scholarly journals Density of surface charge is a more predictive factor of the toxicity of cationic carbon nanoparticles than zeta potential

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Maud Weiss ◽  
Jiahui Fan ◽  
Mickaël Claudel ◽  
Thomas Sonntag ◽  
Pascal Didier ◽  
...  
Keyword(s):  
Charge Density ◽  
Surface Charge ◽  
Airway Inflammation ◽  
Surface Charge Density ◽  
Airway Epithelial Cells ◽  
Mucus Production ◽  
Ζ Potential ◽  
Viability Loss

Abstract Background A positive surface charge has been largely associated with nanoparticle (NP) toxicity. However, by screening a carbon NP library in macrophages, we found that a cationic charge does not systematically translate into toxicity. To get deeper insight into this, we carried out a comprehensive study on 5 cationic carbon NPs (NP2 to NP6) exhibiting a similar zeta (ζ) potential value (from + 20.6 to + 26.9 mV) but displaying an increasing surface charge density (electrokinetic charge, Qek from 0.23 to 4.39 µmol/g). An anionic and non-cytotoxic NP (NP1, ζ-potential = − 38.5 mV) was used as control. Results The 5 cationic NPs induced high (NP6 and NP5, Qek of 2.95 and 4.39 µmol/g, respectively), little (NP3 and NP4, Qek of 0.78 and 1.35 µmol/g, respectively) or no (NP2, Qek of 0.23 µmol/g) viability loss in THP-1-derived macrophages exposed for 24 h to escalating NP dose (3 to 200 µg/mL). A similar toxicity trend was observed in airway epithelial cells (A549 and Calu-3), with less viability loss than in THP-1 cells. NP3, NP5 and NP6 were taken up by THP-1 cells at 4 h, whereas NP1, NP2 and NP4 were not. Among the 6 NPs, only NP5 and NP6 with the highest surface charge density induced significant oxidative stress, IL-8 release, mitochondrial dysfunction and loss in lysosomal integrity in THP-1 cells. As well, in mice, NP5 and NP6 only induced airway inflammation. NP5 also increased allergen-induced immune response, airway inflammation and mucus production. Conclusions Thus, this study clearly reveals that the surface charge density of a cationic carbon NP rather than the absolute value of its ζ-potential is a relevant descriptor of its in vitro and in vivo toxicity.

17,18-Epoxyeicosatetraenoic Acid Inhibits TNF-α-Induced Inflammation in Cultured Human Airway Epithelium and LPS-Induced Murine Airway Inflammation

2021 ◽  
pp. 194589242110276
Author(s):  
Shiori Hara ◽  
Ichiro Tojima ◽  
Shino Shimizu ◽  
Hideaki Kouzaki ◽  
Takeshi Shimizu
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Neutrophil Infiltration ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Mucus Production ◽  
Chemokine Production ◽  
In Vivo Effects

Background 17,18-Epoxyeicosatetraenoic acid (17,18-EpETE), an eicosapentaenoic acid metabolite, is generated from dietary oil in the gut, and antiinflammatory activity of 17,18-EpETE was recently reported. Objective To evaluate the inhibitory effects of 17,18-EpETE in airway inflammation, we examined in vitro and in vivo effects on mucus production, neutrophil infiltration, and cytokine/chemokine production in airway epithelium. Methods Nasal tissue localization of G protein-coupled receptor 40 (GPR40), a receptor of 17,18-EpETE, was determined by immunohistochemical staining. Expression of GPR40 mRNA in nasal mucosa of chronic rhinosinusitis (CRS) patients and control subjects was determined by reverse transcription-polymerase chain reaction (RT-PCR). The in vitro effects on airway epithelial cells were examined using normal human bronchial epithelial cells and NCI-H292 cells. To examine the in vivo effects of 17,18-EpETE on airway inflammation, we induced goblet cell metaplasia, mucus production, and neutrophil infiltration in mouse nasal epithelium by intranasal lipopolysaccharide (LPS) instillation. Results GPR40 is mainly expressed in human nasal epithelial cells and submucosal gland cells. RT-PCR analysis revealed that the expression of GPR40 mRNA was increased in nasal tissues from CRS patients compared with those from control subjects. 17,18-EpETE significantly inhibited tumor necrosis factor (TNF)-α-induced production of interleukin (IL)-6 , IL-8, and mucin from cultured human airway epithelial cells dose dependently, and these antiinflammatory effects on cytokine production were abolished by GW1100, a selective GPR40 antagonist. Intraperitoneal injection or intranasal instillation of 17,18-EpETE significantly attenuated LPS-induced mucus production and neutrophil infiltration in mouse nasal epithelium. Inflammatory cytokine/chemokine production in lung tissues and bronchoalveolar lavage fluids was also inhibited. Conclusion These results indicate that 17,18-EpETE plays a regulatory role in mucus hypersecretion and neutrophil infiltration in nasal inflammation. Local or systemic administration may provide a new therapeutic approach for the treatment of intractable airway disease such as CRS.

