Priming of Phosphatidic Acid Production by Staurosporine in f-Met-Leu-Phe-Stimulated Human Neutrophils—Correlation with Respiratory Burst

Rais, Samira; Pédruzzi, Eric; Dang, My-Chan; Giroud, Jean‐Paul; Hakim, Jacques; Périanin, Axel

doi:10.1016/s0898-6568(97)00116-2

Cited by 22 publications

(20 citation statements)

References 57 publications

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“…Staurosporine, a serine/threonine protein kinase and PKC inhibitor, was found to increase both fMLP-stimulated O 2 Ϫ generation and PtdIns(3,4,5)P 3 accumulation to levels equal to or higher than those observed with TNF-␣ priming. This rather surprising "priming" effect of staurosporine has also been observed by other workers (27); however, the mechanism remains to be defined. More importantly, the lack of inhibition observed with radicicol, a selective tyrosine kinase inhibitor that lacks activity against the G␤␥-regulated PI3-kinase (28) but abolished p85-regulated PI3-kinase activity in BTSM cells (Fig.…”

Section: Figuresupporting

confidence: 77%

“…Genistein was effective only at concentrations Ͼ10 M, suggesting that its effect may be due to inhibition of alternative (nontyrosine) kinases. Staurosporine is a broad-spectrum serine/threonine protein kinase and protein kinase C (PKC) inhibitor that has the paradoxical ability to augment rather than inhibit agonist-stimulated respiratory burst activity in neutrophils (27) . Fig.…”

Section: )P 3 Generationmentioning

confidence: 99%

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Regulation of Phosphatidylinositol 3-Kinase Activity and Phosphatidylinositol 3,4,5-Trisphosphate Accumulation by Neutrophil Priming Agents

Cadwallader

Condliffe

McGregor

et al. 2002

The Journal of Immunology

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Neutrophil priming by agents such as TNF-α and GM-CSF causes a dramatic increase in the response of these cells to secretagogue agonists and affects the capacity of neutrophils to induce tissue injury. In view of the central role of phosphatidylinositol 3-kinase (PI3-kinase) in regulating NADPH oxidase activity we examined the influence of priming agents on agonist-stimulated phosphatidylinositol 3,4,5-trisphosphate (PtdIns(3,4,5)P3) accumulation in human neutrophils. Pretreatment of neutrophils with TNF-α or GM-CSF, while not influencing fMLP-stimulated PtdIns(3,4,5)P3 accumulation at 5 s, caused a major increase in PtdIns(3,4,5)P3 at later times (10–60 s), which paralleled the augmented superoxide anion (O2−) response. The intimate relationship between PtdIns(3,4,5)P3 accumulation and O2− release was confirmed using platelet-activating factor, which caused full but transient priming of both responses. Likewise, LY294002, a PI3-kinase inhibitor, and genistein, a tyrosine kinase inhibitor, caused parallel inhibition of O2− generation and PtdIns(3,4,5)P3 accumulation; in contrast, radicicol, which inhibits receptor-mediated activation of p85 PI3-kinase, had no effect on either response. Despite major increases in PI3-kinase activity observed in p85 and anti-phosphotyrosine immunoprecipitates in growth factor-stimulated smooth muscle cells, no such increase was observed in primed/stimulated neutrophils. In contrast, both fMLP and TNF-α alone caused a 3-fold increase in PI3-kinase activity in p110γ PI3-kinase immunoprecipitates. p21ras activation (an upstream regulator of PI3-kinase) was unaffected by priming. These data demonstrate that timing and magnitude of PtdIns(3,4,5)P3 accumulation in neutrophils correlate closely with O2− generation, that PI3-kinase-γ is responsible for the enhanced PtdIns(3,4,5)P3 production seen in primed cells, and that factors other than activation of p21ras underlie this response.

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Section: Figuresupporting

confidence: 77%

Section: )P 3 Generationmentioning

confidence: 99%

Regulation of Phosphatidylinositol 3-Kinase Activity and Phosphatidylinositol 3,4,5-Trisphosphate Accumulation by Neutrophil Priming Agents

Cadwallader

Condliffe

McGregor

et al. 2002

The Journal of Immunology

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“…Human blood was preferred to that of mice since it is suitable for the purification of large numbers of leukocytes for further investigation of drug effects in vitro. Among leukocytes, PMN were chosen for further study of the Sbb effect, since this cell type is a suitable model for clarifying the mode of action of drugs (11,13,24,26). In addition, PMN were reported to ingest L. major in vivo and to control the parasite load (21).…”

