scholarly journals Phagocytosis in human platelets: localization of acid phosphatase- positive phagosomes following latex uptake

Blood ◽  
1976 ◽  
Vol 47 (5) ◽  
pp. 833-840 ◽  
Author(s):  
JC Lewis ◽  
JE Maldonado ◽  
kg Mann
Keyword(s):  
Acid Phosphatase ◽  
Polymorphonuclear Leukocytes ◽  
Open Channel ◽  
Human Platelets ◽  
Channel System ◽  
Latex Particles ◽  
Phagocytic Process ◽  
Progressive Accumulation

Abstract Incubation of human platelets in plasma containing a suspension of latex particles for 1–90 min resulted in progressive accumulation of particles in the open-channel system, followed by localization of latex in electron-opaque vacuoles. After 60 min, acid phosphatase was localized within latex-containing vacuoles. The periodate-alkaline- bismuth reaction intensely stained external membranes and membranes of the open-channel system. Membranes of latex-containing organelles were not stained. Latex phagocytosis was independent of both anticoagulant choice and aspirin effects. Our results indicate that the platelet can act as a true phagocyte, and we suggest that the phagocytic process is chronologically similar to that reported for polymorphonuclear leukocytes.

scholarly journals Phagocytosis in human platelets: localization of acid phosphatase- positive phagosomes following latex uptake

Blood ◽  
1976 ◽  
Vol 47 (5) ◽  
pp. 833-840 ◽  
Author(s):  
JC Lewis ◽  
JE Maldonado ◽  
kg Mann
Keyword(s):  
Acid Phosphatase ◽  
Polymorphonuclear Leukocytes ◽  
Open Channel ◽  
Human Platelets ◽  
Channel System ◽  
Latex Particles ◽  
Phagocytic Process ◽  
Progressive Accumulation

Incubation of human platelets in plasma containing a suspension of latex particles for 1–90 min resulted in progressive accumulation of particles in the open-channel system, followed by localization of latex in electron-opaque vacuoles. After 60 min, acid phosphatase was localized within latex-containing vacuoles. The periodate-alkaline- bismuth reaction intensely stained external membranes and membranes of the open-channel system. Membranes of latex-containing organelles were not stained. Latex phagocytosis was independent of both anticoagulant choice and aspirin effects. Our results indicate that the platelet can act as a true phagocyte, and we suggest that the phagocytic process is chronologically similar to that reported for polymorphonuclear leukocytes.

Increased Protein Synthesis by Human Platelets during Phagocytosis of Latex Particles in Vitro

1976 ◽  
Vol 35 (02) ◽  
pp. 350-357 ◽  
Author(s):  
Hana Bessler ◽  
Galila Agam ◽  
Meir Djaldetti
Keyword(s):  
Protein Synthesis ◽  
Fold Increase ◽  
Human Platelets ◽  
Polystyrene Latex ◽  
Latex Particles ◽  
The Third ◽  
Platelet Protein ◽  
Dose Dependent ◽  
Phagocytotic Activity

SummaryA three-fold increase of protein synthesis by human platelets during in vitro phagocytosis of polystyrene latex particles was detected. During the first two hours of incubation, the percentage of phagocytizing platelets and the number of latex particles per platelet increased; by the end of the third hour, the first parameter remained stable, while the number of latex particles per cell had decreased.Vincristine (20 μg/ml of cell suspension) inhibited platelet protein synthesis. This effect was both time- and dose-dependent. The drug also caused a decrease in the number of phagocytizing cells, as well as in their phagocytotic activity.

The Influence of Ascorbic Acid on Platelet Structure and Function

1975 ◽  
Vol 34 (01) ◽  
pp. 050-062
Author(s):  
Dale H Cowan ◽  
Richard C Graham ◽  
Patricia Shook ◽  
Ronda Griffin
Keyword(s):  
Ascorbic Acid ◽  
Open Channel ◽  
Channel System ◽  
Short Intervals ◽  
Platelet Survival ◽  
Artifactual Changes ◽  
Survival Studies ◽  
And Function ◽  
Induced Aggregation ◽  
Platelet Structure

