Generation of superoxide anion and chemiluminescence by human monocytes during phagocytosis and on contact with surface-bound immunoglobulin G.

Johnston, Richard B.; Lehmeyer, Joyce E.; Guthrie, L A

doi:10.1084/jem.143.6.1551

Cited by 220 publications

(69 citation statements)

References 13 publications

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“…This suggestion is in accordance with the present finding that neutrophils, whose number declined sharply on elicitation, emitted more intense chemiluminescence when compared with macrophages. In fact, this supports the earlier reports by Johnston et al [29] and Sagone et al [30] that granulocytes are capable of producing a more intense peak of chemiluminescence than monocytes/macrophages. However, in human blood, such differences in peak chemiluminescence have been attributed to differences in their ability to produce hydroxyl radicals [31].…”

Section: Resultssupporting

confidence: 81%

Free Radicals and Detoxification Enzymes of Inflammatory Peritoneal Neutrophils and Macrophages.

Alaudeen¹,

Weidemann²

1997

J. Clin. Biochem. Nutr.

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SummaryIn our study to elucidate the biochemical basis of macrophage activation, we noted a transient surge (within 24 h) in neutrophil number in the peritoneal cavity following the injection of thioglycollate. By day 2 the peritoneal cell population consisted predominantly of vacuolated macrophages. In order to understand the possible cause of the above short-lived increase in neutrophils, we compared the capacity to produce toxic free radicals (by measuring luminol-dependent chemiluminescence) and the activities of detoxification enzymes, namely, glutathione peroxidase and glutathione reductase, between neutrophils (day-1 cells) and the day-2 cells, which were predominantly macrophages. The results show that the neutrophils obtained 1 day after elicitation by thioglycollate produced an intense burst of luminol-dependent chemiluminescence, approximately 7-fold greater than that of the day-2 macrophages. This was true despite a markedly enhanced oxygen consumption by the latter compared with that by the neutrophils. In addition there were marked differences in the onset and duration of the response. Investigations on the activities of detoxification enzymes, especially glutathione peroxidase and glutathione reductase, which are known to be coupled to the oxidative segment of the pentose phosphate pathway, revealed neutrophils to have a reduced capacity to detoxify free radicals and peroxides in comparison with elicited macrophages. These findings suggest that the neutrophils, despite their enhanced capacity to emit toxic free radicals and peroxides, are less efficient in protecting themselves, which ultimately may cause cell death and, as a consequence, a decline in their cell number at the site of inflammation.

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Section: Resultssupporting

confidence: 81%

Free Radicals and Detoxification Enzymes of Inflammatory Peritoneal Neutrophils and Macrophages.

Alaudeen¹,

Weidemann²

1997

J. Clin. Biochem. Nutr.

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“…When suiperoxidle di smutitase a(In catalase, which hlad been heated to dlestroy enizymatic activity, were added, no inhibitory effect on cell lysis was ohserved. It wats ascertained that 50 mM miannitol did not (18)(19)(20)(21), annd it is seen from our results that the process of ADCC, phagocytosis, and postphaigocytic events are intimately correlated, allthouigh no ca'usal relation mav be deduced friom these results.…”

Section: Introductionmentioning

confidence: 46%

Role of oxygen in antibody-dependent cytotoxicity mediated by monocytes and neutrophils.

