Demonstration of a specific neutrophil receptor for a cell-derived chemotactic factor.

Spilberg, Isaias; Mehta, J M

doi:10.1172/jci109282

Cited by 53 publications

(18 citation statements)

References 10 publications

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“…Colchicine, at concentrations of 10 (21). The data stummarized above would indicate the appearance of CCF in vivo in the synovial fluid of the animnals injected with MSU.…”

Section: Resultsmentioning

confidence: 86%

“…In the binding assays, 1 x 107 human PMN were incubated at 37°C in a total volume of 0.5 ml of Hanks' balanced saline solution, pH 7.4, which contained 0.1% bovine serum albumin (BSA) with either 125I-CCF (final concentration 0.24 J±M) or 1251-CCF and various concentrations of synovial fluid from the animals injected with either crystals, or FMLP which served as control. We have previously shown that FMLP does not compete with 125I-CCF for binding sites in the cell membrane (21). After 60 min of incubation, 0.5 ml ice-cold Hanks'-0.1% BSA solution was added, followed by centrifugation in a microfuge (model B, Beckman Instruments, Inc., Spinco Div., Palo Alto, Calif.) at 8,000 g for 2 min.…”

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confidence: 99%

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Mechanism of Action of Colchicine in Acute Urate Crystal-Induced Arthritis

et al. 1979

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A B S T R A C T Phagocytosis of urate crystals by human or rabbit neutrophils induces the synthesis and release of a glycoprotein, the crystal-induced chemotactic factor (CCF), which is chemotactically active both in vitro and in vivo. It has been proposed that CCF is a prime mediator of the acute gouty attack. Colchicine has been shown to decrease the production and release of this factor in vitro. In these studies, colchicine, at nonleukopenic doses, is shown to abrogate the acute arthritis induced by monosodium urate crystals in rabbits, but to have no effect upon the arthritis induced by the injection of the purified cell-derived chemotactic factor. Serum colchicine levels were 0.48-0.58 ,uM at 30 min and 0.12-0.3 AM at 90 min after intravenous injection of 0.2 mg/kg colchicine. Peripheral blood polymorphonuclear leukocytes obtained from colchicine-treated animals migrated normally towards a chemotactic stimulus but failed to produce CCF after phagocytosis of monosodium urate crystals. The dialyzed synovial fluid from rabbits injected with microcrystalline sodium urate contained chemotactic activity that was not present when animals were also given intravenous colchicine or injected intra-articularly with the chemotactic factor formyl-methionyl-leucyl-phenylalanine.Furthermore, the synovial fluid from rabbits injected with microcrystalline sodium urate significantly decreased 1251-CCF binding to neutrophils. The binding of '25I-CCF to its neutrophil receptor was not significantly reduced by the synovial fluid of colchicinetreated rabbits nor by the synovial fluid ofcontrol rabbits injected with the chemotactic factor formyl-methionylleucyl-phenylalanine. Colchicine (10 and 0.1 AM) was shown to have no effect upon the binding of 125I_CCF to its cell receptor.

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“…Colchicine, at concentrations of 10 (21). The data stummarized above would indicate the appearance of CCF in vivo in the synovial fluid of the animnals injected with MSU.…”

Section: Resultsmentioning

confidence: 86%

mentioning

confidence: 99%

Mechanism of Action of Colchicine in Acute Urate Crystal-Induced Arthritis

et al. 1979

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“…These responses are initiated by the binding of the chemoattractant to specific cell surface receptors (17,(22)(23)(24)(25)(26)(27) The amplitudes of these responses revealed a shallow perpendicular scattering coupled with a prominent transmission response. In addition, CB markedly attenuated the relaxation of the slow response upon fMet-Leu-Phe stimulation (Fig.…”

Section: Discussionmentioning

confidence: 99%

Rapid changes in light scattering from human polymorphonuclear leukocytes exposed to chemoattractants. Discrete responses correlated with chemotactic and secretory functions.

Yuli¹,

Snyderman²

1984

J. Clin. Invest.

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“…Whereas these assays often yield a great deal of information, they measure the end result of a complex series of events including the binding of chemotactic factors to the plasma membrane (20)(21)(22)(23)(24), the induction oftransmembrane signals (25,26), the reorganization of cytoskeletal elements (27), the assumption of an elongated, polarized configutation (19), and finally, actual cell movement. The measurement of chemotaxis in vitro, particularly by mononuclear cells, requires a lengthy assay period ranging from 60-90 min using even the quickest procedures (2) Depletion or enrichment of peroxidase-positive cells in mononuclear cell suspensions.…”

Section: Introductionmentioning

confidence: 99%

Monocyte Responsiveness to Chemotactic Stimuli is a Property of a Subpopulation of Cells that can Respond to Multiple Chemoattractants

Cianciolo¹,

Snyderman²

1981

J. Clin. Invest.

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A B S T R A C T The chemotactic migration of leukocytes is preceded by an alteration in the cells' shape from round to a characteristic polar configuration. We have developed an assay that shows that human monocytes, when exposed to chemoattractant in suspension, assume this polarized shape. The three types ofchemoattractants studied, a chemotactic lymphokine, complement-activated serum, and the N-formylated oligopeptides, all induced polarization in a time, temperature, and dose-dependent fashion.

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Demonstration of a specific neutrophil receptor for a cell-derived chemotactic factor.

Cited by 53 publications

References 10 publications

Mechanism of Action of Colchicine in Acute Urate Crystal-Induced Arthritis

Mechanism of Action of Colchicine in Acute Urate Crystal-Induced Arthritis

Rapid changes in light scattering from human polymorphonuclear leukocytes exposed to chemoattractants. Discrete responses correlated with chemotactic and secretory functions.

Monocyte Responsiveness to Chemotactic Stimuli is a Property of a Subpopulation of Cells that can Respond to Multiple Chemoattractants

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