scholarly journals The antioxidant resveratrol down-regulates inflammation in an in-vitro model of Pseudomonas aeruginosa infection of lung epithelial cells

2013 ◽  
Vol 91 (3) ◽  
pp. 248-255 ◽  
Author(s):  
Ashley M. Cerqueira ◽  
Neelam Khaper ◽  
Simon J. Lees ◽  
Marina Ulanova
Keyword(s):  
Oxidative Stress ◽  
Pseudomonas Aeruginosa ◽  
Inflammatory Response ◽  
A549 Cells ◽  
Surface Expression ◽  
Lung Epithelial Cells ◽  
Cell Surface Expression ◽  
Intercellular Adhesion Molecule ◽  
Ros Generation ◽  
Lung Epithelial

Pseudomonas aeruginosa is a Gram-negative opportunistic pathogen that can cause severe pulmonary infection in immunocompromized individuals. During the infectious process, P. aeruginosa provokes a potent inflammatory response and induces the release of reactive oxygen species (ROS). Cells undergo oxidative stress when cellular antioxidants are unable to effectively scavenge and detoxify ROS, resulting in lung damage. Resveratrol (3,5,4′-trihydroxystilbene) is a natural polyphenolic compound with recognized antioxidant effects. We hypothesized that owing to its antioxidant activities, resveratrol can attenuate an inflammatory response in P. aeruginosa-infected cells. Lung epithelial A549 cells were pre-treated with 100 μmol/L of resveratrol for 5 h, followed by infection with P. aeruginosa. Intracellular ROS generation was used as an indicator of P. aeruginosa-induced oxidative stress, and cell surface expression of Fas receptor and activation of caspases-3 and -7 as indicators of apoptosis. We also measured the surface expression of intercellular adhesion molecule (ICAM)-1 and enzymes related to inflammation and redox signaling. Resveratrol significantly reduced ROS generation, ICAM-1, and human beta-defensin-2 expression, as well as the markers of apoptosis in A549 cells infected with P. aeruginosa, and up-regulated glutathione peroxidase, suggesting its potential therapeutic role in protecting the lungs against the deleterious effects of P. aeruginosa infection.

scholarly journals Comparative Toxic Effects of Manufactured Nanoparticles and Atmospheric Particulate Matter in Human Lung Epithelial Cells

2020 ◽  
Vol 18 (1) ◽  
pp. 22
Author(s):  
Yun Wu ◽  
Mei Wang ◽  
Shaojuan Luo ◽  
Yunfeng Gu ◽  
Dongyang Nie ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Atmospheric Particulate Matter ◽  
Toxic Effects ◽  
Ros Generation ◽  
Atmospheric Particulate ◽  
Significant Difference ◽  
Lung Epithelial

Although nanoparticles (NPs) have been used as simplified atmospheric particulate matter (PM) models, little experimental evidence is available to support such simulations. In this study, we comparatively assessed the toxic effects of PM and typical NPs (four carbonaceous NPs with different morphologies, metal NPs of Fe, Al, and Ti, as well as SiO2 NPs) on human lung epithelial A549 cells. The EC50 value of PM evaluated by cell viability assay was 148.7 μg/mL, closest to that of SiO2 NPs, between the values of carbonaceous NPs and metal NPs. All particles caused varying degrees of reactive oxygen species (ROS) generation and adenosine triphosphate (ATP) suppression. TiO2 NPs showed similar performance with PM in inducing ROS production (p < 0.05). Small variations between two carbonaceous NPs (graphene oxides and graphenes) and PM were also observed at 50 μg/mL. Similarly, there was no significant difference in ATP inhibition between carbonaceous NPs and PM, while markedly different effects were caused by SiO2 NP and TiO2 NP exposure. Our results indicated that carbonaceous NPs could be served as potential surrogates for urban PM. The identification of PM model may help us further explore the specific roles and mechanisms of various components in PM.

scholarly journals Flavonoid Fraction of Orange and Bergamot Juices Protect Human Lung Epithelial Cells from Hydrogen Peroxide-Induced Oxidative Stress

2015 ◽  
Vol 2015 ◽  
pp. 1-14 ◽  
Author(s):  
Nadia Ferlazzo ◽  
Giuseppa Visalli ◽  
Antonella Smeriglio ◽  
Santa Cirmi ◽  
Giovanni Enrico Lombardo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Human Lung ◽  
Antioxidant Properties ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Food Sources ◽  
Plant Metabolites ◽  
Lung Epithelial ◽  
Flavonoid Fraction

