scholarly journals Reactivation of Desensitized Formyl Peptide Receptors by Platelet Activating Factor: A Novel Receptor Cross Talk Mechanism Regulating Neutrophil Superoxide Anion Production

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e60169 ◽  
Author(s):  
Huamei Forsman ◽  
Karin Önnheim ◽  
Emil Andréasson ◽  
Karin Christenson ◽  
Anna Karlsson ◽  
...  
Keyword(s):  
Cross Talk ◽  
Superoxide Anion ◽  
Platelet Activating Factor ◽  
Peptide Receptors ◽  
Superoxide Anion Production ◽  
Formyl Peptide Receptors ◽  
Anion Production ◽  
Formyl Peptide ◽  
Neutrophil Superoxide ◽  
Receptor Cross Talk

A novel receptor cross-talk between the ATP receptor P2Y2 and formyl peptide receptors reactivates desensitized neutrophils to produce superoxide

2014 ◽  
Vol 323 (1) ◽  
pp. 209-217 ◽  
Author(s):  
Karin Önnheim ◽  
Karin Christenson ◽  
Michael Gabl ◽  
Joachim C. Burbiel ◽  
Christa E. Müller ◽  
...  
Keyword(s):  
Cross Talk ◽  
Peptide Receptors ◽  
Formyl Peptide Receptors ◽  
Formyl Peptide ◽  
Receptor Cross Talk

scholarly journals Eugenol prevents fMLF-induced superoxide anion production in human neutrophils by inhibiting ERK1/2 signaling pathway and p47phox phosphorylation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Amina Chniguir ◽  
Coralie Pintard ◽  
Dan Liu ◽  
Pham My-Chan Dang ◽  
Jamel El-Benna ◽  
...  
Keyword(s):  
Superoxide Anion ◽  
Human Neutrophils ◽  
Syzygium Aromaticum ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Reduction Assay ◽  
Cytochrome C Reduction ◽  
Phenolic Group ◽  
Anti Oxidant ◽  
Neutrophil Superoxide

AbstractEugenol is a polyphenol extracted from Syzygium aromaticum essential oil. It is known to have anti-inflammatory and chemoprotective properties as well as a potent anti-oxidant activity due the presence of its phenolic group. In this study, we examined the effects of eugenol on neutrophil superoxide production, a key process involved in innate immunity and inflammation. Superoxide anion generationin human neutrophils was measured by cytochrome c reduction assay. Western blotting was used to analyze the phosphorylation of, p47phox, MAPKinases (p38 and ERK1/2), MEK1/2 and Raf, key proteins involved in the activation of NADPH oxidase. Pretreatment of neutrophils by increasing concentrations (2.5 µg/mL–20 µg/mL) of eugenol for 30 min, inhibited significantly (p < 0.001) superoxide anion generation induced by the chemotactic peptide formyl-Met-Leu-Phe (fMLF) with an IC50 of 5 µg/mL. Phorbolmyristate acetate (PMA)-stimulated O2− production was affected only at the highest eugenol concentration (20 µg/mL). Results showed that eugenol decreased the phosphorylation of p47phox onSer-345 and Ser-328, the translocation of p47phox to the membranesand the phosphorylation of Raf, MEK1/2 and ERK1/2 proteins. Taken together, our results suggest that eugenol inhibits the generation of superoxide anion by neutrophils via the inhibition of Raf/MEK/ERK1/2/p47phox-phosphorylation pathway.

Local Anesthetic Effects on Priming and Activation of Human Neutrophils

2001 ◽  
Vol 95 (1) ◽  
pp. 113-122 ◽  
Author(s):  
Markus W. Hollmann ◽  
Ariane Gross ◽  
Niko Jelacin ◽  
Marcel E. Durieux
Keyword(s):  
Signaling Pathway ◽  
Local Anesthetics ◽  
Superoxide Anion ◽  
Platelet Activating Factor ◽  
Target Site ◽  
Polymorphonuclear Neutrophil ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Site Of Action

Background Local anesthetics (LAs) have been shown to inhibit human polymorphonuclear neutrophil (hPMN) functions in vitro, but mechanisms are poorly understood. In this study the authors determined how LAs affect superoxide anion production of hPMNs primed with platelet-activating factor (PAF). The authors studied which pharmacologic properties of LAs are important for this action and assessed the LA site of action within the PAF signaling pathway. Methods Metabolic activity of primed and/or activated hPMNs were measured using the cytochrome-c assay. hPMNs were incubated with several LAs for 1 h to assess interference with PAF signaling. Using protein kinase C (PKC) inhibitors, the PKC activator phorbol myristate acetate (PMA), and the phospholipase C (PLC) antagonist U-73122, we studied involvement of PKC and PLC in the priming process. Pertussis toxin (PTX) was used to characterize the G proteins mediating this pathway. Combined administration of lidocaine with PMA or PTX was used to determine the LA site of action within the priming pathway. Results Platelet-activating factor effectively primed hPMNs. Ester LAs (tetracaine and benzocaine) exerted the most profound inhibitory effect on PAF-primed hPMNs, whereas inhibitory potency of amide LAs increased with decreased charged fraction. The major PAF-induced priming pathway is PLC- and PKC-dependent and mainly Gq-mediated. The main target site for LA in this pathway is located upstream of PKC. Conclusions Local anesthetics in clinically relevant concentrations inhibit superoxide anion production of PAF-primed hPMNs. Effects on priming by these compounds might explain, at least in part, the previously unexplained difference between concentrations of LAs required for their antiinflammatory action in vitro and in vivo. This study suggests a target site for LAs within a Gq-coupled signaling pathway.

