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PubMed1977

Quantitative phagocytosis by human polymorphonuclear leucocytes. Use of radiolabelled emulsions to measure thae rate of phagocytosis.

A new micro-method for the quantitative measurement of phagocytosis by neutrophils is described. The material used for phagocytosis consists of a radioactive oil emulsion coated with E. coli lipopolysaccharide. Uptake of radioactive material is a function of cell number, duration of incubation, dilution of serum used for opsonization, content of lipopolysaccharide and concentration of emulsion. This method can be used to quantify rapidly and precisely phagocytosis rates of as few as 5 x 10(4)-10(6) polymorphonuclear leucocytes and the opsonic activity of 10 microliter serum.

Albumins↗

PubMed1984

Further studies on the application of the micromethod of phagocytosis using cadmium microcrystals as phagocytosis particles.

The use of Cd microcrystals together with a monolayer technique using small quantities of whole blood offers several advantages for routine studies of phagocytosis. The original method by Miler was especially minimized with regard to the necessary quantity of serum. Homologous serum was replaced by heterologous guinea-pig serum and the method was simplified by the omission of opsonization. A comparison of the stimulatory effect of inactivated and native serum as well as the inhibition of phagocytosis by trypan blue allows us to characterize Cd-phagocytosis as complement-dependent.

Cadmium↗

PubMed1970

Failure of Immune Sera to Enhance Significantly Phagocytosis of Staphylococus aureus: Nonspecific Adsorption of Phagocytosis-Promoting Factors.

Serum from rabbits immunized with either heat-killed or live nonencapsulated Staphylococcus aureus failed further to enhance phagocytosis and intracellular killing of the homologous organism by either normal rabbit polymorphonuclear leukocytes or monocytes, when compared with normal rabbit serum. These immune sera did, however, show an increase in agglutinating and precipitating antibody level. Adsorption of normal human serum with some gram-positive and gram-negative bacteria, yeast, and some inert particles significantly reduced the phagocytosis-promoting factors of the serum. It would seem, then, that nonencapsulated S. aureus differs from other pathogenic bacteria in that the humoral antibacterial factors promoting its phagocytosis and intracellular killing are not significantly enhanced by infection or immunization.

Journal Article↗

PubMed1982

The phagocytosis capacity assay: a new radiometric phagocytosis test for clinical use.

A radiometric technique is described for measuring phagocytosis which does not require separation of extra- and intracellular microorganisms. Following phagocytosis of optimally opsonized yeast cells (Saccharomyces cerevisiae) by mononuclear cells (MNC) or granulocytes, yeast cells remaining extracellular are labeled with [75Se]L-selenomethionine. To measure the phagocytic capacity of the cell population investigated, 1-4 x 10(6) leukocytes are incubated with 5, 10, 20, 30 and 40 x 10(6) yeast cells/ml for testing. Depending on the actual number of phagocytes in the cell populations investigated, different optimal yeast cell concentrations may be determined. Provided measurements are carried out at these optima even moderate effects of therapy can be detected. In a preliminary study of 22 patients with Hodgkin's disease it was shown, that the phagocytic activity of the MNC fraction was higher, but the activity of granulocytes lower, than that of the healthy controls. After combined chemotherapy the above mentioned values returned to normal. This simple, exact method is recommended for clinical use.

Granulocytes↗

PubMed1976

2-Deoxyglucose selectively inhibits Fc and complement receptor-mediated phagocytosis in mouse peritoneal macrophages II. Dissociation of the inhibitory effects of 2-deoxyglucose on phagocytosis and ATP generation.

Macrophages incubated in 2-deoxy-D-glucose (2-dG)-containing medium showed a marked decrease in cellular ATP content, and were unable to ingest IgG- and complement-coated erythrocytes via the corresponding membrane receptors for these ligands. However, the inhibitory effects of 2-dG on Fc- and C3 receptor-mediated phagocytosis were not a consequence of lowered macrophage ATP levels since addition of glucose or mannose to the culture medium restored the capacity of the macrophages to ingest IgG- and C3-coated particles without increasing ATP levels. These results indicate that Fc- and C3 receptor-mediated phagocytosis (opsonin dependent) differs qualitatively from the ingestion of latex and zymosan particles (opsonin independent); they suggest that the same regulatory molecules govern the responses of phagocytic cells to signals initiated by both the Fc and C3 receptors. The possibility that these molecules are regulated by glycosylation is discussed.

