Human neutrophils produce free radicals from the cell-zymosan interface during phagocytosis and from the whole plasma membrane when stimulated with calcium ionophore A23187

Hirai, Kei-Ichi; Moriguchi, Keiichi; Wang, Guoying

doi:10.1016/0014-4827(91)90124-d

Cited by 36 publications

(15 citation statements)

References 34 publications

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“…However, these scavengers had less of an effect in this system than in the system using the PMN sonicates. This minor effect could be explained by recent electron microscopic-histochemical studies (Vissers et al, 1985;Hirai et al, 1991). These studies have demonstrated that PMNs, activated by specific agonists, release active oxygens only at the area of contact between PMNs and nonphagocytosable surfaces or phagocytosable particles, which is hence inaccessible to macromolecules such as scavenger proteins.…”

Section: Discussionmentioning

confidence: 92%

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1993

British J Pharmacology

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The mechanism of polymorphonuclear leukocyte (PMN)‐dependent platelet adhesion to cultured endothelial cells induced by platelet‐activating factor (PAF) was investigated to determine whether PMNs release or generate any factor(s) capable of inducing platelet adhesion, and the roles of prostacyclin and endothelium‐derived relaxing factor (EDRF). Cell‐free supernatants, sonicates or rapid filtrates of PAF‐stimulated PMN suspensions did not induce platelet adhesion to endothelial cells, but the PMN sonicates induced platelet adhesion when endothelial cells were pretreated with both aspirin and NG‐nitro‐lm‐arginine (l‐NOARG). Its microphotograph showed that mainly platelet aggregates adhered to the endothelial cell surface. Platelet adhesion induced by the PMN sonicates to aspirin‐ and l‐NOARG‐pretreated endothelial cells was dose‐dependently prevented by OP‐41483 (1–100 nm), and slightly by l‐arginine (1 mm). The inhibition of platelet adhesion by OP‐41483 and l‐arginine was potentiated by their combination. WEB 2170 (3 μm), a PAF antagonist, inhibited platelet adhesion induced by the PMN sonicates. However, PAF alone did not induce significant platelet adhesion to aspirin‐ and l‐NOARG‐treated endothelial cells. Platelet adhesion induced by the PMN sonicates was not suppressed by AA‐861 and indomethacin. However, both superoxide dismutase and catalase significantly inhibited platelet adhesion, and, in combination, their inhibitory effect was synergistically potentiated. Mannitol had no effect. It was also significantly inhibited by α1‐antitrypsin, whereas chymostatin and elastatinal had no effect. PAF‐induced platelet adhesion to endothelial cells in the presence of intact PMNs was not suppressed by indomethacin and AA‐861, or by protease inhibitors. SOD alone, and in combination with catalase, caused a slight but significant inhibition, while catalase and mannitol by themselves had no effect. PMN‐induced platelet adhesion was slightly inhibited by OP‐41483 (100 nm). l‐Arginine (1 mm) alone had no effect, but slightly potentiated the effect of OP‐41483. This platelet adhesion was not accompanied by suppression of prostacyclin synthesis. The results with the PMN sonicates show that prostacyclin, EDRF and active oxygens are important modulators of intercellular interactions between platelets and endothelial cells. These results further suggest that the mechanism of intact PMN‐dependent platelet adhesion is primarily through platelet‐endothelial cell interactions in which leukocyte‐derived active oxygens play a role, but does not involve platelet‐platelet interactions inhibitable by prostacyclin.

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Section: Discussionmentioning

confidence: 92%

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Hirafuji

Satoh

1993

British J Pharmacology

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“…PMNs were mixed with OPZ and incubated in a cerium medium containing CeCl 3 and glucose in physiological saline before fixation (Ohno et al, 1982;Hirai et al, 1991). The glucose is the source for NADPH through the monophosphate shunt in living PMNs.…”

Section: Discussionmentioning

confidence: 99%

Electron microscopic identification of hydrogen peroxide detected in fixed human polymorphonuclear leukocytes during phagocytosis

Moriguchi

Ohno

2014

Okajimas Folia Anat. Jpn.

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Summary: Polymorphonuclear leukocytes (PMNs) engaged in phagocytosis produce reactive oxygen species (ROS), such as those that occur in an activated NADPH oxidase reaction, to eliminate ingested microorganisms. The translocation of NADPH oxidase components to produce antimicrobial free radicals from the vesicles to the phagosomes may be important. Hydrogen peroxide (H 2 O 2 ) derived from O 2 -has been observed by electron microscopy using a cerium method. However, 2'-7'-dichlorofluorescin diacetate can also detect H 2 O 2 through fluorescence. The main objective of the present study was to measure the H 2 O 2 -dependent fluorescence of PMNs after opsonized zymosan A (OPZ) phagocytosis using a microplate reader under different fixation conditions, including 0.5, 1, and 10% glutaraldehyde (GA) individually for 1, 5, 10, or 30 min. An additional objective was to visualize, through the use of electron microscopic cytochemistry, the process of H 2 O 2 generation in OPZ phagocytic fixed PMNs. The fixed PMNs showed that the largest fluorescent value was produced by a concentration of 0.5% GA for all fixation times. This suggested that the fixation of PMNs with a high concentration of GA inhibited phagocytosis and produced ROS. In the fixed PMNs, electron microscopic results showed that after 1 min of mixing, some PMNs attached to particles and exhibited mild deposits in their secretory vesicles. When PMNs engulfed particles, free radical-producing vesicles had enhanced reaction deposits 10 min later and fused to the phagosomal membrane, releasing numerous free radicals into the lumen. Time-dependent H 2 O 2 production was enhanced in the secretory vesicles, some of which were fused exactly to the phagosome membranes.

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“…However, Brieland et al [3] reported that translocation of PKC is not necessary for the O-2 generation in macrophages. Microscopic analysis to visualize O-2 generated by human neutrophils was first reported by Nathan et al [22], and more recently by Hirai et al [11]. They showed that the cytochemical reaction is localized in phagocytic vacuoles and at areas of the plasma membrane attached to forein particle, but the free surface of the plasma membrane is completely devoid of reaction products.…”

Section: Discussionmentioning

confidence: 99%

Immunoelectron Microscopy of Protein Kinase C in Resting and Phagocytosing Macrophages.

Fujimoto

Nakano

Ogawa

1997

Acta Histochem. Cytochem

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Human neutrophils produce free radicals from the cell-zymosan interface during phagocytosis and from the whole plasma membrane when stimulated with calcium ionophore A23187

Cited by 36 publications

References 34 publications

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Roles of prostacyclin, EDRF and active oxygens in leukocyte‐dependent platelet adhesion to endothelial cells induced by platelet‐activating factor in vitro

Electron microscopic identification of hydrogen peroxide detected in fixed human polymorphonuclear leukocytes during phagocytosis

Immunoelectron Microscopy of Protein Kinase C in Resting and Phagocytosing Macrophages.

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