Effects Of Pyocyanin Research Articles

The Effi ciency of Purifi ed Pyocyanin from Pseudomonas aeruginosa in Disruption of Biofi lm Formation by Candida albicans Causing Oral Candidiasis

Candida albicans is the most usually isolated species in invasive oral candidiasis, which is a major health concern in underdeveloped nations. So pyocyanin was screened in Pseudomonas aeruginosa and found that the highest level of productivity in King A medium appeared compared with cetrimide agar, also, the productivity was increased in presence of sweet potato in comparison with soya bean. The pyocyanin was purifi ed with silica gel chromatography as a single peak with high purity. C. albicans causing oral candidiasis is considered a stronger producer of biofi lms. The eff ect of pyocyanin on Candida biofi lm formation was inhibited with increasing incubation concentration and with increasing incubation period and the percentage of biofi lm inhibition reached 73–87% after 72 hours.

Effect of Pyocyanin on gene expression of norA gene in Staphylococcus aureus and SMR gene in Serratia marcescense

Background: The antibiotics active against Multidrug resistant bacteria have several limitations for their use, which include less clinical experience, During the continuing COVID-19 epidemic, limiting use has been difficult because most hospitalized COVID-19 patients receive antibiotics as a defense against subsequent bacterial infection. , Efflux pumps remove drugs and are linked to biofilm formation, making infections more difficult to treat due to a lack of therapeutic choices and necessitating new antimicrobial tactics. Pyocyanin is a secondary blue redox-active metabolite and a large family member of phenazines, tricyclic compounds. Phenazine has been utilized as a biological pesticide against several harmful microorganisms because of its antibacterial properties. Methods: Total RNA from ( Staphylococcus aureus obtained from respiratory tract diagnosed as MDR and Serratia marcescens obtained from co-infection Covid 19 )were isolated . The gene expression of the norA gene efflux pump of S. aureus, which was normalized to the rpoB HKG, and the smr gene efflux pump of Serratia marcescens, which was normalized to the Adnalyate Kinaze enzyme, was studied using quantitative real-time RT PCR on the extracted RNA.

Pyocyanin, a Pathogen-Associated Ligand of the Aryl Hydrocarbon Receptor, as a Novel Therapeutic Target for Septic Cachexia

Upon completion, participant will be able to list one effect of pyocyanin on body weight and adipose tissue that may lead to novel therapeutic strategies for cachexia in septic patients.

Caspase-3-dependent Cell Death in B lymphocyte Caused by Pseudomonas aeruginosa Pyocyanin

Objective: The aim of this study was to investigate cellular responses of B lymphocyte to the exposure of pyocyanin and the role of caspase-3 in its molecular mechanism. Methods: B lymphocytes (Raji cells) were cultured overnight prior to the experiments. Cell culture in five replications were then exposed to various concentrations of pyocyanin and incubated for 24 h in antibiotics-free medium. MTT assay was performed to analyze the cytotoxicity effect of pyocyanin. In separated experiments, the cells were cultured with pyocyanin and addressed for cell morphological analysis using phase contrast microscope. To study the mechanism involved in pyocyanin-induced cellular damage, immunocytochemical analysis was run for the identification of active caspase-3 protein expression. Results: The results of this study showed that cell viability was decreased in pcyocyanin-treated groups. Statistical analysis using ANOVA (p < 0.05) demonstrated significant different between groups with significant value of 0.000. Pyocyanin induced cell death on B lymphocyte in dose-dependent manner. Nuclear fragmentation was observed in pyocyanin-induced cell death; furthermore, caspase-3 was expressed clearly in cell cytoplasm after 24 h incubation. Conclusion: It is concluded that pyocyanin is capable of inducing cell death on B lymphocyte. Caspase-3 may play important role in the molecular mechanism of pyocyanin-induced cell death. DOI: 10.14693/jdi.v22i2.403

Pyocyanin inhibits both nitric oxide-dependent and -independent relaxation in porcine coronary arteries.