Adenosine Triphosphate↗

PubMed2005

Phagocytosis of Salmonella montevideo by human neutrophils: immune adherence increases phagocytosis, whereas the bacterial surface determines the route of intracellular processing.

Complement-opsonized particles become immune adherent to complement receptor 1 (CR1 or CD35) on human erythrocytes, allowing particles to be ingested by phagocytes in the liver and the spleen. We investigated the role that immune adherence plays in the uptake and killing of Salmonella montevideo by human neutrophils. Exposure to serum induced loss of flagella and facilitated immune adherence, which was followed by more-efficient phagocytosis and killing, compared with that after exposure to serum-opsonized, free bacteria. One correlate of bacterial killing is the fusion of phagosomes with lysosomes, which can be monitored by Lyso-Tracker or lysosomal-associated membrane protein 2 colocalization with the intracellular bacteria. At 5 min, phagolysosmal fusion was significantly faster for immune-adherent bacteria than for non-immune-adherent bacteria, but, by 35 min, the difference between the 2 groups was minimal. Immune adherence also facilitated the ingestion of antibody complement-opsonized fluorescent microspheres, but, unlike bacteria, most internalized microspheres failed to fuse with lysosomes. However, addition of lipopolysaccharide, a Toll-like receptor ligand, to microspheres directed their intracellular trafficking, resulting in rapid lysosomal fusion. Thus, immune adherence facilitates phagocytosis, but the route of intracellular processing depends on the molecular nature of the target and is independent of host complement and antibody.

Bacterial Adhesion↗

PubMed1989

Myelin phagocytosis by peritoneal macrophages in organ cultures of mouse peripheral nerve. A new model for studying myelin phagocytosis in vitro.

Organ cultures of degenerating nerve fascicles were exposed to cultured macrophages obtained by peritoneal lavage. Invasion of the nerve fascicle by phagocytes was shown by prelabeling with carbon and with electron microscopy. There was massive active phagocytosis of degenerating myelin sheaths. The invading phagocytic cell population was identified as Fc receptor-positive, Mac-1-positive macrophages by immunocytochemistry. The Schwann cell population persisted without significant myelin phagocytosis. The vitality of the Schwann cell population was shown by subsequent reimplantation of the organ cultures into host animals. The reimplants had retained their ability to remyelinate regenerating axon sprouts. These observations were made in cultures exposed to cytostatic agents. If cytostatic agents were omitted, there was proliferation of endogenous phagocytes in the nerve fascicles without added peritoneal cells. These endogenous phagocytes were identified as proliferating resident monocytes and were positive for the Fc receptor and Mac-1 markers. This model allows studies on how monocytes recognize and digest degenerating myelin apart from surviving Schwann cells.

Animals↗

PubMed2005

CCR7 ligand-enhanced phagocytosis of various antigens in mature dendritic cells-time course and antigen distribution different from phagocytosis in immature dendritic cells.

CC chemokine receptor 7 (CCR7) is selectively expressed on mature dendritic cells (DC). The CCR7 ligands, CC chemokine ligand (CCL) 19 and CCL21, facilitate migration of mature DC from the peripheral tissues to regional lymph nodes. We previously demonstrated that CCR7 ligands induced rapid receptor-mediated endocytosis of dextran in mature DC. In the present study, we further examined the effects of CCR7 ligands on endocytosis of other kinds of antigen, mannosilated bovine serum albumin (Mann-BSA), Escherichia coli(E. coli), or ovalbumin-containing immune complex (OVA-IC), by mature DC. We found that CCR7 ligands enhanced the endocytosis of Mann BSA, E. coli, and OVA-IC in mature DC but not in immature DC. The endocytosis of BSA was not enhanced by CCR7 ligands. Furthermore, the phagocytosis of OVA-IC was significantly inhibited by anti-Fcgamma receptor III/II antibody. These results demonstrate that CCR7 ligands enhance only receptor-mediated endocytosis by mature DC. When rapidly phagocytosed E. coli were traced in CCL19-treated mature DC, most of the phagocytosed E. coli did not colocalize with the lysosomal marker: lysosome-associated membrane protein-1 (Lamp-1), whereas most of E. coli taken up relatively slowly by immature DC colocalized with Lamp-1. These results suggest that phagocytosis of antigens by immature and mature DC plays different functional roles.