The ζ-Potential of Kaolinite Particles

1956 ◽  
Vol 9 (4) ◽  
pp. 450 ◽  
Author(s):  
N Street ◽  
AS Buchanan
Keyword(s):  
Charge Density ◽  
Surface Charge ◽  
Electrophoretic Mobility ◽  
Surface Charge Density ◽  
Considerable Increase ◽  
Ionic Species ◽  
Ζ Potential ◽  
Potentiometric Titrations ◽  
Kaolinite Suspension

Electrophoretic mobility measurements, and both conductometric and potentiometric titrations, were carried out on a kaolinite suspension throughout its neutralization by various bases. The concentration of the ionic species present was calculated from the conductometric and potentiometric titrations, and the true ζ-potential calculated from the electrophoretic mobility by Stigter and Mysels's (1955) method. The results indicate that a discontinuity exists in the adsorption of ions in the vicinity of pH 6.5-7.0 causing a considerable increase in the surface charge density of the particles.

scholarly journals Blockade of Airway Inflammation by Kaempferol via Disturbing Tyk-STAT Signaling in Airway Epithelial Cells and in Asthmatic Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Ju-Hyun Gong ◽  
Daekeun Shin ◽  
Seon-Young Han ◽  
Sin-Hye Park ◽  
Min-Kyung Kang ◽  
...  
Keyword(s):  
Oral Administration ◽  
Airway Inflammation ◽  
Airway Epithelium ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Bronchial Inflammation ◽  
Stat Signaling ◽  
Socs3 Expression

Asthma is characterized by bronchial inflammation causing increased airway hyperresponsiveness and eosinophilia. The interaction between airway epithelium and inflammatory mediators plays a key role in the asthmatic pathogenesis. Thein vitrostudy elucidated inhibitory effects of kaempferol, a flavonoid found in apples and many berries, on inflammation in human airway epithelial BEAS-2B cells. Nontoxic kaempferol at ≤20 μM suppressed the LPS-induced IL-8 production through the TLR4 activation, inhibiting eotaxin-1 induction. Thein vivostudy explored the demoting effects of kaempferol on asthmatic inflammation in BALB/c mice sensitized with ovalbumin (OVA). Mouse macrophage inflammatory protein-2 production and CXCR2 expression were upregulated in OVA-challenged mice, which was attenuated by oral administration of ≥10 mg/kg kaempferol. Kaempferol allayed the airway tissue levels of eotaxin-1 and eotaxin receptor CCR3 enhanced by OVA challenge. This study further explored the blockade of Tyk-STAT signaling by kaempferol in both LPS-stimulated BEAS-2B cells and OVA-challenged mice. LPS activated Tyk2 responsible for eotaxin-1 induction, while kaempferol dose-dependently inhibited LPS- or IL-8-inflamed Tyk2 activation. Similar inhibition of Tyk2 activation by kaempferol was observed in OVA-induced mice. Additionally, LPS stimulated the activation of STAT1/3 signaling concomitant with downregulated expression of Tyk-inhibiting SOCS3. In contrast, kaempferol encumbered STAT1/3 signaling with restoration of SOCS3 expression. Consistently, oral administration of kaempferol blocked STAT3 transactivation elevated by OVA challenge. These results demonstrate that kaempferol alleviated airway inflammation through modulating Tyk2-STAT1/3 signaling responsive to IL-8 in endotoxin-exposed airway epithelium and in asthmatic mice. Therefore, kaempferol may be a therapeutic agent targeting asthmatic diseases.