Plasma-Mediated Neutrophil Activation during Acute Myocardial Infarction: Role of Platelet-Activating Factor

1995 ◽  
Vol 89 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Tomasz Siminiak ◽  
Robin M. Egdell ◽  
Daniel J. O'Gorman ◽  
Julian F. Dye ◽  
Desmond J. Sheridan
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Superoxide Anion ◽  
Platelet Activating Factor ◽  
Neutrophil Activation ◽  
Polymorphonuclear Neutrophils ◽  
Polymorphonuclear Neutrophil ◽  
Plasma Samples ◽  
Superoxide Anion Production ◽  
Anion Production

1. Polymorphonuclear neutrophils are involved in the development of myocardial injury during ischaemia through the release of free oxygen radicals and by adhesion of activated polymorphonuclear neutrophils to endothelium, resulting in plugging of coronary capillaries. Polymorphonuclear neutrophil activation may be a result of contact with ligands expressed by endothelial cells and/or a response to soluble stimuli released from ischaemic tissue to the plasma. 2. To investigate this we studied plasma-mediated polymorphonuclear neutrophil activation in vitro using plasma samples collected from 14 patients with acute myocardial infarction at time of admission and 6 h and 1, 2, 5 and 7 days later. Plasma samples were incubated with washed polymorphonuclear neutrophils isolated from healthy donors. Expression of adhesion molecules CD18/CD11b integrin and L-selectin (Leu-8) were measured by flow cytometry and superoxide anion production in polymorphonuclear neutrophils was measured by chemiluminescence. 3. Plasma samples obtained 6 h and 1 day after admission were capable of inducing CD18/CD11b antigen expression, superoxide anion production and L-selectin shedding in the washed polymorphonuclear neutrophils, and this effect was significant when compared with plasma taken at 5 and 7 days after admission. 4. The plasma-mediated polymorphonuclear neutrophil stimulation was prevented when the PMN were pretreated with platelet-activating factor receptor antagonists BN52021 or BN50739. The platelet-activating factor concentrations detected in the plasma samples were not higher than those detected in plasma from healthy subjects. 5. These findings suggest that during acute myocardial infarction peripheral plasma contains soluble stimuli capable of inducing polymorphonuclear neutrophil integrin expression, L-selectin shedding and oxygen free radical production and that platelet-activating factor appears to act as an autocrine polymorphonuclear neutrophil stimulus.

Superoxide anion production and degranulation of rat neutrophils in response to acetaldehyde-altered liver cell membranes

1986 ◽  
Vol 71 (3) ◽  
pp. 313-318 ◽  
Author(s):  
A. J. K. Williams ◽  
R. E. Barry
Keyword(s):  
Liver Cell ◽  
Superoxide Anion ◽  
Cell Membranes ◽  
Membrane Vesicles ◽  
Enzyme Release ◽  
Superoxide Anion Production ◽  
Liver Membrane ◽  
Anion Production ◽  
Neutrophil Superoxide ◽  
Altered Liver

1. Rat liver membrane vesicles were exposed to acetaldehyde, with or without reduction of the resultant adducts formed. 2. Superoxide anion production and degranulation of rat neutrophils, upon stimulation with the liver membrane vesicles, were measured by cytochrome c reduction before and after the addition of superoxide dismutase, and β-glucuronidase release respectively. 3. Preincubation with acetaldehyde significantly enhanced superoxide anion production by both the reduced and non-reduced membrane samples (1.7-fold and 4.4-fold, respectively). 4. Preincubation with acetaldehyde significantly enhanced degranulation (1.5-fold) of neutrophils in response to the non-reduced membranes only. The reductive process itself caused a marked increase (2.4-fold) in the ability of the membrane vesicles to stimulate degranulation. 5. Cytochalasin B, an inhibitor of phagocytosis, did not reduce degranulation, implying that it occurred as a consequence of cell surface stimulation. 6. Neutrophil superoxide anion production and lysosomal enzyme release in response to acetaldehyde-altered liver cell membranes could be an important mechanism of hepatocyte injury in alcoholic liver disease.

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