Characterization of the A549 Cell Line as a Type II Pulmonary Epithelial Cell Model for Drug Metabolism

Foster, Kimberly A.; Oster, Christine G.; Mayer, Mary M.; Avery, Michael L.; Audus, Kenneth L.

doi:10.1006/excr.1998.4172

Cited by 566 publications

(367 citation statements)

References 20 publications

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“…Recent study has revealed that the human alveolar type 2 cells internalized nanoparticles less efficiently than the human alveolar type 1 cells [47]. Since A549 cells are representatives of the alveolar epithelial type 2-like cells [15] it is reasonable to suppose that this fact might underlie less efficient MNPs entrance into the human lung tumor cells compared with the human lung diploid cells. Moreover, Ge et al [44] have reported recently that positively charged magnetite nanoparticles are more efficiently taken up into KB cells due to electrostatic attraction to the negatively charged cell membrane than negatively charged particles.…”

Section: Discussionmentioning

confidence: 99%

“…To overcome this gap in our knowledge, two human lung cell lines, A549 and HEL 12469 were used to investigate the internalization and cytotoxicity of MNPs with different surface modifications commonly used in biomedical research. The human lung adenocarcinoma epithelial cell line A549 is a valuable in vitro model of human alveolar epithelial type 2 cells [15]. This cell line has been widely utilized in the studies of alveolar epithelium function [16] and drug delivery via the lung route [17].…”

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confidence: 99%

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The intensity of internalization and cytotoxicity of superparamagnetic iron oxide nanoparticles with different surface modifications in human tumor and diploid lung cells

Mesárošová

Cĭampor²,

Závišová³

et al. 2012

neo

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The human lung adenocarcinoma epithelial (A549) cells and the human embryo lung (HEL 12469) cells were used to investigate the uptake and cytotoxicity of magnetite nanoparticles (MNPs) with different chemically modified surfaces. MNPs uptake was an energy-dependent process substantially affected by the serum concentration in the culture medium. Internalized MNPs localized in vesicle-bound aggregates were observed in the cytoplasm, none in the nucleus or in mitochondria. All MNPs induced a dose-and time-dependent increase in cytotoxicity in both human lung cell lines. The cytotoxicity of MNPs increased proportionally with the particle size. Since the cytotoxicity of MNPs was nearly identical when the doses were equalized based on particle surface area, we suppose that the particle surface area rather than the surface modifications per se underlay the cytotoxicity of MNPs. In general, higher internalized amount of MNPs was found in HEL 12469 cells compared with A549 cells. Accordingly, the viability of the human embryo lung cells was reduced more substantially than that of the adenocarcinoma lung cells. The weak MNPs uptake into A549 cells might be of biomedical relevance in cases where MNPs should be used as nanocarriers for targeted drug delivery in tumor tissue derived from alveolar epithelial cells.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

The intensity of internalization and cytotoxicity of superparamagnetic iron oxide nanoparticles with different surface modifications in human tumor and diploid lung cells

Mesárošová

Cĭampor²,

Závišová³

et al. 2012

neo

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“…These cells display properties of type II alveolar epithelial cells and also form polarized barriers when grown on permeable filters (10,(17)(18)(19). A549 cells were maintained in Ham's F-12K medium with 2 mM L-glutamine 1.5 g/L NaHCO 3 , 10% FBS, and 100 U of penicillin/streptomycin.…”

Section: Growth and Maintenance Of Epithelial Cellsmentioning

confidence: 99%

Polymorphonuclear Cell Transmigration Induced by Pseudomonas aeruginosa Requires the Eicosanoid Hepoxilin A3