The effects of the Pseudomonas aeruginosa virulence factor pyocyanin (PCN) on the contractile function of porcine coronary arteries was investigated in vitro. Artery rings (5 mm) were suspended in organ baths containing Krebs' solution for the measurement of isometric tension. The effect of PCN on resting and precontracted coronary arteries was initially investigated with various agents. Arteries were precontracted with prostaglandin (PG) F2α or potassium chloride and endothelium-dependent relaxations were induced by various agents in the presence of PCN. Pyocyanin (0.1-10 μmol/L) evoked small-amplitude, dose-dependent contractions in resting porcine coronary arteries. In addition, PCN amplified the contractile response to PGF2α , but did not alter responses to carbachol. Pyocyanin (0.1-10 μmol/L) significantly inhibited endothelium-dependent relaxations evoked by neurokinin A. Pyocyanin also inhibited relaxations evoked by diethylamine nitric oxide (a nitric oxide donor), forskolin (an adenylate cyclase activator), dibuytyryl-cAMP (a cAMP analogue), 8-bromo-cGMP (a cGMP analogue) and P1075 (a KATP channel activator), but not isoprenaline (β-adrenoceceptor agonist). These results indicate that physiological concentrations of PCN interfere with multiple intracellular processes involved in vascular smooth muscle relaxation, in particular pathways downstream of nitric oxide release. Thus, PCN may alter normal vascular function in patients infected with P. aeruginosa.

Novel Lipophilic Probe for Detecting Near-Membrane Reactive Oxygen Species Responses and Its Application for Studies of Pancreatic Acinar Cells: Effects of Pyocyanin and L-Ornithine

The aim of this study was to develop a fluorescent reactive oxygen species (ROS) probe, which is preferentially localized in cellular membranes and displays a strong change in fluorescence upon oxidation. We also aimed to test the performance of this probe for detecting pathophysiologically relevant ROS responses in isolated cells. We introduced a novel lipophilic ROS probe dihydrorhodamine B octadecyl ester (H2RB-C18). We then applied the new probe to characterize the ROS changes triggered by inducers of acute pancreatitis in pancreatic acinar cells. We resolved ROS changes produced by L-ornithine, L-arginine, cholecystokinin-8, acetylcholine, taurolithocholic acid 3-sulfate, palmitoleic acid ethyl ester, and the bacterial toxin pyocyanin. Particularly prominent ROS responses were induced by pyocyanin and L-ornithine. These ROS responses were accompanied by changes in cytosolic Ca(2+)concentration ([Ca(2+)]i), mitochondrial membrane potential (ΔΨ), and NAD(P)H concentration. The study describes a novel sensitive lipophilic ROS probe. The probe is particularly suitable for detecting ROS in near-membrane regions and therefore for reporting the ROS environment of plasma membrane channels and pumps. In our experimental conditions, the novel probe was more sensitive than 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein (CM-H2DCF) and dihydrorhodamine123 (H2R123) and allowed us to resolve ROS responses to secretagogues, pyocyanin, and L-ornithine. Changes in the fluorescence of the new probe were particularly prominent in the peripheral plasma membrane-associated regions. Our findings suggest that the new probe will be a useful tool in studies of the contribution of ROS to the pathophysiology of exocrine pancreas and other organs/tissues.

Production of pyocyanin pigment from Pseudomonas aeruginosa strains and investigation of the antimicrobial effect of pyocyanin on other microorganisms

Production of pyocyanin pigment from Pseudomonas aeruginosa strains and investigation of the antimicrobial effect of pyocyanin on other microorganisms

Inhibition of Myeloperoxidase by Phenazine‐Based Bacterial Metabolites: Implications for Cystic Fibrosis

Cystic fibrosis (CF) patients have chronic airway inflammation due to persistent neutrophil influx in response to bacterial infection, most notably Pseudomonas aeruginosa (PA). Neutrophils express myeloperoxidase (MPO), an enzyme that catalyzes the formation of hypochlorous acid to kill bacteria in the lungs of CF patients. Pyocyanin (PYO) and 1‐hydroxyphenazine (1‐HP) are metabolites abundantly produced by PA, known to cause detrimental effects in the lung; however, the effect of PYO and 1‐HP on MPO activity is not known. We hypothesized that PA produce PYO and 1‐HP as a means of inhibiting MPO and incapacitating this important mammalian host defense mechanism. In order to test this hypothesis, we utilized colorimetric assays of MPO activity in the presence or absence of 1‐HP or PYO. Our data indicate that 1‐HP and PYO inhibit both the peroxidase and chlorination activities of MPO. The data suggest that 1‐HP and PYO can modulate MPO activity and presumably decreasing its antibactericidal functions, and thus acting as a mechanism by which PA can thrive in the CF airway. Identifying the effects PYO and 1‐HP have on MPO will influence overall strategies for therapeutic treatments in cystic fibrosis.