SummaryTo determine the effect on platelet behavior of transient exposure of platelets to ascorbic acid, studies of platelet function and ultrastructure were done before exposure to ascorbic acid at pH 6.5, during exposure to pH 6.5, and after restoration of pH to pre-acidifìcation levels. The effect of ascorbic acid (A. A.) was compared to that of HCl and citric acid (C. A.). ADP- and collagen-induced aggregation of normal platelets were significantly impaired by both A. A. and C. A. but were less affected by HCl. The release of 14C-serotonin was significantly reduced by each agent. The ultra-structure of normal platelets brought to pH 6.5 by A.A. was normal. After neutralization, there was marked dilatation of the open channel system and loss of the disc shape. When platelets were brought to pH 6.5 by A. A., then neutralized, the aggregates which formed after stimulation by ADP or collagen were smaller than normal, the platelets were less closely approximated, and degranulation was less complete. The data show that exposure of platelets to ascorbic acid for short intervals impairs their function when measured after restoration of pH to levels compatible with maximal responses. Platelet survival studies using autologous platelets labelled with 51Cr in the presence or absence of ascorbic acid showed that the recovery of normal platelets was unaffected by ascorbic acid, whereas recovery of platelets from patients with idiopathic thrombocytopenic purpura, idiopathic thrombocythemia, and alcohol-related thrombocytopenia was markedly reduced. The injury resulting from the use of ascorbic acid in preparing platelets for studies of platelet survival in patients with disorders affecting platelets may impair the recovery of the cells, resulting in artifactual changes in the survival studies.

scholarly journals Ultrastructural Study of Platelet Aggregation by Mouse 15091A Tumor Cells

1977 ◽  
Author(s):  
G.J. Stewart ◽  
R.A. Kuprionas ◽  
G.J. Gasic ◽  
J. Catalfamo ◽  
G.P. Gasic
Keyword(s):  
Platelet Aggregation ◽  
Tumor Cells ◽  
Lysosomal Enzymes ◽  
Culture Medium ◽  
Open Channel ◽  
Channel System ◽  
Transmission Electron ◽  
Spherical Vesicles ◽  
Aggregation Of Platelets ◽  
Soluble Material

Most tumor cells cause aggregation of platelets in heparinized plasma via material shed into culture medium. In this study we investigated the events by transmission electron microscopy. Freshly washed cells were covered with closely spaced microvilli, many of which pinched off during 1 hour of incubation at 37°C. Both cells and shed microvilli were membrane enclosed. Shed microvilli became spherical vesicles containing cytoplasm. Platelets aggregated when stirred with incubated tumor cells or shed material. The aggregates were composed of platelets that showed pseudopod formation, centralization of granules and increase in the open channel system. Platelets around the periphery of aggregates had bulbous portions free of granules (ballooning) but many granules remained in platelets in the interior of aggregates suggesting that release of lysosomal enzymes may have been somewhat limited. Aggregates resembled those induced by ADP rather than by thrombin. Tumor cells were not incorporated into the aggregates. Vesicles were not selectively associated with platelets prior to or during aggregation. While some vesicles were incorporated into aggregates, it appeared that this was a consequence rather than the cause of aggregation. Therefore, vesicles may have produced soluble material that induced platelet aggregation.

scholarly journals DIGESTION AND THE DISTRIBUTION OF ACID PHOSPHATASE IN BLEPHARISMA

1968 ◽  
Vol 37 (2) ◽  
pp. 329-344 ◽  
Author(s):  
Herbert M. Dembitzer
Keyword(s):  
Electron Microscopy ◽  
Acid Phosphatase ◽  
Golgi Apparatus ◽  
Acid Phosphatase Activity ◽  
Food Vacuole ◽  
Vacuolar Membrane ◽  
Latex Particles ◽  
Pinocytotic Vesicles ◽  
Food Vacuoles ◽  
Separate System

Suspensions of Blepharisma intermedium were fed latex particles for 5 min and then were separated from the particles by filtration. Samples were fixed at intervals after separation and incubated to demonstrate acid phosphatase activity. They were subsequently embedded and sectioned for electron microscopy. During formation of the food vacuole, the vacuolar membrane is acid phosphatase-negative. Within 5 min, dumbbell-shaped acid phosphatase-positive bodies, possibly derived from the the acid phosphatase-positive Golgi apparatus, apparently fuse with the food vacuole and render it acid phosphatase-positive. A larger type of acid phosphatase-positive, vacuolated body may also fuse with the food vacuole at later stages. At about 20 min after formation, acid phosphatase-positive secondary pinocytotic vesicles pinch off from the food vacuoles and approach a separate system of membrane-bounded spaces. By 1 hr after formation, the food vacuole becomes acid phosphatase-negative, and the undigested latex particles are voided into the membrane-bounded spaces. The membrane-bounded spaces are closely associated with the food vacuole at all stages of digestion and are generally acid phosphatase-negative. Within the membrane-bounded spaces, dense, pleomorphic, granular bodies are found, in which are embedded mitochondria, paraglycogen granules, membrane-limited acid phosphatase-containing structures, and Golgi apparatuses. The granular bodies may serve as vehicles for the transport of organelles through the extensive, ramifying membrane-bounded spaces.