Hurley

Siccardi

Mrsny

et al. 2004

The Journal of Immunology

161

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Lung inflammation resulting from bacterial infection of the respiratory mucosal surface in diseases such as cystic fibrosis and pneumonia contributes significantly to the pathology. A major consequence of the inflammatory response is the recruitment and accumulation of polymorphonuclear cells (PMNs) at the infection site. It is currently unclear what bacterial factors trigger this response and exactly how PMNs are directed across the epithelial barrier to the airway lumen. An in vitro model consisting of human PMNs and alveolar epithelial cells (A549) grown on inverted Transwell filters was used to determine whether bacteria are capable of inducing PMN migration across these epithelial barriers. A variety of lung pathogenic bacteria, including Klebsiella pneumoniae, Escherichia coli, and Pseudomonas aeruginosa are indeed capable of inducing PMN migration across A549 monolayers. This phenomenon is not mediated by LPS, but requires live bacteria infecting the apical surface. Bacterial interaction with the apical surface of A549 monolayers results in activation of epithelial responses, including the phosphorylation of ERK1/2 and secretion of the PMN chemokine IL-8. However, secretion of IL-8 in response to bacterial infection is neither necessary nor sufficient to mediate PMN transepithelial migration. Instead, PMN transepithelial migration is mediated by the eicosanoid hepoxilin A3, which is a PMN chemoattractant secreted by A549 cells in response to bacterial infection in a protein kinase C-dependent manner. These data suggest that bacterial-induced hepoxilin A3 secretion may represent a previously unrecognized inflammatory mechanism occurring within the lung epithelium during bacterial infections.

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“…Cells are grown at confluence in DMEM + 10%FCS, 2 mM L-glutamine, 50 IU/ml penicillin, 50 µg/ml streptomycin, at 5%CO 2 − 95% air atmosphere. Routine subcultures (passages 89-92) were done at onetwentieth split ratios by incubation with 0.025 g/100 ml trypsin −0.02 g/100 ml EDTA in calcium-and magnesiumfree PBS for 10 min at 37 • C. Moreover, A549 cells have been shown to exhibit metabolic and transport properties consistent with type II pulmonary epithelial cells in vivo, and importantly, they do not functionally differentiate in culture to a cell type capable of liquid-phase endocytosis like type I alveolar epithelial cells (Foster et al 1998). A more recent study has shown that A549 cells still have the ability to form adherent and tight junctions when grown to confluence (Kawkitinarong et al 2004).…”

Section: Cell Culture Pfc Exposure and Cell Viabilitymentioning

confidence: 99%

Perfluorocarbon induces alveolar epithelial cell response through structural and mechanical remodeling

Dias¹,

Planus²,

Angely³

et al. 2018

Biomech Model Mechanobiol

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During total liquid ventilation, lung cells are exposed to perfluorocarbon (PFC) whose chemophysical properties highly differ from standard aqueous cell feeding medium (DMEM). We herein perform a systematic study of structural and mechanical properties of A549 alveolar epithelial cells in order to characterize their response to PFC exposure, using DMEM as control condition. Changes in F-actin structure, focal adhesion density and glycocalyx distribution are evaluated by confocal fluorescent microscopy. Changes in cell mechanics and adhesion are measured by multiscale magnetic twisting cytometry (MTC). Two different microrheological models (single Voigt and power law) are used to analyze the cell mechanics characterized by cytoskeleton (CSK) stiffness and characteristic relaxation times. Cell-matrix adhesion is analyzed using a stochastic multibond deadhesion model taking into account the non-reversible character of the cell response, allowing us to quantify the adhesion weakness and the number of associated bonds. The roles of F-actin structure and glycocalyx layer are evaluated by depolymerizing F-actin and degrading glycocalyx, respectively. Results show that PFC exposure consistently induces F-actin remodeling, CSK softening and adhesion weakening. These results demonstrate that PFC triggers an alveolar epithelial cell response herein evidenced by a decay in intracellular CSK tension, an adhesion weakening and a glycocalyx layer redistribution. These PFC-induced cell adjustments are consistent with the hypothesis that cells respond to a decrease in adhesion energy at cell surface. This adhesion energy can be even further reduced in the presence of surfactant adsorbed at the cell surface.

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Characterization of the A549 Cell Line as a Type II Pulmonary Epithelial Cell Model for Drug Metabolism

Cited by 566 publications

References 20 publications

The intensity of internalization and cytotoxicity of superparamagnetic iron oxide nanoparticles with different surface modifications in human tumor and diploid lung cells

The intensity of internalization and cytotoxicity of superparamagnetic iron oxide nanoparticles with different surface modifications in human tumor and diploid lung cells

Polymorphonuclear Cell Transmigration Induced by Pseudomonas aeruginosa Requires the Eicosanoid Hepoxilin A3

Perfluorocarbon induces alveolar epithelial cell response through structural and mechanical remodeling

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