Liver sinusoidal endothelial cells and acute non‐oxidative hepatic injury induced by Pseudomonas aeruginosa pyocyanin

The liver sinusoidal endothelial cell (LSEC) is damaged by many toxins, including oxidants and bacterial toxins. Any effect on LSECs of the Pseudomonas aeruginosa virulence factor, pyocyanin, may be relevant for systemic pseudomonal infections and liver transplantation. In this study, the effects of pyocyanin on in vivo rat livers and isolated LSECs were assessed using electron microscopy, immunohistochemistry and biochemistry. In particular, the effect on fenestrations, a crucial morphological aspect of LSECs was assessed. Pyocyanin treatment induced a dose-dependent reduction in fenestrations in isolated LSECs. In the intact liver, intraportal injection of pyocyanin (11.9 microM in blood) was associated with a reduction in endothelial porosity from 3.4 +/- 0.2% (n = 5) to 1.3 +/- 0.1% (n = 7) within 30 min. There were decreases in both diameter and frequency of fenestrations in the intact endothelium. There was also a decrease in endothelial thickness from 175.8 +/- 5.8 to 156.5 +/- 4.0 nm, an endothelial pathology finding previously unreported. Hepatocyte ultrastructure, liver function tests and immunohistochemical markers of oxidative stress (3-nitrotyrosine and malondialdehyde) were not affected. Pyocyanin induces significant ultrastructural changes in the LSEC in the absence of immunohistochemical evidence of oxidative stress or hepatocyte injury pointing to a novel mechanism for pyocyanin pathogenesis.

Mechanisms of action of Pseudomonas aeruginosa pyocyanin on human ciliary beat in vitro.

Pyocyanin is a blue redox active pigment produced by Pseudomonas aeruginosa. It is present at concentrations of up to 10(-4) M in sputa from patients with cystic fibrosis and bronchiectasis who are heavily colonized with this organism. Pyocyanin, at physiologically relevant concentrations, slows human nasal ciliary beat frequency (CBF) in vitro and leads to disruption of the epithelium. Pyocyanin-induced slowing of CBF after 2 h was associated with a significant fall in intracellular cyclic AMP (cAMP) (90%) and ATP (66%) and was reversible after the pyocyanin was removed by washing. These effects were not mediated through interaction with neutrophils. The pyocyanin-induced fall in CBF was not affected by EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid], pyrazinamide, 8-phenyltheophylline, indomethacin, or antioxidants, including catalase (500 U/ml), superoxide dismutase, and N-acetylcysteine. Ciliary slowing was, however, prevented (> 70%) by isobutylmethylxanthine and forskolin, both of which increase intracellular cAMP, and also by the cAMP analog, dibutyryl cAMP. There was also a concomitant protection against the fall in both cAMP and ATP. These agents also delayed the onset of epithelial disruption associated with pyocyanin treatment. In contrast, treatment with the iron chelator desferrioxamine prevented epithelial disruption, although it had no effect on pyocyanin-induced slowing of CBF. It appears that ciliary slowing can be dissociated from epithelial disruption and that the effects of pyocyanin on CBF are associated with a fall in both intracellular cAMP and ATP.

Effect of Pyocyanin and I-Hydroxyphenazine on the Assay of Lactate Dehydrogenase Activity

Effect of Pyocyanin and I-Hydroxyphenazine on the Assay of Lactate Dehydrogenase Activity

Effects of pyocyanine, a phenazine dye from Pseudomonas aeruginosa, on oxidative burst and bacterial killing in human neutrophils

The effects of pyocyanine (phenazinium, 1-hydroxy-5-methyl-hydroxide, inner salt) on oxidative burst in human polymorphonuclear leukocytes were studied by several different approaches. In a cell- and enzyme-free system, pyocyanine oxidized NADPH. The reduced pyocyanine could be measured by its reaction with ferricytochrome c. It was shown by this assay that resting as well as phorbol myristate acetate- or zymosan-stimulated granulocytes reduced pyocyanine. The effect was independent of mitochondria, as cytoplasts were similarly active. Measurement of the hexose monophosphate shunt in intact granulocytes in the presence of pyocyanine indicated a concentration-dependent activation of the shunt without the generation of O2-, suggesting that pyocyanine oxidizes NADPH to NADP+ when it enters granulocytes. Intracellular NADPH in granulocytes was indeed lowered by almost 40% after incubation with pyocyanine. It is by this shuttling of reduction equivalents, leading to the partial depletion of NADPH, that pyocyanine affects the observed concentration-dependent partial inhibition of the phorbol myristate acetate- and zymosan-stimulated generation of O2-. A further consequence was that the intracellular killing of Staphylococcus aureus was also partially suppressed, particularly at higher loads of granulocytes with bacteria. Phagocytosis was not inhibited by pyocyanine concentrations as high as 500 microM. Pyocyanine did not affect the intracellular killing of Pseudomonas aeruginosa. The possible relevance of these findings to the course of mixed hospital infections in immunocompromised patients is discussed.

Effect of pyocyanin and 1-hydroxyphenazine on in vivo tracheal mucus velocity.

