Investigation on the antibacterial activity of electronic cigarette liquids (ECLs): a proof of concept study

2020 ◽  
Vol 21 ◽  
Author(s):  
Virginia Fuochi ◽  
Massimo Caruso ◽  
Rosalia Emma ◽  
Aldo Stivala ◽  
Riccardo Polosa ◽  
...  
Keyword(s):  
Antibacterial Activity ◽  
Bacterial Species ◽  
A549 Cells ◽  
Bactericidal Effect ◽  
Minimal Bactericidal Concentration ◽  
Viability Assay ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Background: The key ingredients of e-cigarettes liquid are commonly propane-1,2-diol (also called propylene glycol) and propane-1,2,3-triol (vegetal glycerol) and their antimicrobial effects are already established. The nicotine and flavors which are often present in e-liquids can interfere with the growth of some microorganisms. Objective: The effect of the combining these elements in e-liquids is unknown. The aim of the study was to investigate the possible effects of these liquids on bacterial growth in the presence or absence of nicotine and flavors. Methods: Susceptibilities of pathogenic strains (Klebsiella pneumoniae, Staphylococcus aureus, Pseudomonas aeruginosa, Acinetobacter baumannii, Escherichia coli, Enterococcus faecalis and Sarcina lutea) were studied by means of a multidisciplinary approach. Cell viability and antioxidant assays were also evaluated. Results: All e-liquids investigated showed antibacterial activity against at least one pathogenic strain. A higher activity was correlated to the presence of flavors and nicotine. Discussion: In most cases the value of minimal bactericidal concentration is equal to the value of minimal inhibitory concentration showing that these substances have a bactericidal effect. This effect was observed in concentrations up to 6.25% v/v. Antioxidant activity was also correlated to presence of flavors. Over time, the viability assay in human epithelial lung A549 cells showed a dose-dependent inhibition of cell growth. Conclusion: Our results have shown that flavors considerably enhance the antibacterial activity of propane-1,2-diol and propane-1,2,3-triol. This study provides important evidence that should be taken into consideration in further investigative approaches, to clarify the different sensitivity of the various bacterial species to e-liquids, including the respiratory microbiota, to highlight the possible role of flavors and nicotine.

Prejunctional inhibition of vasoactive intestinal peptide release

1987 ◽  
Vol 253 (1) ◽  
pp. G7-G12 ◽  
Author(s):  
J. R. Grider ◽  
G. M. Makhlouf
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Muscle Relaxation ◽  
Dependent Manner ◽  
Basal Tone ◽  
Peptide Release ◽  
Dependent Inhibition ◽  
Motor Nerves ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

The role of vasoactive intestinal peptide (VIP) and its homologue, peptide histidine isoleucine (PHI), as neurotransmitters of inhibitory motor nerves of the gut, were examined in strips of guinea pig taenia coli and gastric fundic muscle. The stoichiometry of VIP release and muscle relaxation was determined in the presence and absence of the bee venom peptide, apamin, and the existence of prejunctional VIP/PHI receptors capable of regulating VIP/PHI release was explored. In both types of muscle, relaxation induced by field stimulation was proportional to the amount of VIP released. Apamin inhibited relaxation and VIP release in a dose-dependent manner: maximal relaxation was inhibited by 85–96% at 10(-7)-10(-6) M apamin. Analysis of residual responses showed that apamin did not affect the stoichiometry of VIP release and muscle relaxation. Because apamin had no effect on basal tone or on relaxation induced by exogenous VIP, its effect on neurally induced relaxation was attributed to inhibition of VIP release. Both secretin and PHI inhibited neurally induced VIP release in the two types of muscle. At the optimal concentration of 10(-7) M, secretin inhibited VIP release by 52%, whereas the closer neural homologue, PHI, abolished VIP release. The dose-dependent inhibition of VIP release by PHI, which is cosynthesized and coreleased with VIP, indicates the existence of prejunctional inhibitory VIP/PHI autoreceptors capable of regulating VIP/PHI release.