It has been reported that oxidant/antioxidant imbalance triggers cell damage that in turn causes a number of lung diseases. Flavonoids are known for their health benefits, andCitrusfruits juices are one of the main food sources of these secondary plant metabolites. The present study was designed to evaluate the effect of the flavonoid fraction of bergamot and orange juices, on H2O2-induced oxidative stress in human lung epithelial A549 cells. First we tested the antioxidant properties of both extracts in cell-free experimental models and then we assayed their capability to prevent the cytotoxic effects induced by H2O2. Our results demonstrated that bothCitrusjuice extracts reduce the generation of reactive oxygen species and membrane lipid peroxidation, improve mitochondrial functionality, and prevent DNA-oxidative damage in A549 cells incubated with H2O2. Our data indicate that the mix of flavonoids present in both bergamot and orange juices may be of use in preventing oxidative cell injury and pave the way for further research into a novel healthy approach to avoid lung disorders.

scholarly journals Quercetin Prevents LPS-Induced Oxidative Stress and Inflammation by Modulating NOX2/ROS/NF-kB in Lung Epithelial Cells

Molecules ◽  
2021 ◽  
Vol 26 (22) ◽  
pp. 6949
Author(s):  
 Ok-Joo Sul ◽  
Seung Won Ra
Keyword(s):  
Oxidative Stress ◽  
Nuclear Translocation ◽  
A549 Cells ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Lung Epithelial Cells ◽  
Tnf Α ◽  
Lung Epithelial ◽  
Cytokine Tumor Necrosis Factor ◽  
Inflammatory Processes ◽  
Mrna And Protein Expression

Oxidative stress caused by the production of reactive oxygen species (ROS) plays a major role in inflammatory processes. We hypothesized that modulation of ROS via quercetin may protect against oxidative stress and inflammation. Thus, this study aimed to investigate the effects of quercetin on oxidative stress and inflammation in lung epithelial A549 cells. The lipopolysaccharide (LPS)-induced elevation of intracellular ROS levels was reduced after quercetin treatment, which also almost completely abolished the mRNA and protein expression of nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) induced by LPS stimulation. In addition, quercetin suppressed the nuclear translocation of nuclear factor kappa B (NF-κB) and reduced levels of inflammatory cytokine tumor necrosis factor (TNF)-α, interleukin (IL)-1, and IL-6, which had increased significantly after LPS exposure. Our data demonstrated that quercetin decreased ROS-induced oxidative stress and inflammation by suppressing NOX2 production.

The effects of PM10 particles and oxidative stress on macrophages and lung epithelial cells: modulating effects of calcium-signaling antagonists

2007 ◽  
Vol 292 (6) ◽  
pp. L1444-L1451 ◽  
Author(s):  
David M. Brown ◽  
Laura Hutchison ◽  
Kenneth Donaldson ◽  
Vicki Stone
Keyword(s):  
Oxidative Stress ◽  
Calcium Antagonist ◽  
Epithelial Cells ◽  
Calcium Signaling ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Tnf Α ◽  
Lung Epithelial

We have previously examined the ability of air pollution particles (PM10) to promote release of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) from human peripheral blood mononuclear cells and demonstrated a role for calcium as a signaling molecule in this process. We have now studied the ability of oxidative stress induced by a synthetic oxidant tert-butyl hydroperoxide (tBHP) to induce TNF-α production via calcium signaling in the mouse macrophage cell line (J774). The oxidant tBHP significantly increased intracellular calcium and the release of TNF-α in J774 cells, an effect that was reduced to control levels by inhibition of calcium signaling with verapamil, BAPTA-AM, and W-7. This study also investigated interactions between PM10-treated macrophages and epithelial cells by using conditioned medium (CM) from PM10-treated mononuclear cells to stimulate the release of the neutrophil chemoattractant chemokine IL-8 from A549 lung epithelial cells. TNF-α protein release was demonstrated in human mononuclear cells after PM10 treatment, an effect that was inhibited by calcium antagonists. Treatment of A549 cells with monocyte/PM10 CM produced increased IL-8 release that was reduced with CM from monocyte/PM10/calcium antagonist treatments. The expression of ICAM-1 was increased after incubation with CM from monocyte/PM10 treatment, and this increase was prevented by treatment with CM from monocyte/PM10/calcium antagonist. These data demonstrate a link between oxidative stress, calcium, and inflammatory mediator production in macrophages and lung epithelial cells.