Borregaard¹,

Kragballe²

1980

J. Clin. Invest.

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A B S T R A C T The antibody-dependent cell-mediated cytoxicity (ADCC) by human monocytes and neutrophils was investigated by measuiriing the release of 'chromate from prelabeled erythrocytes coated with immunoglobulin G. ADCC was found to be positively correlated to phagocytosis of 51Cr-labeled erythrocytes and to the postphagocytic events of the effector cells, activation of the hexose monophosphate shunt, and degranulation.Exclusion of oxygen from the incubatioin media halved the ADCC by both cell types without affecting phagocytosis or degranutilation. Likewise, ADCC by cells from patients suffering from chronic granulomatous disease (CGD) was only half the intensity of ADCC by cells from normals. Inhibitors of mitochondrial respiration were without depressing effect on ADCC. Azide, which in addition to its blocking action on oxydative phosphorylation also inhibits catalase and myeloperoxidase, resulted in a -40% stimulation of ADCC by cells from normals but was without effect oIn ADCC by cells from CGD patients. The hydroxyl radical scavenger, mannitol, significantly depressed ADCC by cells from normals (P < 0.01) but was without effect on cells from CGD patients. Azide and mannitol also were without effect on ADCC by normal cells when oxygen was excluded.In a xanthine-xanthiine oxidase system, erythrocytes were effectively lysed. This lysis was inhibited by catalase, superoxide dismutase, and mannitol. When comparable concentrations of gltucose oxidase were tused no lysis was observed. H202 either alone or in combination with azidle did not lyse erythrocytes.It is suggested that ADCC by 1)oth monocytes and neutrophils is partly dependent on the generation of hydroxyl ra(licals by the effector cells.

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“…Using a more sensitive and specific fluorometric assay (20) we found that monocytes release _20% of the amount of hydrogen peroxide generated by neutrophils. Several studies indicate that human monocytes also generate superoxide anions during phagocytosis (10,13 These findings may contribute to our understanding of monocyte function. Monocytes kill bacteria less efficiently than PMN (8,9,33).…”

Section: Discussionmentioning

confidence: 99%

“…With various stimulating agents, monocytes produced 20-70% of the chemiluminescence generated by neutrophils. Release of superoxide by monocytes amounted to -60% of the production by PMIN (13).…”

Section: Introductionmentioning

confidence: 99%

Differences in Oxygen Metabolism of Phagocytosing Monocytes and Neutrophils

Reiß¹,

Roos²

1978

J. Clin. Invest.

182

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A B S T R A C T The oxidative metabolism of monocytes and polymorphonuclear leukocytes from human peripheral blood was studied in resting and phagocytosing cells. Monocytes, like neutrophils, showed an increase in oxygen consumption during phagocytosis with a concurrent release of superoxide anions and hydrogen peroxide. Both oxygen products are highly reactive agents with potential bactericidal activity. Neutrophils consumed two and a half times as much oxygen, generated about twice as much superoxide, and released five times as much hydrogen peroxide as monocytes did. Monocytes generated superoxide and hydrogen peroxide at equivalent rates.Antimycin A, a specific mitochondrial respiratory chain inhibitor, depressed the oxygen consumption of monocytes by -70% but had no effect on neutrophil respiration. Therefore, the oxygen consumed by phagocytosing monocytes appeared to be metabolized in two distinct processes: =-30% of the oxygen is converted to hydrogen peroxide, whereas the remaining 70% is metabolized via the mitochondrial respiratory chain. The release of superoxide and hydrogen peroxide was unaffected by antimycin in either cell type.Phagocytosis of zymosan particles by monocytes was nearly abolished by antimycin, whereas no effect was noted with neutrophils. Thus, phagocytosis appears to be highly dependent on oxidative phosphorylation in monocytes but not in polymorphonuclear leukocytes. Moreover, in monocytes treated with antimycin, an addition of opsonized zymosan particles induced stimulation of the oxidative metabolism without occurrence of ingestion.

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Generation of superoxide anion and chemiluminescence by human monocytes during phagocytosis and on contact with surface-bound immunoglobulin G.

Cited by 220 publications

References 13 publications

Free Radicals and Detoxification Enzymes of Inflammatory Peritoneal Neutrophils and Macrophages.

Free Radicals and Detoxification Enzymes of Inflammatory Peritoneal Neutrophils and Macrophages.

Role of oxygen in antibody-dependent cytotoxicity mediated by monocytes and neutrophils.

Differences in Oxygen Metabolism of Phagocytosing Monocytes and Neutrophils

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