Electrokinetic properties of thylakoids in in vitro cultured Gypsophila paniculata plants

2000 ◽  
Vol 27 (11) ◽  
pp. 1085
Author(s):  
Virjinia R. Doltchinkova ◽  
Katia Georgieva ◽  
Veneta Kapchina-Toteva ◽  
Juergen Polle
Keyword(s):  
Charge Density ◽  
Surface Charge ◽  
Surface Charge Density ◽  
Light Emission ◽  
Chlorophyll Synthesis ◽  
Photochemical Activity ◽  
Delayed Fluorescence ◽  
Fluorescence Induction ◽  
Gypsophila Paniculata

In vitro cultured Gypsophila paniculata L. plants were used as a model to evaluate the effect of some cytokinins and anticytokinins on thylakoid surface charge. Influence of the cytokinins N-6-furfurylaminopurine (kinetin) and N1-(2-chloro-4-pyridyl)-N2-phenylurea (4-PU-30), cytokinin antagonists 2-chloro-4-cyclobutylamino-6-ethylamino-1,3,5-triazine and N-(4-pyridyl)-O-(4-chlorophenyl) carbamate on the pigment content, surface charge density (s ), fluorescence induction kinetics and millisecond-delayed light emission was studied. Our results showed that the chlorophyll (a+b) content significantly decreased after the 1st and the 2nd month of G. paniculata growth in the presence of the cytokinins kinetin and 4-PU-30. In our model system, cytokinins enhanced the number of open lateral buds and, as a consequence, more shoots per explant. Hence, chlorophyll synthesis was not inhibited but so-called ‘dilution of the pigments’ was available. Anticytokinins inhibited the formation of more than one shoot, and the chlorophyll content was not influenced significantly. The phenylurea cytokinin 4-PU-30 and anticytokinins increased the electrophoretic mobility, zeta potential and surface charge density of thylakoids after a longer time of treatment. Making thylakoid membranes more negatively charged, phenylurea cytokinin and anticytokinins increased the aggregation of the complexes and the energization of the membrane. Our results showed that plant growth regulators decreased the primary photochemical activity of photosystem II (estimated by the ratio Fv/Fm) and delayed fluorescence intensity in the 1st month. However, no significant changes were observed in these parameters in the 2nd month.

scholarly journals ζ-POTENTIAL AND SURFACE CHARGE DENSITY OF TANNIC ACID-TREATED NYLON 6 FIBERS IN ACID DYE SOLUTIONS

1981 ◽  
Vol 37 (6) ◽  
pp. T241-T246 ◽  
Author(s):  
Shinji Ogasawara ◽  
Hiromasa Asami ◽  
Yoshifumi Kimura ◽  
Shigetaka Kuroiwa
Keyword(s):  
Charge Density ◽  
Surface Charge ◽  
Tannic Acid ◽  
Surface Charge Density ◽  
Nylon 6 ◽  
Acid Dye ◽  
Ζ Potential ◽  
Dye Solutions

scholarly journals Mucus Release and Airway Constriction by TMEM16A May Worsen Pathology in Inflammatory Lung Disease

2021 ◽  
Vol 22 (15) ◽  
pp. 7852
Author(s):  
Raquel Centeio ◽  
Jiraporn Ousingsawat ◽  
Inês Cabrita ◽  
Rainer Schreiber ◽  
Khaoula Talbi ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Airway Disease ◽  
Airway Epithelial Cells ◽  
Mucus Secretion ◽  
Airway Epithelial ◽  
Mucus Production ◽  
Airway Constriction ◽  
Goblet Cell Differentiation

Activation of the Ca2+ activated Cl- channel TMEM16A is proposed as a treatment in inflammatory airway disease. It is assumed that activation of TMEM16A will induce electrolyte secretion, and thus reduce airway mucus plugging and improve mucociliary clearance. A benefit of activation of TMEM16A was shown in vitro and in studies in sheep, but others reported an increase in mucus production and airway contraction by activation of TMEM16A. We analyzed expression of TMEM16A in healthy and inflamed human and mouse airways and examined the consequences of activation or inhibition of TMEM16A in asthmatic mice. TMEM16A was found to be upregulated in the lungs of patients with asthma or cystic fibrosis, as well as in the airways of asthmatic mice. Activation or potentiation of TMEM16A by the compounds Eact or brevenal, respectively, induced acute mucus release from airway goblet cells and induced bronchoconstriction in mice in vivo. In contrast, niclosamide, an inhibitor of TMEM16A, blocked mucus production and mucus secretion in vivo and in vitro. Treatment of airway epithelial cells with niclosamide strongly inhibited expression of the essential transcription factor of Th2-dependent inflammation and goblet cell differentiation, SAM pointed domain-containing ETS-like factor (SPDEF). Activation of TMEM16A in people with inflammatory airway diseases is likely to induce mucus secretion along with airway constriction. In contrast, inhibitors of TMEM16A may suppress pulmonary Th2 inflammation, goblet cell metaplasia, mucus production, and bronchoconstriction, partially by inhibiting expression of SPDEF.