Anti-nociceptive activity of a few structurally related trimethoxy flavones and possible mechanisms involved

2016 ◽  
Vol 27 (2) ◽  
Author(s):  
Jagan Nadipelly ◽  
Vijaykumar Sayeli ◽  
Parimala Kadhirvelu ◽  
Jaikumar Shanmugasundaram ◽  
Binoy Varghese Cheriyan ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Hot Water ◽  
Dependent Manner ◽  
Tail Immersion ◽  
Dopaminergic Mechanisms ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
Definite Role

AbstractThe present study was designed to investigate the anti-nociceptive activity of a few structurally related trimethoxy flavones (7,2′,3′-TMF, 7,2′,4′-TMF, 7,3′,4′-TMF and 7,5,4′-TMF) and the possible mechanisms involved.Anti-nociceptive activity was evaluated in mice by employing acetic acid-induced writhing, formalin-induced nociception and hot water tail immersion methods. The involvement of opioid, GABAergic, tryptaminergic, adrenergic and dopaminergic mechanisms and KTrimethoxy flavones exhibited a significant and dose-dependent inhibition of acetic acid writhing. The paw-licking response time was reduced both in the early and late phases of formalin nociception in a dose-dependent manner by trimethoxy flavones. A significant increase in tail withdrawal latency time was also observed after trimethoxy flavones treatment. These observations revealed the potential anti-nociceptive action of the investigated trimethoxy flavones. Pretreatment with naloxone and bicuculline significantly attenuated the reduction of abdominal constrictions produced by all the tested trimethoxy flavones indicating a definite role of opioid and GABAergic mechanisms in the anti-nociceptive effect of trimethoxy flavones. The anti-nociceptive action elicited by various trimethoxy flavones was differently modulated by glibenclamide, ondansetron, yohimbine and sulpiride.The investigated trimethoxy flavones exhibited promising anti-nociceptive activity in various nociceptive models, and multiple mechanisms are involved in the anti-nociceptive activity of these compounds.

Regulation of phosphatidylcholine and phosphatidylethanolamine synthesis in rat hepatocytes by 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR)

2002 ◽  
Vol 362 (1) ◽  
pp. 97-104 ◽  
Author(s):  
Martin HOUWELING ◽  
Wil KLEIN ◽  
Math J. H. GEELEN
Keyword(s):  
Cellular Uptake ◽  
Rat Hepatocytes ◽  
Cellular Level ◽  
Membrane Phospholipids ◽  
Main Target ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

The present study was undertaken to study the role of AMP-activated kinase (AMPK) in the biosynthesis of two major membrane phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Incubation of rat hepatocytes with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), an activator of AMPK, produced dose-dependent inhibition of the incorporation of [3H]choline and [3H]ethanolamine into PC and PE, respectively. Determination of the cellular uptake of choline and ethanolamine showed that the reduced synthesis of PC and PE did not result from impaired uptake of these two precursors. The decreased synthesis of PC was not mirrored by a reduction in the activities of the enzymes of the CDP-choline pathway. The diminution of PE biosynthesis, however, was paralleled by a depressed activity of CTP:phosphoethanolamine cytidylyltransferase (ET), the pace-setting enzyme of the CDP-ethanolamine pathway. AICAR treatment of hepatocytes stimulated the conversion of choline into betaine, indicating that reduced PC synthesis most probably resulted from a decrease in the availability of choline. In addition, AICAR induced a 50% reduction in the cellular level of diacylglycerols, which may further impair the synthesis of PC and PE. The results thus indicate that AICAR inhibits the biosynthesis of PC and PE and that the effect is exerted at different sites in the two pathways. Increased oxidation of choline to betaine is the main target of AICAR in the PC pathway, whereas inhibition of ET activity is the locus of AICAR action in the PE pathway.

scholarly journals The role of GTP in prostaglandin E1 stimulation of adenylate cyclase in platelet membranes

1983 ◽  
Vol 214 (1) ◽  
pp. 231-234 ◽  
Author(s):  
J M Stein ◽  
B R Martin
Keyword(s):  
Adenylate Cyclase ◽  
Prostaglandin E1 ◽  
Platelet Membrane ◽  
Cyclase Activity ◽  
Adenylate Cyclase Activity ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
Stimulation Of

Adenylate cyclase activity in platelet membrane preparations was measured in the presence of prostaglandin E1 (PGE1), GTP and a non-hydrolysable analogue of GDP, guanosine 5′-[beta-thio]diphosphate (GDP[beta S]). A dose-dependent inhibition of adenylate cyclase by GDP[beta S] was observed that could be reversed either by adding increased amounts of GTP or of PGE1.

scholarly journals The role of glutathione reductase in maintaining human granulocyte function and sensitivity to exogenous H2O2

Blood ◽  
1987 ◽  
Vol 69 (2) ◽  
pp. 493-500 ◽  
Author(s):  
HJ Cohen ◽  
EH Tape ◽  
J Novak ◽  
ME Chovaniec ◽  
P Liegey ◽  
...  
Keyword(s):  
Glutathione Reductase ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Glutathione Cycle ◽  
Granulocyte Function ◽  
Dose Dependent ◽  
Generating System ◽  
Shape Changes ◽  
Exogenous H2o2