Animals↗

PubMed1991

Fluorescence assay to monitor phagocytosis by blood-clot derived polymorphonuclear leucocytes. 1. Study of patients with diabetes and phagocytosis of different staphylococcal species.

A recently developed simple and rapid fluorescence assay of phagocytosis by polymorphonuclear leucocytes (PMNs) was used to compare the phagocytic activity of PMNs from diabetic patients and healthy people. Differences in phagocytosis have been described in these systems. Different bacterial strains were used to challenge the phagocytic capabilities of bacterial ingestion and killing for both patient and control groups. Staphylococcus epidermidis derived from clinical isolates was prone to faster ingestion and more rapid killing once the bacteria were intracellular, compared with S. epidermidis derived from normal skin. The pathogen, S. aureus, though ingested rapidly, was not so easily killed. PMNs from diabetics appeared to ingest S. aureus and kill ingested pathogenic bacteria not as effectively as PMNs from healthy volunteers. These difference were not found for non-pathogenic skin isolates of S. epidermidis.

Blood Coagulation↗

PubMed1984

[Current theories of phagocytosis and methodological problems in the study of phagocytosis defects in diabetics].

The process of phagocytosis on bacteria is described: recognition of the bacterium by C3b- and Fc-receptors and possibly lektin-like substances on PMN surfaces; ingestion by an actin-myosin interaction in a local Ca++ gradient; simultaneous activation of a NADPH-oxidase and oxidative attack of the bacterial membrane. Special aspects: opsonization, dependence of the rate of phagocytosis on day-time, conditions of diabetics.

Actins↗

PubMed1983

Cytophilic receptors for foreignness and some factors which influence phagocytosis by invertebrate leucocytes: in vitro phagocytosis by amoebocytes of the snail Lymnaea stagnalis.

By means of in vitro phagocytosis it was demonstrated that macrophage-like blood cells of an invertebrate (amoebocytes of the pond snail Lymnaea stagnalis) possess cytophilic receptors for foreignness. These receptors are lectin molecules which are reversibly bound to the surface of the cells. Phagocytosis is dependent, beyond recognition of foreignness, on temperature and pH, and on the feeding condition of the snails.

Agglutinins↗

PubMed1996

CR3 (alphaM beta2; CD11b/CD18) restores IgG-dependent phagocytosis in transfectants expressing a phagocytosis-defective Fc gammaRIIA (CD32) tail-minus mutant.

Previous studies have suggested that complement receptors cooperate with Fc receptors to mediate Ab-dependent effector functions. In the present study, we tested the capacity of complement receptor type 3 (CR3; alphaM beta2; CD11b/CD18) to participate in Fc gammaRIIA (CD32)-mediated phagocytosis. To test this hypothesis, we transfected a phagocytosis-defective tail-minus mutant of Fc gammaRIIA into fibroblasts that did or did not express CR3. As controls, cells exposed to the transfection protocol but not expressing either CR3 or Fc gammaRIIA constructs were also selected. Expression of cell surface receptors was confirmed by both flow cytometry and fluorescence microscopy. Cells were tested for their ability to bind and internalize IgG-opsonized erythrocytes and for surface proximity of CR3 and Fc gammaRIIA using resonance energy transfer techniques. Resonance energy transfer studies showed a physical proximity between CR3 and Fc gammaRIIA on cell surfaces. Cells expressing only the tail-minus mutant of Fc gammaRIIA were unable to internalize erythrocytes but showed significant binding ability. In contrast, cells expressing both mutant Fc gammaRIIA and CR3 internalized opsonized erythrocytes. These results show that CR3 can complement the phagocytic function of defective Fc gammaRIIA. These data suggest that CR3 is capable of transducing a phagocytic signal generated by Fc gammaRIIA recognition events that mediates internalization of IgG-opsonized targets.

