A new way for inducing a respiratory burst in guinea pig neutrophils

Rossi, Filippo; Bianca, Vittorina Della; Davoli, A.

doi:10.1016/0014-5793(81)81177-5

Cited by 21 publications

(3 citation statements)

References 21 publications

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“…Our results indicate that while the two events may be coupled, the increase in membrane depolarization is not a sine qua non for the enhancement of the oxidative burst induced by pretreatment with GM-CSF,h. These findings support the results of others (Della Bianca et al, 1983;Simchowitz and Spilberg, 1979;Rossi et al, 1981;Mottola and Romeo, 1982), as well as our own (Tauber and Simons, 19831, which have questioned the role of depolarization as an essential signal for activation of 0; anion generation.…”

Section: Discussionsupporting

confidence: 95%

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSF_rh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Sullivan¹,

Fredette²,

Leavitt³

et al. 1989

Journal Cellular Physiology

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When human granulocytes that have been primed with recombinant human granulocyte-macrophage colony-stimulating factor (GM-CSFrh) are activated by ligands that stimulate the respiratory burst, the amount of superoxide anion (O2-) they generate is significantly increased. We have found that the accelerated rate of O2- release occurring under these conditions is accompanied by an antecedent increase in membrane depolarization. We examined the nature of the enhancement of membrane depolarization in GM-CSFrh-primed granulocytes and investigated its relationship to the increase in O2- generation by N-formyl methionylleucylphenylalanine (fMLP)-activated granulocytes. We found that augmented depolarization could not be accounted for by a change in the resting membrane potential induced by the growth factor and was still present after either blocking passive transmembrane Na+ movement with dimethylamiloride or by increasing the membrane's permeability to K+ with valinomycin. When their ability to depolarize was virtually eliminated by dissipating the transmembrane K+ gradient, GM-CSFrh-pretreated cells continued to generate more O2- after fMLP than did control cells. These results indicate that augmentation of the granulocyte's ability to generate O2- anions, which is induced by priming with GM-CSFrh, is independent both of the resting transmembrane potential and of alterations in the extent of membrane potential change induced by stimuli such as fMLP.

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Section: Discussionsupporting

confidence: 95%

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSF_rh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Sullivan¹,

Fredette²,

Leavitt³

et al. 1989

Journal Cellular Physiology

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“…What could be the role of these voltage-gated currents in signal transduction in microglia? In granulocytes and neutrophils, reduction of K+ and Na+ gradients cause a rise in [Ca2+], that leads to oxidative burst (Rossi et al, 1981;Sullivan et al, 1989). Hyperpolarization of T lymphocytes by the application of a K' ionophore inhibits the rise in [Ca2+Ii caused by antigen receptor binding that leads to activation of the cell (Gray et al, 1987).…”

Section: Patterns Of Current Expression: Relation To Cell Morphologymentioning

confidence: 99%

Voltage‐gated currents expressed by rat microglia in culture

Korotzer

Cotman

1992

Glia

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Using the whole-cell patch-clamp technique, at least three types of voltage-gated currents expressed by cultured rat microglia were identified: an inward rectifier K+ current, a delayed rectifier K+ current (IK), and a Na+ current activated by depolarization. The inward rectifier conductance was activated by hyperpolarization to potentials more negative than -80 mV, depended on the external K+ concentration, and declined over time during whole cell recording, as the cell was internally dialyzed. The delayed rectifier current was activated by depolarization to potentials more positive than -40 mV and the rates of activation and deactivation showed a voltage-dependence similar to such currents seen in other preparations. An inward current possibly carried by Na+ was seen in a small percentage of cells. Recordings had been made from two morphological cell types, namely process-bearing ("ramified") and non-process-bearing ("ameboid"). Each of these currents was present in microglia of both morphological types. However, microglial morphology, which is thought to represent different states of activation, was significantly related to the types of combinations of currents expressed in a given cell.

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“…The respiratory response was measured as 02 consumption at 37°C with a Clark oxygen electrode as previously described (Rossi et al, 1981) using 1.5 x 107 neutrophils, unless otherwise indicated, suspended in the above medium supplemented with 5,ug of cytochalasin B/ml and 2mM-NaN3 in order to avoid the inactivation of the chemotactic peptide used as stimulus.…”

Section: Metabolic Studiesmentioning

confidence: 99%

Cyclic AMP inhibition of fMet-Leu-Phe-dependent metabolic responses in human neutrophils is not due to its effects on cytosolic Ca2+

Togni¹,

Cabrini²,

Virgilio³

1984

Biochemical Journal

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Cyclic AMP powerfully inhibits the fMet-Leu-Phe-dependent respiratory burst and exocytosis of azurophilic and specific granules without affecting Ca2+ release from intracellular stores. The elevation of [Ca2+]i induced by fMet-Leu-Phe is short-lived in cyclic AMP-treated cells and similar to that of untreated cells stimulated in the absence of external Ca2+. Nevertheless, in these latter cells fMet-Leu-Phe induces metabolic activation. We therefore suggest that the inhibitory action of cyclic AMP on neutrophil responses is not due to its effects on [Ca2+]i homoeostasis.

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A new way for inducing a respiratory burst in guinea pig neutrophils

Cited by 21 publications

References 21 publications

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSF_rh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSF_rh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Voltage‐gated currents expressed by rat microglia in culture

Cyclic AMP inhibition of fMet-Leu-Phe-dependent metabolic responses in human neutrophils is not due to its effects on cytosolic Ca2+

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A new way for inducing a respiratory burst in guinea pig neutrophils

Cited by 21 publications

References 21 publications

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSFrh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSFrh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Voltage‐gated currents expressed by rat microglia in culture

Cyclic AMP inhibition of fMet-Leu-Phe-dependent metabolic responses in human neutrophils is not due to its effects on cytosolic Ca2+

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Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSF_rh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production

Effects of recombinant human granulocyte‐macrophage colony‐stimulating factor (GM‐CSF_rh) on transmembrane electrical potentials in granulocytes: Relationship between enhancement of ligand‐mediated depolarization and augmentation of superoxide anion (O) production