Abstract Human granulocytes (polymorphonuclear leukocytes, PMN) produce H2O2 and other reactive oxygen species while undergoing phagocytosis. To examine the role of the glutathione cycle in metabolizing H2O2, we incubated PMN with 1,3-bis (2-chloroethyl) nitrosourea (BCNU). Incubation of PMN with BCNU results in a dose-dependent inhibition of PMN glutathione reductase (GRED), with 50% inhibition occurring at approximately 2 micrograms/mL BCNU. PMN hexose monophosphate shunt activity stimulated with an exogenous H2O2-generating system was inhibited only when the GRED activity was reduced to less than 30% of control. BCNU-treated cells contained lower levels of reduced sulfhydryls and reduced glutathione, which decreased even more in the presence of an exogenous H2O2-generating system. The effect of BCNU and exogenous H2O2 on various aspects of phagocytosis were examined. Exposure of BCNU-treated PMN to an H2O2-generating system resulted in an inhibition of chemotactic peptide-induced shape changes and degranulation. The ability of BCNU-treated cells to produce O2- was diminished only when the PMN were incubated with an H2O2-generating system in the presence of cyanide. Ingestion of opsonized bacteria by BCNU-treated PMN was unaffected by incubation in an H2O2-generating system even in the presence of cyanide. We conclude that PMN GRED is inhibited by BCNU, the ability of PMN to metabolize H2O2 is affected only when GRED is reduced more than 70%, this inhibition affects the glutathione content of these cells, and some, but not all of the phagocytic functions of GRED-inhibited PMN are inhibited after exposure to an H2O2-generating system.

The Role of the CXCR4 Inhibitor AMD3100 in Multiple Myeloma (MM).

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2492-2492
Author(s):  
Irene M. Ghobrial ◽  
Mona Melhem ◽  
Ujjal Singha ◽  
Diane George ◽  
Michael Timm ◽  
...  
Keyword(s):  
Maximum Effect ◽  
Adhesion Assay ◽  
Invasion Assay ◽  
Inhibition Of Proliferation ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent ◽  
Higher Doses ◽  
Serial Dilutions

Abstract We have previously demonstrated that the chemokine receptor CXCR4 and its ligand SDF-1 are important regulators of migration in MM. The objective of this study was to investigate the role of the CXCR4 inhibitor AMD3100 (Sigma, MO) on proliferation, survival, migration, adhesion and invasion in MM. MM cell lines (MM.1S, OPM2 and Kas6/1) were exposed to serial dilutions of SDF-1 (1–100nM) in the presence or absence of the CXCR4 inhibitor AMD3100 (20–100uM) incubated for 16 hrs or the CXCR4 inhibitory antibody MAB171 (RDSystems, MN) 10–800uM or its IgG2 isotype control. Inhibition of proliferation was measured using the MTT proliferation assay. Apoptosis was determined using Annexin V/PI FACS analysis. Migration was determined using a transwell migration assay (Costar, Corning, NY). Cells treated with serial concentrations of AMD3100 or vehicle (sterile water) were washed, placed in serum free medium for two hours, then placed in the migration chambers with 1% FCS medium in the presence of SDF–1 20nM (a concentration previously determined to induce maximum migration in MM cells). After 4 hours of incubation, cells that migrated to the lower chambers were counted. Similarly, adhesion was determined using an adhesion assay (EMD Biosciences, CA) with 96 well plated coated with fibronectin and using MM cells treated with serial dilutions of AMD3100 or vehicle in the presence or absence of serial concentrations of SDF-1 (10–30nM). Invasion was determined using the invasion assay (EMD Biosciences, CA). Serial concentrations of SDF-1 induced a bell-shaped migration curve in MM cells with 10–30nM inducing maximum migration (324% compared to untreated control) while higher doses of SDF-1 (100nM) did not induce migration in all MM cells tested. AMD3100 induced a dose dependent inhibition of migration in MM cells treated with 20nM SDF-1. The maximum effect was demonstrated at 25uM with 48% migration as compared to control. Higher doses of AMD3100 (50–100uM) did not further inhibit migration. The anti-CXCR4 antibody demonstrated a dose dependent inhibition of migration. Anti-CXCR4 10uM inhibited migration to 53% and 200uM to 35%. The effects of higher doses of anti-CXCR4 were not significantly different as compared to 200uM. Serial concentrations of SDF-1 (10–100) induced a dose-response increase in adhesion to fribronectin with 10nM increasing adhesion by 202% as compared to untreated cells and 100nM 462% indicating activation of alpha4 beta1 integrin on MM cells. AMD3100 100uM inhibited adhesion at all doses by 55% as compared to control. Using the invasion assay, SDF-1 100nM induced maximal invasion of MM cells. The effect of SDF-1 on invasion was not abrogated by AMD3100. AMD3100 did not induce significant apoptosis or inhibition of proliferation at all tested doses, in the presence or absence of 20–100nM SDF-1. In summary, AMD3100 inhibited migration and adhesion of MM cells, but not invasion indicating that invasion occurs through non-CXCR4 dependent mechanisms. AMD3100 did not induce apoptosis or inhibition of proliferation indicating that its effect is specific on migration and adhesion. Further experiments to test its role on homing of MM cells in vivo are underway. The future use of this novel agent as an inhibitor of homing of MM cells in clinical trials may be warranted. Supported in part by an ASH Scholar Award and an MMRF grant.