Products of the bacterium Pseudomonas aeruginosa have been shown to slow the beating of human respiratory tract cilia in vitro. We have tested the effects of two of these compounds, pyocyanin and 1-hydroxyphenazine (given as a bolus dose dissolved in 2 microliters Ringer solution), on tracheal mucus velocity of radiolabeled erythrocytes in anesthetized guinea pigs. 1-Hydroxyphenazine (200 ng) caused a rapid slowing of tracheal mucus velocity (maximum fall 47% at 20 min) with recovery by 1 h. The effect of pyocyanin was slower in onset, 600 ng causing 60% reduction in tracheal mucus velocity at 3 h, and no recovery occurred. A combination of pyocyanin and 1-hydroxyphenazine produced an initial rapid slowing equivalent to the same dose of 1-hydroxyphenazine given alone, but the later slowing attributed to pyocyanin was greater than the same dose administered alone. This study demonstrates one mechanism by which products of P. aeruginosa may facilitate its colonization of the respiratory tract.

Effects of pyocyanine, a blue pigment from Pseudomonas aeruginosa, on separate steps of T cell activation: Interleukin 2 (IL 2) production, IL 2 receptor formation, proliferation and induction of cytolytic activity

Pyocyanine was isolated by chloroform extraction of cultures of Pseudomonas aeruginosa, and purified by thin layer chromatography. The effects of pyocyanine on the various stages of T cell activation were studied with concanavalin A-stimulated CBA/J mouse splenocytes. At 12.5 microM concentration pyocyanine totally inhibited Con A-dependent proliferation and development of cytotoxic effector cells. Protein and RNA synthesis was only 50% inhibited at this concentration. Inhibitory doses of pyocyanine were nontoxic, in that cell viability was maintained, and the inhibitory effects were reversible after removal of the drug. Pyocyanine did not interfere with interleukin 2 synthesis, nor did it affect the lytic stage of cytotoxic effector T cells. However, T blasts generated by Con A in the presence of pyocyanine did not grow in response to IL2 even in the absence of pyocyanine, and IL2 receptors, detected by indirect immunofluorescence with the receptor-specific monoclonal antibody AMT-13, were diminished in pyocyanine-treated cells. Pyocyanine also inhibited IL2-dependent proliferation of T blasts with fully developed IL2 receptors. The substance thus interferes with several discrete stages of T cell activation.

Pyocyanin and metabolic pathways in liver slices in vitro

The effect of pyocyanin, an oxidation-reduction mediator, on the metabolism of 14C-labeled mannose, fructose, glycerol, pyruvate, acetate, propionate, butyrate, and CO2 in rat-liver slices has been studied. In general, pyocyanin markedly increased the oxidation to CO2 of those substrates expected to be metabolized significantly via the phosphogluconate pathway. However, while fructose and glycerol are presumed to enter the Embden-Meyerhof pathway at the triose level, glycerol but not fructose oxidation to CO2 was increased by pyocyanin addition. Pyocyanin decreased the incorporation of the labeled substrates into glycogen and fatty acids and also the oxidation of pyruvate, acetate, propionate, and butyrate to CO2. Pyocyanin thus appears to have effects on pathways in addition to the phosphogluconate pathway.

The effects of pyocyanine and of lithium on the development and respiration of the eggs of two echinoderms

The effects of pyocyanine and of lithium on the development and respiration of the eggs of two echinoderms

Effect of Pyocyanin on Cerebral Metabolism.

ConclusionPyocyanin administered in vivo produces an increased cerebral oxygen utilization which may be followed by a decrease. These changes are accompanied by symptoms of disturbed function of th...

The effect of pyocyanine on the respiration of some normal tissues and tumours

The effect of pyocyanine on the respiration of some normal tissues and tumours

The effect of pyocyanine on the respiration of some normal tissues and tumours

The effect of pyocyanine on the respiration of some normal tissues and tumours

PYOCYANINE, AN ACCESSORY RESPIRATORY ENZYME

Pyocyanine, the blue pigment of B. pyocyaneus, can increase the respiration of living cells to a great degree (maximum observed increase 24-fold). The reversibility of its oxidation and reduction is responsible for this. The effect is non-species-specific and has been observed in varying degrees with B. pyocyaneus, Staphylococcus aureus, Pneumococcus Type III, and the red blood corpuscles of rabbits. The effect of pyocyanine is dependent on the presence of another respiratory ferment sensitive to potassium cyanide and carbon monoxide. The increase of respiration induced by pyocyanine is paralleled by an increase in the respiratory quotient. The pyocyanine catalysis is not indiscriminately effective in all oxidations, but only in the oxidation of certain substances closely associated with the bacterial body.