Myeloperoxidase-Based Chemiluminescence of Polymorphonuclear Leukocytes and Monocytes

McNally, J. A.; Bell, Andrew S.

doi:10.1002/(sici)1099-1271(199603)11:2<99::aid-bio404>3.0.co;2-3

Cited by 42 publications

(16 citation statements)

References 15 publications

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“…Hydrogen peroxide, O 2 -. , and myeloperoxidase are implicated in CL generated by monocytes stimulated with PMA and fMLP (McNally and Bell, 1996). However, in our hands, CL induced by tumour cells was not dependent on hydrogen peroxide generation because catalase had no effect.…”

Section: Discussioncontrasting

confidence: 67%

Induction of reactive oxygen intermediates in human monocytes by tumour cells and their role in spontaneous monocyte cytotoxicity

et al. 1999

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SummaryThe present study examined the ability of human monocytes to produce reactive oxygen intermediates after a contact with tumour cells. Monocytes generated oxygen radicals, as measured by luminol-enhanced chemiluminescence and superoxide anion production, after stimulation with the tumour, but not with untransformed, cells. The use of specific oxygen radical scavengers and inhibitors, superoxide dismutase, catalase, dimethyl sulphoxide and deferoxamine as well as the myeloperoxidase inhibitor 4-aminobenzoic acid hydrazide, indicated that chemiluminescence was dependent on the production of superoxide anion and hydroxyl radical and the presence of myeloperoxidase. The tumour cell-induced chemiluminescent response of monocytes showed different kinetics from that seen after activation of monocytes with phorbol ester. These results indicate that human monocytes can be directly stimulated by tumour cells for reactive oxygen intermediate production. Spontaneous monocyte-mediated cytotoxicity towards cancer cells was inhibited by superoxide dismutase, catalase, deferoxamine and hydrazide, implicating the role of superoxide anion, hydrogen peroxide, hydroxyl radical and hypohalite. We wish to suggest that so-called 'spontaneous' tumoricidal capacity of freshly isolated human monocytes may in fact be an inducible event associated with generation of reactive oxygen intermediates and perhaps other toxic mediators, resulting from a contact of monocytes with tumour cells.

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Section: Discussioncontrasting

confidence: 67%

Induction of reactive oxygen intermediates in human monocytes by tumour cells and their role in spontaneous monocyte cytotoxicity

et al. 1999

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“…The level of reactive oxygen generated by phagocytes was assayed by CL measurements using lucigenin or luminol. Lucigenin-amplified CL predominantly monitors the initial O 2 Ϫ production, whereas luminol is a suitable substrate to measure reactions linked to the release of lysosomal MPO into the surrounding medium (2,19,23,43). Porin-treated PMN showed a reduction in luminol-enhanced CL when they were stimulated with zymosan, latex particles, gonococci, or cytochalasin B plus FMLP (Fig.…”

Section: Discussionmentioning

confidence: 99%

“…This CL reaction can be amplified by addition of the indicators luminol or lucigenin (4,14). These indicators measure different stages of the reaction since lucigenin reacts directly with O 2 Ϫ , whereas luminol-enhanced light emission is due to oxidation of luminol by oxygen derivatives resulting primarily from MPO-catalyzed reactions (16,19,23,43).…”

mentioning

confidence: 99%

Neisseria gonorrhoeaePorin Modifies the Oxidative Burst of Human Professional Phagocytes