scholarly journals Murine granulocytic cell adhesion to bone marrow hemonectin is mediated by mannose and galactose

Blood ◽  
1995 ◽  
Vol 86 (1) ◽  
pp. 135-140 ◽  
Author(s):  
BA Sullenbarger ◽  
MS Petitt ◽  
P Chong ◽  
MW Long ◽  
MS Wicha
Keyword(s):  
Bone Marrow ◽  
Cell Adhesion ◽  
Cell Attachment ◽  
Lectin Binding ◽  
Specific Attachment ◽  
Dependent Inhibition ◽  
Apparent Decrease ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

Hemonectin (HN) is a bone marrow (BM) protein that promotes specific attachment of immature granulocytes and their precursors within the BM. We report that HN is a glycoprotein containing both mannose and galactose residues, and provide evidence that these carbohydrates mediate granulocytic cell adhesion to HN. Carbohydrate structure was determined by digoxigenin-conjugated lectin binding to HN and indicated the presence of mannose, galactose, sialic acid, and the absence of fucose-linked oligosaccharides. The role of carbohydrates in mediating cell adhesion was examined by chemical and enzymatic deglycosylation. Deglycosylation of HN with trifluoromethanesulfonic acid, which cleaves N- and O-linked oligosaccharides, inhibits 66% of cell attachment to HN, and results in an apparent decrease in molecular weight from 60 to 50 kD. Enzymatic deglycosylation with endo-B-N-acetylglucosaminidase H, which hydrolyzes specific N-linked mannose residues, inhibits 30% of cell adhesion to HN. Finally, the role of these specific sugars in hemonectin-mediated cell adhesion was confirmed with neoglycoprotein blocking. Preincubation of BM cells with mannosyl- and galactosyl-BSA probes produces a dose-dependent inhibition of cell attachment to HN, whereas fucosyl-BSA does not inhibit cell adhesion to HN. These results show that mannose and galactose partially mediate adhesion of BM granulocytes to HN.

scholarly journals CXCL9 and CXCL11 Chemokines Modulation by Peroxisome Proliferator-Activated Receptor-α Agonists Secretion in Graves’ and Normal Thyrocytes

2010 ◽  
Vol 31 (5) ◽  
pp. 780-780
Author(s):  
Alessandro Antonelli ◽  
Silvia Martina Ferrari ◽  
Silvia Frascerra ◽  
Cinzia Pupilli ◽  
Caterina Mancusi ◽  
...  
Keyword(s):  
Peroxisome Proliferator ◽  
Rt Pcr ◽  
Thyroid Cells ◽  
Peroxisome Proliferator Activated Receptor ◽  
Dependent Inhibition ◽  
Pparγ Agonists ◽  
Dose Dependent Inhibition ◽  
And Control ◽  
Dose Dependent

ABSTRACT Context Peroxisome proliferator-activated receptor (PPAR)-α has been shown to exert immunomodulatory effects in autoimmune disorders. However, until now, no data were present in the literature about the effect of PPARα activation on CXCL9 and CXCL11 chemokines in general or on secretion of these chemokines in thyroid cells. Objective and Design The presence of PPARα and PPARγ has been evaluated by RT-PCR in Graves’ disease (GD) and control cells in primary culture. Furthermore, we have tested the role of PPARα and PPARγ activation on CXCL9 and CXCL11 secretion in GD and control cells after stimulation of these chemokines secretion with IFNγ and TNFα. Results This study shows the presence of PPARα and PPARγ in GD and control cells. A potent dose-dependent inhibition by PPARα-agonists was observed on the cytokines-stimulated secretion of CXCL9 and CXCL11 in GD and control cells. The potency of the PPARα agonists used was maximum on the secretion of CXCL9, reaching about 90% of inhibition by fenofibrate and 85% by ciprofibrate. The relative potency of the compounds was different with each chemokine; for example, gemfibrozil exerted a 55% inhibition on CXCL11, whereas it had a weaker activity on CXCL9 (40% inhibition). PPARα agonists were stronger (ANOVA, P < 0.001) inhibitors of CXCL9 and CXCL11 secretion in thyrocytes than PPARγ agonists. Conclusions Our study shows the presence of PPARα in GD and control thyrocytes. PPARα activators are potent inhibitors of the secretion of CXCL9 and CXCL11, suggesting that PPARα may be involved in the modulation of the immune response in the thyroid.

