Biochemical characteristics of phagocytosis in the P388 D1 cell

Goodell, Estelle M.; Bilgin, Suna; Carchman, Richard A.

doi:10.1016/0014-4827(78)90035-6

Cited by 20 publications

(4 citation statements)

References 16 publications

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“…The effect of prostaglandin E2 on 0 may be at least partially accounted for by a change in intracellular cAMP concentration. Furthermore, db-cAMP, which is sufficient to decrease fluidity, decreases phagocytosis of opsonized particles (Goodell et al, 1978).…”

Section: Discussionmentioning

confidence: 99%

Influence of immune complexes on macrophage membrane fluidity: a nanosecond fluorescence antisotropy study

Petty¹,

Niebylski²,

Francis³

1987

Biochemistry

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Time-resolved fluorescence anisotropy (TRFA) and steady-state anisotropy measurements and fluorescence intensification microscopic observations were made on RAW264 macrophages labeled with 1,6-diphenyl-1,3,5-hexatriene (DPH) or 1-[4-(trimethylammonio)phenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH). Microscopic analysis revealed that the fluorescent probe DPH was found in association with plasma membranes and small vesicles. Macrophages treated with immune complexes could not be distinguished from untreated cells, indicating that the same membrane compartments were labeled. The probe TMA-DPH was exclusively localized to the plasma membrane. Steady-state anisotropy measurements indicated that in vitro culture conditions did not significantly affect membrane fluidity. TRFA measurements were conducted to determine the physical properties of macrophage membranes during immune recognition and endocytosis. Data were analyzed by iterative deconvolution to yield phi, the rotational correlation time, and r infinity, the limiting anisotropy. These parameters may be interpreted as the "fluidity" and order parameter of the membrane environment, respectively. Typical values for untreated macrophages were phi = 7.8 ns and r infinity = 0.12. Binding and endocytosis of immune complexes prepared in 4-fold antigen excess increase these values to phi = 22.1 ns and r infinity = 0.15. However, receptor-independent phagocytosis of latex beads decreases these values to phi = 2.2 ns and r infinity = 0.10. Addition of catalase before, but not after, immune complex incubation with cells diminishes the effect upon membrane structure, suggesting that H2O2 participates in fluidity changes. Pretreatment of macrophages with the membrane-impermeable sulfhydryl blocker p-(chloromercuri)benzenesulfonic acid also diminished these effects.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 99%

Influence of immune complexes on macrophage membrane fluidity: a nanosecond fluorescence antisotropy study

Petty¹,

Niebylski²,

Francis³

1987

Biochemistry

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“…It seems likely that cAMP is a participant at some level in the combined ligand and epinephrine-mediated depression of phagocytosis. Several reagents that are known to elevate cAMP levels depress phagocytosis (Cox and Karnovsky, 1973;Lima et al, 1974;Goodell et al, 1978). Furthermore, phagocytosis stimulates increased levels of intracellular cAMP (Seyberth et al, 1973;Goodell et al, 1978).…”

Section: Potential Mechanismsmentioning

confidence: 99%

“…Several reagents that are known to elevate cAMP levels depress phagocytosis (Cox and Karnovsky, 1973;Lima et al, 1974;Goodell et al, 1978). Furthermore, phagocytosis stimulates increased levels of intracellular cAMP (Seyberth et al, 1973;Goodell et al, 1978). In the case of antibody-dependent phago-cytosis, the Fc receptor stimulates cAMP formation (Nitta and Suzuki, 1982).…”

Section: Potential Mechanismsmentioning

confidence: 99%

Combinative ligand‐receptor interactions: Epinephrine depresses RAW264 macrophage antibody‐dependent phagocytosis in the absence and presence of met‐enkephalin

Petty

Berg

1988

Journal Cellular Physiology

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Macrophages have been shown to possess cell surface receptors for opiates and catecholamines. The abilities of these ligands to affect RAW264 macrophage antibody-dependent effector activity directed against sheep red blood cells were tested. Phagocytosis was measured by the uptake of 51Cr labeled erythrocytes and optical microscopy. Cytolysis was measured by 51Cr-release assays. Met-enkephalin increased specific antibody-dependent phagocytosis in a dose-dependent fashion; the optimal dose was found to be 10(-8) M. Epinephrine diminished phagocytosis in a dose-dependent manner exhibiting a maximal inhibition at 10(-4)-10(-5) M. This inhibition can be blocked by propranolol. The combined effects of simultaneous treatment with met-enkephalin and epinephrine were measured. At the several doses tested, the combined effects of these two ligands on the amount of phagocytosis were equivalent to or more inhibitory than epinephrine alone. Thioglycolate-elicited murine peritoneal macrophages demonstrated similar responses to epinephrine, met-enkephalin, and their combination. Therefore, in vitro models more closely approximating in vivo neuroregulation of macrophage function demonstrate phagocytic inhibition.

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“…Cell Culture P388D1 macrophage-like cells (Koren et al, 1975;Snyderman et al, 1977;Goodell et al, 1978) were grown as adherent monolayers in 75-ml tissue culture flasks (Fal-con), with Dulbecco's modified Eagle's minimal essential medium (DMEM, Gibco) supplemented with 10% fetal calf serum (FCS, Gibco), 100 U/ml penicillin and 100 pg/ml streptomycin, and routinely subcultured by vigorous pipetting. For fibrin gel cultures, the cells were seeded into 35-mm fibrin-coated dishes (Falcon) and grown for 2-3 days before the start of the experiments.…”

Section: Preparation Of Three-dimensional Fibrin Gelsmentioning

confidence: 99%

Phorbol ester stimulates macrophage invasion of fibrin matrices

Castellucci

Montesano

1988

Anat. Rec.

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Macrophages migrate through a fibrin-rich extracellular matrix in chronic inflammation, wound healing, and other pathophysiological processes. To investigate the factors that might influence the ability of mononuclear phagocytes to invade fibrin matrices, we cultured macrophage-like P388D1 cells as well as resident and thioglycollate-elicited mouse peritoneal macrophages on three-dimensional fibrin gels, and we examined the effect of agents known to stimulate a variety of macrophage functions, including the production of fibrinolytic enzymes. Cells grown on fibrin gels under control conditions, as well as cells treated with either bacterial lipopolysaccharide or concanavalin A, remained confined to the gel surface. In contrast, the tumor promoter 4 beta-phorbol 12-myristate 13-acetate (PMA) induced both P388D1 cells and peritoneal macrophages to invade the underlying fibrin matrix. The invasive behavior of PMA-treated P388D1 cells was not affected by protease inhibitors of various specificities. These results demonstrate that certain exogenous signals can profoundly modify the ability of macrophages to migrate through fibrin matrices.

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Biochemical characteristics of phagocytosis in the P388 D1 cell

Cited by 20 publications

References 16 publications

Influence of immune complexes on macrophage membrane fluidity: a nanosecond fluorescence antisotropy study

Influence of immune complexes on macrophage membrane fluidity: a nanosecond fluorescence antisotropy study

Combinative ligand‐receptor interactions: Epinephrine depresses RAW264 macrophage antibody‐dependent phagocytosis in the absence and presence of met‐enkephalin

Phorbol ester stimulates macrophage invasion of fibrin matrices

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