Styrene induces an inflammatory response in human lung epithelial cells via oxidative stress and NF-κB activation

2008 ◽  
Vol 231 (2) ◽  
pp. 241-247 ◽  
Author(s):  
Carmen Röder-Stolinski ◽  
Gundula Fischäder ◽  
Gertie Janneke Oostingh ◽  
Ralph Feltens ◽  
Franziska Kohse ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cells ◽  
Inflammatory Response ◽  
Human Lung ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Human Lung Epithelial Cells

scholarly journals A549 Lung Epithelial Cells Grown as Three-Dimensional Aggregates: Alternative Tissue Culture Model for Pseudomonas aeruginosa Pathogenesis

2005 ◽  
Vol 73 (2) ◽  
pp. 1129-1140 ◽  
Author(s):  
A. J. Carterson ◽  
K. Höner zu Bentrup ◽  
C. M. Ott ◽  
M. S. Clarke ◽  
D. L. Pierson ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Pseudomonas Aeruginosa ◽  
Epithelial Cells ◽  
Three Dimensional ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
A549 Lung ◽  
Scanning Electron

ABSTRACT A three-dimensional (3-D) lung aggregate model was developed from A549 human lung epithelial cells by using a rotating-wall vessel bioreactor to study the interactions between Pseudomonas aeruginosa and lung epithelial cells. The suitability of the 3-D aggregates as an infection model was examined by immunohistochemistry, adherence and invasion assays, scanning electron microscopy, and cytokine and mucoglycoprotein production. Immunohistochemical characterization of the 3-D A549 aggregates showed increased expression of epithelial cell-specific markers and decreased expression of cancer-specific markers compared to their monolayer counterparts. Immunohistochemistry of junctional markers on A549 3-D cells revealed that these cells formed tight junctions and polarity, in contrast to the cells grown as monolayers. Additionally, the 3-D aggregates stained positively for the production of mucoglycoprotein while the monolayers showed no indication of staining. Moreover, mucin-specific antibodies to MUC1 and MUC5A bound with greater affinity to 3-D aggregates than to the monolayers. P. aeruginosa attached to and penetrated A549 monolayers significantly more than the same cells grown as 3-D aggregates. Scanning electron microscopy of A549 cells grown as monolayers and 3-D aggregates infected with P. aeruginosa showed that monolayers detached from the surface of the culture plate postinfection, in contrast to the 3-D aggregates, which remained attached to the microcarrier beads. In response to infection, proinflammatory cytokine levels were elevated for the 3-D A549 aggregates compared to monolayer controls. These findings suggest that A549 lung cells grown as 3-D aggregates may represent a more physiologically relevant model to examine the interactions between P. aeruginosa and the lung epithelium during infection.

scholarly journals Ethanol Decreases Inflammatory Response in Human Lung Epithelial Cells by Inhibiting the Canonical NF-kB-Pathway

2017 ◽  
Vol 43 (1) ◽  
pp. 17-30 ◽  
Author(s):  
Katharina Mörs ◽  
Jason-Alexander Hörauf ◽  
Shinwan Kany ◽  
Nils Wagner ◽  
Ramona Sturm ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Acute Inflammation ◽  
Human Lung ◽  
A549 Cells ◽  
Lung Epithelial Cells ◽  
Neutrophil Adhesion ◽  
Lung Epithelial ◽  
Nuclear Levels ◽  
Human Lung Epithelial Cells

Background/Aims: Alcohol (ethanol, EtOH) as significant contributor to traumatic injury is linked to suppressed inflammatory response, thereby influencing clinical outcomes. Alcohol-induced immune-suppression during acute inflammation (trauma) was linked to nuclear factor-kappaB (NF-ĸB). Here, we analyzed alcohol`s effects and mechanisms underlying its influence on NF-ĸB-signaling during acute inflammation in human lung epithelial cells. Methods: A549-cells were stimulated with interleukin (IL)-1β, or sera from trauma patients (TP) or healthy volunteers, with positive/negative blood alcohol concentrations (BAC), and subsequently exposed to EtOH (170 Mm, 1h). IL-6-release and neutrophil adhesion to A549 were analyzed. Specific siRNA-NIK mediated downregulation of non-canonical, and IKK-NBD-inhibition of canonical NF-ĸB signaling were performed. Nuclear levels of activated p50 and p52 NF-ĸB-subunits were detected using TransAm ELISA. Results: Both stimuli significantly induced IL-6-release (39.79±4.70 vs. 0.58±0.8 pg/ml) and neutrophil adhesion (132.30±8.80 vs. 100% control, p<0.05) to A549-cells. EtOH significantly decreased IL-6-release (22.90±5.40, p<0.05) and neutrophil adherence vs. controls (105.40±14.5%, p<0.05). IL-1β-induced significant activation of canonical/p50 and non-canonical/p52 pathways. EtOH significantly reduced p50 (34.90±23.70 vs. 197.70±36.43, p<0.05) not p52 activation. Inhibition of canonical pathway was further increased by EtOH (less p50-activation), while p52 remained unaltered. Inhibition of non-canonical pathway was unchanged by EtOH. Conclusion: Here, alcohol`s anti-inflammatory effects are mediated via decreasing nuclear levels of activated p50-subunit and canonical NF-ĸB signaling pathway.

Sign in / Sign up

Export Citation Format

Share Document