3T3 Cells↗

PubMed1986

Phagocytosis of latex particles by leucocytes. I. Dependence of phagocytosis on the size and surface potential of particles.

A series of latex particles, having different sizes and surface structures, were prepared and the dependence of phagocytosis of latex particles by leucocytes on the particle size and surface potential was investigated by measuring the oxygen consumption of leucocytes. Most of the phagocytic behaviour in the initial stages can be explained by susceptibility of particles to heterocoagulation i.e. attachment of small particles (latex particles) onto large particles (leucocytes) by the colloidal attractive force between the two kinds of particles. Specific behaviour for fine particles seems to be attributed to the contribution of steric stabilization by the hydrated layer on the particle surface and to the inability for the leucocytes to recognize very fine particles as foreign materials.

Humans↗

PubMed2006

The Osler slide, a demonstration of phagocytosis from 1876 Reports of phagocytosis before Metchnikoff's 1880 paper.

Recently at the Medical Historical Museum of McGill University, Dr. Rick Fraser discovered a microscope slide prepared in 1876 from the lung of a patient with pneumoconiosis. Photomicrographs show the presence of coal dust particles in alveolar cells. This case and several related ones had been reported in 1875 by William Osler, who also had demonstrated the cellular uptake of carbon particles in kittens injected with India ink. In 1869 a Philadelphia physician described the uptake of bacteria by leukocytes in saliva and urine. Both investigators postulated a protective role for this cellular phenomenon. Neither of these reports has been generally cited in histories of immunology. These two papers are summarized here along with a short review of other reports describing phagocytosis which predating Metchnikoff's entrance into the field.

Allergy and Immunology↗

PubMed2005

Light-induced oxidation of photoreceptor outer segment phospholipids generates ligands for CD36-mediated phagocytosis by retinal pigment epithelium: a potential mechanism for modulating outer segment phagocytosis under oxidant stress conditions.

Clearance by the retinal pigment epithelium (RPE) of shed photoreceptor outer segments (OSs), a tissue with one of the highest turnover rates in the body, is critical to the maintenance and normal function of the retina. We hypothesized that there is a potential role for photo-oxidation in OS uptake by RPE via scavenger receptor-mediated recognition of structurally defined lipid peroxidation products. We now demonstrate that specific structurally defined oxidized species derived from arachidonyl, linoleoyl, and docosahexanoyl phosphatidylcholine may serve as endogenous ligands on OSs for uptake by RPE via the scavenger receptor CD36. Mass spectrometry studies of retinal lipids recovered from dark-adapted rats following physiological light exposure demonstrate in vivo formation of specific oxidized phosphatidylcholine molecular species possessing a CD36 recognition motif, an oxidatively truncated sn-2 acyl group with a terminal gamma-hydroxy(or oxo)-alpha,beta-unsaturated carbonyl. Cellular studies using RPE isolated from wild-type versus CD36 null mice suggest that CD36 plays a role in engulfment, but not initial binding, of OSs via these oxidized phospholipids. Parallel increases in OS protein-bound nitrotyrosine, a post-translational modification by nitric oxide (NO)-derived oxidants, were also observed, suggesting a possible role for light-induced generation of NO-derived oxidants in the initiation of OS lipid peroxidation. Collectively, these studies suggest that intense light exposure promotes "oxidative tagging" of photoreceptor outer segments with structurally defined choline glycerophospholipids that may serve as a physiological signal for CD36-mediated phagocytosis under oxidant stress conditions.

Animals↗

PubMed1976

Inhibition of phagocytosis by cryptococcal polysaccharide: dissociation of the attachment and ingestion phases of phagocytosis.