Section: Resultsmentioning

confidence: 99%

“…One of these, staurosporine, is a bacterial alkaloid known as a potent inhibitor of PKC. This agent also stimulates G protein (19) and phospholipase D (PLD) activity (19,24) and primes fMLP-induced PLD activity in a manner that is correlated with the respiratory burst of PMN (26). Another agent, okadaic acid, an inhibitor of protein phosphatase 2A, also primes PLD activity (13) and respiratory bursts (12).…”

Section: Discussionmentioning

confidence: 99%

“…Human venous blood, heparinized at 10 U/ml, was obtained from healthy volunteers. PMN were isolated by a first-step sedimentation of whole blood on 2% dextran T500 followed by centrifugation of the granulocyte-rich supernatant on a cushion of a mixture of Ficoll and Hypaque (Eurobio, Les Ulis, France) as previously described (26). The purified PMN (97%) were subjected to hypotonic lysis, washed, and resuspended in Hanks balanced salt solution (HBSS) (pH 7.4) containing 10 mM HEPES.…”

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confidence: 99%

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Sodium Stibogluconate (Pentostam) Potentiates Oxidant Production in Murine Visceral Leishmaniasis and in Human Blood

Rais

Périanin

Lenoir

et al. 2000

Antimicrob Agents Chemother

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Sodium stibogluconate (Sbb), a leishmanicidal drug, was studied for its in vivo effect on the formation of reactive oxygen species (ROS), assessed by chemiluminescence (CL) in the whole blood of mice infected with Leishmania infantum. Stimulation of ROS formation induced ex vivo by zymosan particles or the protein kinase C activator phorbol myristate acetate (PMA) was reduced by approximately 25% (P < 0.05) after infection of mice. Treatment of infected mice with Sbb (50 to 400 mg/kg of body weight) enhanced the blood CL induced by zymosan and PMA (47 to 96%, P < 0.01). The drug potentiation effect also occurred in uninfected mice. In vitro treatment of normal human blood with Sbb (1, 10, or 100 g/ml) for 1 h primed the CL response to PMA (29 to 54%). The priming effect of Sbb was also observed on the production of superoxide by isolated polymorphonuclear leukocytes stimulated either by PMA and zymosan or by the chemoattractants N-formylMet-Leu-Phe and platelet-activating factor. These data provide the first evidence of priming of the phagocyte respiratory burst by Sbb. This novel property of Sbb may contribute to the drug's leishmanicidal effect.

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Response of cyclic AMP by DMSO differentiated HL‐60 cells exposed to electric interferential current after prestimulation

Sontag¹

2004

Bioelectromagnetics

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The action of interferential current (IFC) upon intracellular content of cyclic adenosine monophosphate (cAMP) after prestimulation with the chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (fMLP) has been investigated. Human promyelocytes (HL-60) differentiated to granulocytes by dimethylsulphoxide (DMSO) have been treated with different concentrations of fMLP. This enhances their cAMP content. The half maximal effective concentration (EC50) was about 4 nM. Exposure to IFC with modulation frequencies of 35 and 125 Hz (5 min, 250 microA/cm2) after prestimulation with various concentrations of fMLP had no enhancing effect at low or high concentrations of fMLP. In contrast, at medium concentrations in the range of about 100 pM fMLP, a significant enhancement of cAMP could be observed. This synergistic effect of fMLP and IFC has been examined in detail by varying the modulation frequency, current density, and exposure time. Enhancement of cAMP content could be observed at certain modulation frequencies and exposure times suggesting a window effect, whereas for the current density in the range measured (8.5 microA/cm2-2.5 mA/cm2) a constant enhancement could be observed. The synergistic effect of fMLP and IFC could only be observed in the treatment sequence of fMLP followed by IFC; an inverse sequence had no effect on the cAMP content. .

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Priming of Phosphatidic Acid Production by Staurosporine in f-Met-Leu-Phe-Stimulated Human Neutrophils—Correlation with Respiratory Burst

Cited by 22 publications

References 57 publications

Regulation of Phosphatidylinositol 3-Kinase Activity and Phosphatidylinositol 3,4,5-Trisphosphate Accumulation by Neutrophil Priming Agents

Regulation of Phosphatidylinositol 3-Kinase Activity and Phosphatidylinositol 3,4,5-Trisphosphate Accumulation by Neutrophil Priming Agents

Sodium Stibogluconate (Pentostam) Potentiates Oxidant Production in Murine Visceral Leishmaniasis and in Human Blood

Response of cyclic AMP by DMSO differentiated HL‐60 cells exposed to electric interferential current after prestimulation

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