scholarly journals Early Reduction of SARS-CoV-2 Replication in Bronchial Epithelium by Kinin B2 Receptor Antagonism

2021 ◽  
Author(s):  
Constanze A. Jakwerth ◽  
Martin Feuerherd ◽  
Ferdinand M. Guerth ◽  
Madlen Oelsner ◽  
Linda Schellhammer ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
Early Stage ◽  
Bronchial Epithelium ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Inflammation Model ◽  
Protection Potential

Background: SARS-CoV2 has evolved to enter the host via the ACE2 receptor which is part of the Kinin-kallirein pathway. This complex pathway is only poorly understood in context of immune regulation but critical to control infection. This study examines SARS-CoV2 infection and epithelial mechanisms of the kinin-kallikrein system at the kinin B2 receptor level in SARS-CoV-2 infection that is of direct translational relevance. Methods: From acute SARS-CoV-2-positive patients and -negative controls, transcriptomes of nasal brushings were analyzed. Primary airway epithelial cells (NHBEs) were infected with SARS-CoV-2 and treated with the approved B2R antagonist icatibant. SARS-CoV-2 RNA RT-qPCR, cytotoxicity assays, plaque assays and transcriptome analyses were performed. The treatment effect was further studied in a murine airway inflammation model in vivo. Results: Here, we report a broad and strong upregulation of kallikreins and the kinin B2 receptor (B2R) in the nasal mucosa of acutely symptomatic SARS-CoV-2-positive patients. A B2R antagonist impeded SARS-CoV-2 replication and spread in NHBEs, as determined in plaque assays on Vero E6 cells. B2R antagonism reduced the expression of SARS-CoV-2 entry receptor ACE2 in vitro and in a murine airway inflammation model in vivo. In addition, it suppressed gene expression broadly, particularly genes involved in G-protein-coupled-receptor signaling and ion transport. Conclusions: In summary, this study provides evidence that treatment with B2R antagonists protects airway epithelial cells from SARS-CoV-2 by inhibiting its replication and spread, through the reduction of ACE2 levels and the interference with several cellular signaling processes. Future clinical studies need to shed light on the airway protection potential of approved B2R antagonists, like icatibant, in the treatment of early-stage COVID-19.

scholarly journals Silibinin Attenuates Silica Dioxide Nanoparticles-Induced Inflammation by Suppressing TXNIP/MAPKs/AP-1 Signaling

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 678 ◽  
Author(s):  
Je-Oh Lim ◽  
Na-Rae Shin ◽  
Yun-Soo Seo ◽  
Hyeon-Hwa Nam ◽  
Je-Won Ko ◽  
...  
Keyword(s):  
Airway Inflammation ◽  
Inflammatory Responses ◽  
Underlying Mechanism ◽  
Airway Epithelial Cells ◽  
Protective Effects ◽  
Proinflammatory Mediators ◽  
Cell Counts ◽  
Silica Dioxide

Silica dioxide nanoparticles (SiONPs) have been applied to several fields, such as drug delivery and gene therapy. However, SiONPs are a constituent of fine dust and can induce excessive inflammatory responses in the lungs via the airways. Silibinin, a major component of silymarin, has been known for its anti-oxidant and anti-inflammatory effects. In the present study, we explored the protective effects of silibinin against SiONPs-induced airway inflammation and explored its underlying mechanism of action, focusing on thioredoxin-interacting protein (TXNIP)/mitogen-activated protein kinases (MAPKs) in vitro and in vivo. In SiONPs-stimulated NCI-H292 airway epithelial cells, silibinin treatment effectively suppressed the elevation of the mRNA expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β, which was accompanied by the reduction in the expression of TXNIP, MAPKs, and activator protein-1 (AP-1). In SiONPs-treated mice, silibinin administration inhibited the increase in inflammatory cell counts and proinflammatory mediators, and it alleviated airway inflammation by SiONPs exposure. In addition, silibinin administration effectively suppressed the elevation of TXNIP/MAPKs/AP-1 signaling by SiONPs exposure. Taken together, silibinin effectively inhibited SiONPs-induced inflammatory responses, and this effect was closely related to the inhibition of TXNIP/MAPK/AP-1 signaling. These results suggested that silibinin might be useful for reducing pulmonary inflammation induced by SiONPs.

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