et al. 2000

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A hallmark of infection with the gram-negative bacterium Neisseria gonorrhoeae is the local infiltration and subsequent activation of polymorphonuclear neutrophils. Several gonococcal outer membrane proteins are involved in the interaction with and the activation of these phagocytes, including gonococcal porin, the most abundant protein in the outer membrane. Previous work suggests that this porin plays a role in various cellular processes, including inhibiting neutrophils activation and phagosome maturation in professional phagocytes. Here we investigated the ability of porin to modify the oxidative metabolism of human peripheral blood neutrophils and monocytes in response to particulate stimuli (including live gonococci) and soluble agents. The activation of the oxidative metabolism was determined by chemiluminescence amplified with either luminol or lucigenin. We found that treatment of the phagocytes with porin inhibits the release of reactive oxygen species measured as luminol-enhanced chemiluminescence in response to zymosan, latex particles, and gonococci. The engulfment of these particles was not, however, affected by porin treatment. Similar effects of porin on the chemiluminescence response were observed in cytochalasin B-treated neutrophils exposed to the soluble chemotactic peptide N-formylmethionyl-leucyl-phenylalanine. This indicates that porin selectively inhibits granule fusion with those cellular membranes that are in direct contact with porin, namely, the phagosomal and plasma membranes. This porin-induced downregulation of oxidative metabolism may be a potent mechanism by which gonococci modulate oxygen-dependent reactions by activated phagocytes at inflammation sites.Professional phagocytes such as polymorphonuclear neutrophils (PMN) and peripheral blood monocytes play a crucial role in the host defense against infection with microorganisms.

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“…24 27 34 It has been shown that myeloperoxidase activity is also required for the luminol reaction, together with H 2 O 2 that is generated by the respiratory burst. [35][36][37] Isoluminol, however, does not penetrate neutrophils and so can be used to measure only reactive oxidants that are released from activated neutrophils. 31 32 Isoluminol was therefore used as a probe to determine extracellular release of reactive oxidants.…”

Section: Activation Of Primed and Unprimed Neutrophils By Immune Compmentioning

confidence: 99%

Insoluble and soluble immune complexes activate neutrophils by distinct activation mechanisms: changes in functional responses induced by priming with cytokines

Fossati

Bucknall²,

Edwards³

2002

Annals of the Rheumatic Diseases

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Background: Rheumatoid synovial fluid contains both soluble and insoluble immune complexes that can activate infiltrating immune cells such as neutrophils. Objectives: To determine if these different complexes activate neutrophils through similar or different receptor signalling pathways. In particular, to determine the circumstances which result in the secretion of tissue damaging reactive oxygen metabolites and granule enzymes. Methods: Blood neutrophils were incubated with synthetic soluble and insoluble immune complexes and the ability to generate reactive oxidants tested by luminescence or spectrophotometric assays that distinguished between intracellular and extracellular production. Degranulation of myeloperoxidase and lactoferrin was determined by western blotting. The roles of FcγRII (CD32) and FcγRIIIb (CD16) were determined by incubation with Fab/F(ab′) 2 fragments before activation. The effect of cytokine priming was determined by incubation with GM-CSF. Results: Insoluble immune complexes activated unprimed neutrophils, but most of the oxidants produced were intracellular. This activation required FcγRIIIb, but not FcγRII function. Soluble complexes failed to activate unprimed neutrophils but generated a rapid and extensive secretion of reactive oxygen metabolites when the cells were primed with granulocyte-macrophage colony stimulating factor (GM-CSF). This activity required both FcγRII and FcγRIIIb function. Insoluble immune complexes activated the release of granule enzymes from primed or unprimed neutrophils, but the kinetics of release did not parallel those of secretion of reactive oxygen metabolites. Only primed neutrophils released enzymes in response to soluble complexes. Conclusions: Soluble and insoluble immune complexes activate neutrophils by separate receptor signalling pathways. Profound changes in neutrophil responsiveness to these complexes occur after cytokine priming.

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Myeloperoxidase-Based Chemiluminescence of Polymorphonuclear Leukocytes and Monocytes

Cited by 42 publications

References 15 publications

Induction of reactive oxygen intermediates in human monocytes by tumour cells and their role in spontaneous monocyte cytotoxicity

Induction of reactive oxygen intermediates in human monocytes by tumour cells and their role in spontaneous monocyte cytotoxicity

Neisseria gonorrhoeaePorin Modifies the Oxidative Burst of Human Professional Phagocytes

Insoluble and soluble immune complexes activate neutrophils by distinct activation mechanisms: changes in functional responses induced by priming with cytokines

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