IgA immune aggregates stimulate platelet-activating factor and superoxide anion production by human neutrophils. A comparison with IgG aggregates

Lipids ◽  
1991 ◽  
Vol 26 (12) ◽  
pp. 1231-1235 ◽  
Author(s):  
Paloma Hernando ◽  
Jesus Egido ◽  
Rosario de Nicolas ◽  
Eva Gonzalez
Keyword(s):  
Superoxide Anion ◽  
Platelet Activating Factor ◽  
Human Neutrophils ◽  
Superoxide Anion Production ◽  
Anion Production ◽  
Immune Aggregates

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.

Modulation of human neutrophil function in vitro by gastrin

1997 ◽  
Vol 153 (3) ◽  
pp. 475-483 ◽  
Author(s):  
M De la Fuente ◽  
M Carrasco ◽  
A Hernanz
Keyword(s):  
Superoxide Anion ◽  
Latex Bead ◽  
Human Neutrophils ◽  
Intracellular Camp ◽  
Maximal Effect ◽  
Superoxide Anion Production ◽  
Phagocytic Process ◽  
Anion Production ◽  
Camp Levels

Abstract We have studied the effects in vitro of gastrin-17 and gastrin-34, at concentrations from 10−14 m to 10−6 m, on several of the functions of peripheral blood human neutrophils, i.e. adherence to substrate, mobility (spontaneous and directed by a chemical gradient or chemotaxis), ingestion of inert particles (latex beads) and cells (Candida albicans) and superoxide anion production. Both gastrins inhibited several steps of the phagocytic process of human neutrophils, such as mobility and ingestion. By contrast, these peptides increased adherence and had no effect on superoxide anion production. In general, these effects were significant at peptide concentrations between 10−12 m and 10−8 m with a maximal effect at 10−10 m. In addition, gastrin peptides induced a significant increase in intracellular cAMP levels at 30, 60 and 120 s. Moreover, the inhibitory effect of gastrin-17 on the ingestion capacity of neutrophils (latex bead phagocytosis) was similar to that obtained with EGTA, a well-known extracellular calcium chelating compound. Gastrin-17 was found to inhibit completely the stimulation of latex bead phagocytosis in neutrophils caused by the calcium ionophore A23187. These results suggest that gastrin is a negative modulator of the phagocytic process of human neutrophils, and that this effect might involve an increase in intracellular cAMP levels and a decrease in calcium entry into the cells. Journal of Endocrinology (1997) 153, 475–483

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.

scholarly journals New Anti-Inflammatory Aporphine and Lignan Derivatives from the Root Wood of Hernandia nymphaeifolia

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2286 ◽  
Author(s):  
Chuan-Yen Wei ◽  
Shih-Wei Wang ◽  
Jin-Wang Ye ◽  
Tsong-Long Hwang ◽  
Ming-Jen Cheng ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Superoxide Anion ◽  
Cytochalasin B ◽  
Human Neutrophils ◽  
Superoxide Anion Production ◽  
Natural Sources ◽  
Spectroscopic Analyses ◽  
Anion Production ◽  
Ic50 Values ◽  
Anti Inflammatory

A new aporphine, 3-hydroxyhernandonine (1) and a new lignin, 4′-O-demethyl-7-O-methyldehydropodophyllotoxin (2), have been isolated from the root wood of Hernanadia nymphaeifolia, together with thirteen known compounds (3–15). The structures of these compounds were determined through mass spectrometry (MS) and spectroscopic analyses. The known isolate, 2-O-methyl-7-oxolaetine (3), was first isolated from natural sources. Among the isolated compounds, 3-hydroxyhernandonine (1), 4′-O-demethyl-7-O-methyldehydropodophyllotoxin (2), hernandonine (4), oxohernangerine (5), and oxohernagine (6) displayed inhibition (IC50 values ≤5.72 μg/mL) of superoxide anion production by human neutrophils in response to formyl-l-methionyl-l-leucyl-l-phenylalanine/cytochalasin B (fMLP/CB). In addition, 3-hydroxyhernandonine (1), 4′-O-demethyl-7-O-methyldehydropodophyllotoxin (2), oxohernangerine (5), and oxohernagine (6) suppressed fMLP/CB-induced elastase release with IC50 values ≤5.40 μg/mL.

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.

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