scholarly journals Coxiella burnetiiAcid Phosphatase Inhibits the Release of Reactive Oxygen Intermediates in Polymorphonuclear Leukocytes

2010 ◽  
Vol 79 (1) ◽  
pp. 414-420 ◽  
Author(s):  
J. Hill ◽  
J. E. Samuel
Keyword(s):  
Acid Phosphatase ◽  
Nadph Oxidase ◽  
Polymorphonuclear Leukocytes ◽  
Q Fever ◽  
Reactive Oxygen ◽  
Host Cells ◽  
Reactive Oxygen Intermediates ◽  
Oxygen Intermediates

ABSTRACTCoxiella burnetii, the etiological agent of Q fever, is a small, Gram-negative, obligate intracellular bacterium. Replication ofC. burnetiiduring infection has been shown to be increased by decreasing oxidative stress using p47phox −/−and iNOS−/−micein vivoand by pharmacologic inhibitorsin vitro. Building upon this model, we investigated the role polymorphonuclear leukocytes (PMN) play in the control of infection, since NADPH oxidase-mediated release of reactive oxygen intermediates (ROI) is a primary bactericidal mechanism for these cells that is critical for early innate clearance. Earlier studies suggested thatC. burnetiiactively inhibited release of ROI from PMN through expression of an unidentified acid phosphatase (ACP). Recent genomic annotations identified one open reading frame (CBU0335) which may encode a Sec- and type II-dependent secreted ACP. To test this model, viableC. burnetiipropagated in tissue culture host cells or axenic media,C. burnetiiextracts, or purified recombinant ACP (rACP) was combined with human PMN induced with 4-phorbol 12-myristate 13-acetate (PMA). The release of ROI was inhibited when PMN were challenged with viableC. burnetii,C. burnetiiextracts, or rACP but not when PMN were challenged with electron beam-inactivatedC. burnetii. C. burnetiiextracts and rACP were also able to inhibit PMA-induced formation of NADPH oxidase complex on PMN membranes, suggesting a molecular mechanism responsible for this inhibition. These data support a model in whichC. burnetiieludes the primary ROI killing mechanism of activated PMN by secreting at least one acid phosphatase.

L-663,536 (MK-886) (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-dimethylpropanoic acid), a novel, orally active leukotriene biosynthesis inhibitor

1989 ◽  
Vol 67 (5) ◽  
pp. 456-464 ◽  
Author(s):  
J. Gillard ◽  
A. W. Ford-Hutchinson ◽  
C. Chan ◽  
S. Charleson ◽  
D. Denis ◽  
...  
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Potent Inhibitor ◽  
Human Platelets ◽  
Ionophore A23187 ◽  
Lipoxygenase Inhibitor ◽  
12 Lipoxygenase ◽  
Rat Paw ◽  
Human Polymorphonuclear Leukocytes

L-663,536 (3-[1-(4-chlorobenzyl)-3-t-butyl-thio-5-isopropylindol-2-yl]-2,2-dimethylpropanoic acid) is a potent inhibitor of leukotriene (LT) biosynthesis in intact human polymorphonuclear leukocytes (PMN) (IC50, 2.5 nM). Similarly, L-663,536 inhibited A23187-induced LTB4 formation by rat peripheral blood and elicited PMN. At concentrations where inhibition of leukotriene biosynthesis occurred in human whole blood (1.1 μM), no effect was seen on cyclooxygenase or 12-lipoxygenase, an effect also observed in washed human platelets. The compound had no effect on rat or porcine 5-lipoxygenase indicating that L-663,536 is not a direct 5-lipoxygenase inhibitor. When administered in vivo L-663,536 was a potent inhibitor of antigen-induced dyspnea in inbred rats pretreated with methysergide (ED50, 0.036 mg/kg p.o.) and of Ascaris-induced bronchoconstriction in squirrel monkeys (1 mg/kg p.o.). The compound inhibited leukotriene biosynthesis in vivo in a rat pleurisy model (ED50, 0.2 mg/kg p.o.), an inflamed rat paw model (ED50, 0.8 mg/kg), a model of leukotriene excretion in rat bile following antigen provocation, and a model in the guinea-pig ear where leukotriene synthesis was induced by topical challenge with ionophore A23187 (ED50, 2.5 mg/kg p.o. and 0.6 μg topically). The results indicate that L-663,536 is a potent inhibitor of leukotriene biosynthesis both in vitro and in vivo indicating that the compound is suitable for studying the role of leukotrienes in a variety of pathological situations.Key words: leukotriene, 5-lipoxygenase, polymorphonuclear leukocytes, leukotriene B4, leukotriene inhibitor.