scholarly journals Chick osteocyte-derived protein inhibits osteoclastic bone resorption

1997 ◽  
Vol 322 (1) ◽  
pp. 245-250 ◽  
Author(s):  
Akiko MAEJIMA-IKEDA ◽  
Mari AOKI ◽  
Katsuki TSURITANI ◽  
Kayo KAMIOKA ◽  
Kenji HIURA ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Conditioned Medium ◽  
Bone Cells ◽  
Inhibitory Protein ◽  
Effector Cells ◽  
Pit Formation ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Dose Dependent

In order to investigate the role of osteocytes in bone resorption, we examined the homogenate and conditioned medium from purified chick calvarial osteocytes in a pit-formation assay using unfractionated bone cells from mice. The osteocyte homogenate markedly inhibited pit formation, whereas the conditioned medium of osteocytes had no effect. This inhibitory activity was not the result of cytotoxicity of the homogenate. A novel bone-resorption-inhibitory protein was purified from collagenase-digested chick calvarial fragments enriched in osteocytes. The inhibitory protein, of molecular mass 18.5 kDa, showed significant dose-dependent inhibition of pit formation by unfractionated bone cells from mice and rabbits, and by human giant tumour cells. This protein also inhibited the bone-resorbing activity of purified osteoclasts in the pit-formation assay in the absence of other effector cells. Microinjection of the protein into osteoclasts caused disruption of the podosomes in the cells. The N-terminal 25-amino-acid sequence of the protein showed 68% identity to a part of Rho-GTP-dissociation inhibitor. Thus chick calvarial osteocytes may be involved in the regulation of bone resorption by osteoclasts.

scholarly journals The role of glutathione reductase in maintaining human granulocyte function and sensitivity to exogenous H2O2

Blood ◽  
1987 ◽  
Vol 69 (2) ◽  
pp. 493-500
Author(s):  
HJ Cohen ◽  
EH Tape ◽  
J Novak ◽  
ME Chovaniec ◽  
P Liegey ◽  
...  
Keyword(s):  
Glutathione Reductase ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
Glutathione Cycle ◽  
Granulocyte Function ◽  
Dose Dependent ◽  
Generating System ◽  
Shape Changes ◽  
Exogenous H2o2

Human granulocytes (polymorphonuclear leukocytes, PMN) produce H2O2 and other reactive oxygen species while undergoing phagocytosis. To examine the role of the glutathione cycle in metabolizing H2O2, we incubated PMN with 1,3-bis (2-chloroethyl) nitrosourea (BCNU). Incubation of PMN with BCNU results in a dose-dependent inhibition of PMN glutathione reductase (GRED), with 50% inhibition occurring at approximately 2 micrograms/mL BCNU. PMN hexose monophosphate shunt activity stimulated with an exogenous H2O2-generating system was inhibited only when the GRED activity was reduced to less than 30% of control. BCNU-treated cells contained lower levels of reduced sulfhydryls and reduced glutathione, which decreased even more in the presence of an exogenous H2O2-generating system. The effect of BCNU and exogenous H2O2 on various aspects of phagocytosis were examined. Exposure of BCNU-treated PMN to an H2O2-generating system resulted in an inhibition of chemotactic peptide-induced shape changes and degranulation. The ability of BCNU-treated cells to produce O2- was diminished only when the PMN were incubated with an H2O2-generating system in the presence of cyanide. Ingestion of opsonized bacteria by BCNU-treated PMN was unaffected by incubation in an H2O2-generating system even in the presence of cyanide. We conclude that PMN GRED is inhibited by BCNU, the ability of PMN to metabolize H2O2 is affected only when GRED is reduced more than 70%, this inhibition affects the glutathione content of these cells, and some, but not all of the phagocytic functions of GRED-inhibited PMN are inhibited after exposure to an H2O2-generating system.

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