The effects of cryptococcal polysaccharide and selected serum factors on (i) the attachment of Cryptococcus neoformans to macrophages and (ii) the subsequent ingestion of yeast cells by the macrophages were investigated. Percent attachment was measured after incubation of yeast cells with macrophages at 4 C. Percent engulfment was determined after incubation of yeast cells and macrophages at 37 C. Nonencapsulated yeast cells readily attached to macrophages at the low temperature and were engulfed at a high rate at 37 C, whereas encapsulated yeast cells attached to macrophages at low rates and were engulfed at low rates. Addition of varying doses of purified cryptococcal polysaccharide to nonencapsulated yeast cells inhibited attachment at approximately the same concentration of polysaccharide required for inhibition of engulfment. Nonencapsulated yeast cells that attached to macrophages at 4 C were eluted from the macrophages by addition of purified cryptococcal polysaccharide to the incubation medium. Heat-labile opsonins were not required for attachment of yeast cells to macrophages, but they were necessary for maximal initial rates of phagocytosis. Heat-stable components of serum facilitated attachment of cryptococci, but their most important function appeared to be triggering the ingestion of attached yeast. Specific antiserum had no effect on the attachment and engulfment of nonencapsulated cryptococci, and the antiserum produced only a small enhancement of the engulfment of encapsulated cryptococci.

Animals↗

PubMed1980

Platelet-activating factor in anaphylaxis and phagocytosis. I. Release from human peripheral polymorphonuclears and monocytes during the stimulation by ionophore A23187 and phagocytosis but not from degranulating basophils.

Platelet-activating factor (PAF) is a mediator of a anaphylaxis found initially in basophils and later in mouse and rat macrophages. The purpose of this paper was to determine the cellular origin of PAF released from human leucocytes and to establish if phagocytosis is a more important stimulus for PAF release than anaphylactic reactions. Phagocytic leucocytes (monocytes and PMNs) released PAF, physicochemically analogous to the PAF obtained by anaphylactic reactions in rabbits when challenged with zymosan, zymosan coated with complement, immune complexes, immunoglobulin aggregates or calcium ionophore A23187. Basophils failed to release PAF by anti-human IgE antibody, although positive degranulation and histamine liberaton were found. Pre-incubation of phagocytosing leucocytes with cytochalasin B or colchicine produced a diminution of PAF release, whereas beta-glucuronidase liberation was increased. The addition of carboxypeptidase B did not significantly modify PAF or beta-glucuronidase release. These data indicate that PAF obtained from preparations of human leucocytes comes from monocytes and polymorphonuclears; human basophils do not liberate measurable quantities of PAF, either by anaphylactic stimulus or by neutrophil cationic proteins; liberation of PAF and lysosomal content follow different mechanisms as they have different kinetics and are modified in an opposite way by drugs acting on the cytoskeleton.

Anaphylaxis↗

PubMed1981

Phagocytosis of Serratia marcescens by leukocytes of fresh defibrinated human blood: failure of "natural" human specific anti-O IgG antibodies to enhance phagocytosis.

Defibrination of fresh, peripheral, venous blood from three human adult volunteers resulted in the removal of from 1/5 to 1/2 of leukocytes, as compared with EDTA-anticoagulated aliquots from identical blood samples. However, differential white blood cell proportions were altered only marginally. Bacterial inocula (approximately 1.5 X 10(4) bacteria/ml at 0 time) of selected assay strains of Serratia marcescens were killed by 65 vol% of fresh, defibrinated human blood to the extent of greater than or equal to 97% within 2 hours after exposure, regardless of serum susceptibility or -resistance of the test strains. The addition of 25 vol% of either undiluted or 1:2 diluted commercially available, intravenously applicable, human IgG immunoglobulin preparations. (Gamma-Venin, Sandoglobulin) ot 65 vol% of fresh, defibrinated blood from all three human volunteers failed to enhance combined phagocytic and serum bactericidal activity against all assay strains of S. marcescens examined, despite documented O-agglutinin activity of the IgG immunoglobulin preparations against the majority of the test strains. It was concluded tentatively that "natural" human specific anti-O IgG antibodies failed to enhance phagocytosis in this in vitro system.

Agglutinins↗