“…Conversely, consistent with our findings, alveolar macrophages after in vitro exposure to O 3 did not produce increased amounts of proinflammatory cytokines (20), and exposure of human alveolar macrophages to nitric oxide (NO 2 ), a strong oxidant that may share mechanisms of cellular toxicity with O 3 , resulted in a significant decrease of LPS-stimulated IL-1␤, IL-6, TNF-␣, and transforming growth factor-␤ release (39). Moreover, recent studies where THP-1 cells were used as a model system for cells of monocyte/macrophage lineage showed that short-term exposure to O 3 decreased the chemotactic mobility of THP-1 cells in response to N-formyl-methionyl-leucyl-phenylalanine chemoattractant (46). Therefore, it seems that, in general, the in vitro O 3 effect on macrophages or macrophage-like cells appears to be a decrease in their functional capabilities.…”

Section: Discussionmentioning

confidence: 99%

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

Janic

Umstead

Phelps

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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, a major component of air pollution and a strong oxidizing agent, can lead to lung injury associated with edema, inflammation, and epithelial cell damage. The effects of O 3 on pulmonary immune cells have been studied in various in vivo and in vitro systems. We have shown previously that O 3 exposure of surfactant protein (SP)-A decreases its ability to modulate proinflammatory cytokine production by cells of monocyte/macrophage lineage (THP-1 cells). In this report, we exposed THP-1 cells and/or native SP-A obtained from bronchoalveolar lavage of patients with alveolar proteinosis to O 3 and studied cytokine production and NF-B signaling. The results showed 1) exposure of THP-1 cells to O 3 significantly decreased their ability to express TNF-␣ in response to SP-A; TNF-␣ production, under these conditions, was still significantly higher than basal (unstimulated) levels in filtered air-exposed THP-1 cells; 2) exposure of both THP-1 cells and SP-A to O 3 did not result in any significant differences in TNF-␣ expression compared with basal levels; 3) O 3 exposure of SP-A resulted in a decreased ability of SP-A to activate the NF-B pathway, as assessed by the lack of significant increase and decrease of the nuclear p65 subunit of NF-B and cytoplasmic I B␣, respectively; and 4) O 3 exposure of THP-1 cells resulted in a decrease in SP-A-mediated THP-1 cell responsiveness, which did not seem to be mediated via the classic NF-B pathway. These findings indicate that O 3 exposure may mediate its effect on macrophage function both directly and indirectly (via SP-A oxidation) and by involving different mechanisms.inflammation; tumor necrosis factor-␣; nuclear factor-B; I B␣; surfactant protein A OZONE (O 3 ) IS A MAJOR COMPONENT of photochemical air pollution. Approximately 113 million people live in areas with O 3 levels above the National Ambient Air Quality (NAAQ) standards for the daily exposure limit, noted as a maximum of 0.12 ppm for 1 h or 0.08 ppm cumulative for 8 consecutive hours (1). O 3 is a strong oxidizing agent that can be rapidly converted into a number of reactive oxygen species (ROS). O 3 exposure has been associated with impaired lung function (53) and with the majority of pathological changes localized in the lower airways. Due to its very low water solubility, O 3 cannot effectively penetrate through the thick epithelial lining fluid in the upper airways. However, the thinner lining in the lower airways allows O 3 to interact with various elements of the fluid and the underlying cells.O 3 and other oxidants exhibit their toxicity by reacting with cell proteins and lipids. This interaction often results in edema, inflammation, and epithelial cell damage causing lung injury and surfactant derangement (66, 67). Furthermore, both morphological (6, 7) and biochemical (26, 27) changes in surfactant are observed following O 3 exposure. An extensive body of work has been generated by various groups to support the hypothesis that O 3 -induced changes lead to a compromised immune response in the lung. However,...

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A new approach to evaluate toxicity of gases on mobile cells in culture

Cited by 12 publications

References 18 publications

Characterisation of Mytilus edulis hemocyte subpopulations by single cell time-lapse motility imaging

Characterisation of Mytilus edulis hemocyte subpopulations by single cell time-lapse motility imaging

Inflammatory Response of Monocytes to Ambient Particles Varies by Highway Proximity

Modulatory effects of ozone on THP-1 cells in response to SP-A stimulation

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