scholarly journals The effects of platelet activating factor and retinoic acid on the expression of ELAM-1 and ICAM-1 and the functions of neutrophils

1995 ◽  
Vol 4 (2) ◽  
pp. 103-106 ◽  
Author(s):  
Si-Feng Chen
Keyword(s):  
Retinoic Acid ◽  
Acid Phosphatase ◽  
Polymorphonuclear Leukocytes ◽  
Platelet Activating Factor ◽  
Intercellular Adhesion Molecule ◽  
Microvascular Endothelial Cells ◽  
Intercellular Adhesion Molecule 1 ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Adhesion Rate

Preincubation of pulmonary microvascular endothelial cells (PMVECs) with platelet-activating factor (PAF) for 3.5 h increased the adhesion rate of polymorphonuclear leukocytes (PMNs) to PMVECs from 57.3% to 72.8% (p < 0.01). Preincubation of PMNs with PAF also increased PMN-PMVEC adhesion rate. All-trans retinoic acid (RA) blocked the adherence of untreated PMNs to PAF-pretreated PMVECs but not the adherence of PAF-pretreated PMNs to untreated PMVECs. PAF increased the expression of intercellular adhesion molecule-1 (ICAM-1) and E-selection (ELAM-1) on PMVECs, PMN chemotaxis to zymosan-activated serum and histamine, and PMN aggregation and the release of acid phosphatase from PMNs. Co-incubation of RA inhibited PAF-induced PMN aggregation, the release of acid phosphatase from PMNs, and PMN chemotaxis to zymosan-activated serum and histamine while the expression of ICAM-1 and ELAM-1 did not change. Our results suggest that RA can be used to ameliorate PMN-mediated inflammation.

scholarly journals Characterization of the IgG-Fc receptor on human platelets

Blood ◽  
1982 ◽  
Vol 60 (6) ◽  
pp. 1277-1282 ◽  
Author(s):  
SP Karas ◽  
WF Rosse ◽  
RJ Kurlander
Keyword(s):  
Surface Area ◽  
Polymorphonuclear Leukocytes ◽  
Association Constant ◽  
Fc Receptors ◽  
Human Platelets ◽  
Crosslinked Polymers ◽  
Receptor Sites ◽  
Human Igg1 ◽  
The Mean

To determine quantitatively the number and avidity of receptors for the Fc portion of IgG on human platelets, we have measured the binding to platelets of human monomeric monoclonal IgG, and of small covalently crosslinked polymers of IgG1 labeled with 125I. The binding of labeled IgG1 monomers to platelets is too weak to permit quantitation. The binding of dimers or larger polymers of IgG1 is much more avid (greater at 4 degrees C than 37 degrees C), is readily reversible, and is saturable. The number of receptor sites ranges from 400 to 2000 per platelet and the mean equilibrium association constant (Ka) for the binding of dimers at 4 degrees C is 2.2 x 10(7) M-1 +/- 0.9 x 10(7) M- 1. The binding is specific for the Fc portion of IgG, and IgG1 and IgG3 bind to the receptors much more avidly than IgG2 or IgG4. Unlabeled IgG1 dimers are about 7--8-fold more potent in inhibiting binding than are IgG1 monomers, and larger polymers are even more potent than dimers. Thus, the Fc receptors on platelets bind human IgG1 with the same specificity and similar avidity as Fc receptors on polymorphonuclear leukocytes (PMNs), but PMNs have about 300-fold more receptors per unit of surface area than platelets.

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