Phagocytosis

Mudd, Stuart; McCutcheon, Morton; Lucké, Balduin

doi:10.1152/physrev.1934.14.2.210

Cited by 133 publications

(49 citation statements)

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“…Many previous reports on the mechanism of phagocytosis by polymorphonuclear leucocytes have stressed the importance of the surface properties of both particle and phagocyte (13). In most instances the ingestion of particles was thought to be solely a surface phenomenon in which the metabolism of the host cell played little or no role (14).…”

Section: Discussionmentioning

confidence: 99%

Functional and Metabolic Properties of Polymorphonuclear Leucocytes

Cohn

Morse

1960

The Journal of Experimental Medicine

190

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A previous report on the interaction between rabbit polymorphonuclear leucocytes and various bacterial species described methods whereby it was possible to evaluate quantitatively the localization and fate of the organisms (1). These techniques had certain advantages over the usual stained film methods in that they allowed the simultaneous estimation of both the rate of ingestion and intraleucocytic killing, over prolonged periods of time. This in dtro system seemed suited, therefore, for the evaluation of both the functional and metabolic activities of leucocytes under identical experimental conditions. This report will deal with (a) certain of the metabolic and opsonic requirements for the phagocytosis and intracellular destruction of bacteria, (b) the influence of particle ingestion on the metabolic activities of leucocytes, and (c) the influence of particle ingestion on the functional activities of the cells; i.e., phagocytosis and intracellular bactericidal mechanisms. The following paper will present similar studies on the effects of a lipopolysaccharide endotoxin. Materials and MethodsMedium.--The medium employed for both the phagocytic and metabolic studies consisted of a modified Hanks solution pH 7.4 (2), containing 0.01 per cent crystalline bovine serum albumin and 0.0056 M glucose (hereafter solution HBG1). Fresh normal rabbit serum was present in the majority of experiments at a final concentration of 10 per cent to supply opsonic factors necessary for phagocytosis. Any additions or omissions from this basic medium will be described in Results.Peritoneal Exudates.--The method employed for obtaining polymorphonuclear leucocytes from rabbit peritoneal exudates was described in detail in a previous pubfication (1). In brief, rabbits were injected intraperitoneally with 0.1 per cent glycogen suspended in pyrogen-free isotonic sodium chloride, and the exudate harvested 4 hours later. Such exudates contained *

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Section: Discussionmentioning

confidence: 99%

Functional and Metabolic Properties of Polymorphonuclear Leucocytes

Cohn

Morse

1960

The Journal of Experimental Medicine

190

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“…Of interest is the fact that it is inactive in the pH range (<6.5) that inhibits phagocytosis (13,14). One possibility that is difficult to exclude is that the macromolecular component of the exudate activator contains subpyrogenic quantities of endotoxin.…”

Section: Evidence That Activation Involves Synthesis Of Protein--thementioning

confidence: 99%

Studies on the Pathogenesis of Fever

Moore

Cheuk

Morton

et al. 1970

The Journal of Experimental Medicine

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Rabbit blood leukocytes ~ contain no detectable preformed pyrogen (4) and produce much less pyrogen than exudate leukocytes (about 1/50) when incubated in 0.15 ~ NaC1 (4). 3 After phagocytosis (5) or exposure to endotoxin (6), 3 on the other hand, they produce about the same or even greater amounts of pyrogen than exudate leukocytes. These findings suggest that blood leukocytes must be "activated" to release pyrogen in 0.15 ~ NaC1, and that activation of blood leukocytes automatically takes place after phagocytosis or exposure to endotoxin. The following experiments deal with the process of activation and the presence of an activating factor in acute peritoneal exudates. Materials and MethodsThe procedures used to exclude exogenous pyrogens (7), to prepare suspensions of leukocytes from both rabbit blood (4) and acute peritoneal exudates (7), to generate pyrogen from the cells (7), to assay the amount of pyrogen released (7,8), and to measure the cellular contents and fluid concentrations of Na and K (5, 9) and the fuid concentration of Ca (5, 9) and of protein (7) have all been previously described. Endotoxin (lipopolysaccharide B from Escherichia coli 011 l:B4) was purchased from Difco Laboratories, Detroit, Mich., and cycloheximide (Acti-dione), puromycin dihydrochloride, and acfinomycin D were obtained from Nutritional Biochemicals Corp., Cleveland, Ohio.

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“…Upon activation, human neutrophils exhibit increased oxygen consumption (1), phagocytosis (2), chemotaxis (3), degranulation (4), aggregation (5), and calcium mobilization (6). Three plasma polypeptides, C5a (5, 7), kallikrein (8-1 1), and Factor XIIa (12), which stimulate neutrophils, have been described.…”

Section: Introductionmentioning

confidence: 99%

Fibronectin degradation products containing the cytoadhesive tetrapeptide stimulate human neutrophil degranulation.

Wachtfogel

Abrams²,

Kucich³

et al. 1988

J. Clin. Invest.

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We investigated whether adhesive glycoproteins, such as fibronectin or fibrinogen, could function to provide a nidus for neutrophil degranulation. Elastase release in recalcified plasma was normal in afibrinogenemic plasma, but 73% less in plasma depleted of fibronectin. Proteolytic digests of fibronectin, but not intact fibronectin (50-1,000 gg/ml), induced a concentration-dependent release of neutrophil elastase and lactoferrin. MAbs N293, which recognized the mid-molecule of fibronectin, N294, which was directed toward the 11-kD cell adhesive fragment, and N295, generated against the amino terminal of the 11-kD fragment, inhibited the release of elastase by 7, 24, and 60%, respectively. The cytoadhesive tetrapeptide portion of fibronectin, Arg-Gly-Asp-Ser (250-1,000 pg/ml), released 1.94±0.10 jig/ml of elastase from 107 neutrophils, in contrast to the lack of release by the control hexapeptide, Arg-GlyTyr-Ser-Leu-Gly. Plasmin appeared to be the enzyme responsible for fibronectin cleavage, since neutrophil elastase release in plasma that had been depleted of plasminogen was decreased and reconstitution of plasminogen-deficient plasma with purified plasminogen corrected the abnormal release. Plasmin cleaved fibronectin to multiple degradation products, each < 200 kD. This fibronectin digest released 1.05 jig/ml of elastase from 107 neutrophils. We suggest that the activation of plasminogen leads to the formation of fibronectin degradation products capable of functioning as agonists for neutrophils.

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Phagocytosis

Cited by 133 publications

References 0 publications

Functional and Metabolic Properties of Polymorphonuclear Leucocytes

Functional and Metabolic Properties of Polymorphonuclear Leucocytes

Studies on the Pathogenesis of Fever

Fibronectin degradation products containing the cytoadhesive tetrapeptide stimulate human neutrophil degranulation.

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