Plasmodium falciparumgrowth inhibition by human plateletsin vitro

Parasitology ◽  
1989 ◽  
Vol 99 (3) ◽  
pp. 317-322 ◽  
Author(s):  
F. Peyron ◽  
B. Polack ◽  
D. Lamotte ◽  
L. Kolodie ◽  
P. Ambroise-Thomas
Keyword(s):  
Growth Inhibition ◽  
Human Platelets ◽  
Activated Platelets ◽  
Erythrocyte Lysis ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Host Parasite ◽  
Oxygen Metabolites

SummaryPlatelets take an active part in immunological processes as well as in haemostasis, especially in the host-parasite relationship. Our aim is to assess the growth ofPlasmodium falciparum, cultured in human erythrocytes in the presence of fresh washed human platelets, since thrombocytopaenia is frequently observed during malarial infections. Our results show that platelets induce a dose-related growth inhibition ofP. falciparum. Both proliferation and maturation of intraerythrocytic stages of the parasite are inhibited. This growth inhibition is triggered by the parasite itself as neither specific antibodies nor any other components are needed to activate platelets. Activated platelets are directly toxic since complement is not involved. Furthermore, inhibition is not mediated by erythrocyte lysis or by toxic oxygen metabolites. Platelets induce an inhibition ofP.falciparumgrowth, at leastin vitro, although the importance of their role playedin vivoin malarial immunity has yet to be evaluated.

scholarly journals Host-Parasite Relationship in Cystic Echinococcosis: An Evolving Story

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Alessandra Siracusano ◽  
Federica Delunardo ◽  
Antonella Teggi ◽  
Elena Ortona
Keyword(s):  
Cystic Echinococcosis ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Recent Developments ◽  
Host Parasite ◽  
Human Cystic Echinococcosis

The larval stage ofEchinococcus granulosuscauses cystic echinococcosis, a neglected infectious disease that constitutes a major public health problem in developing countries. Despite being under constant barrage by the immune system,E. granulosusmodulates antiparasite immune responses and persists in the human hosts with detectable humoral and cellular responses against the parasite.In vitroandin vivoimmunological approaches, together with molecular biology and immunoproteomic technologies, provided us exciting insights into the mechanisms involved in the initiation ofE. granulosusinfection and the consequent induction and regulation of the immune response. Although the last decade has clarified many aspects of host-parasite relationship in human cystic echinococcosis, establishing the full mechanisms that cause the disease requires more studies. Here, we review some of the recent developments and discuss new avenues in this evolving story ofE. granulosusinfection in man.

scholarly journals The effect of thrombin on the density distribution of blood platelets: detection of activated platelets in the circulation

Blood ◽  
1983 ◽  
Vol 62 (2) ◽  
pp. 433-438
Author(s):  
B van Oost ◽  
IH van Hien-Hagg ◽  
AP Timmermans ◽  
JJ Sixma
Keyword(s):  
Cardiopulmonary Bypass ◽  
Density Distribution ◽  
Density Gradient Centrifugation ◽  
Blood Platelets ◽  
Gradient Centrifugation ◽  
Buoyant Density ◽  
Human Platelets ◽  
Activated Platelets

The buoyant density of human platelets is decreased after they have been aggregated and induced to secrete their granule content by thrombin. This change in density was detected by discontinuous density gradient centrifugation using arabinogalactan (Stractan) solutions. The density decrease was dependent on the thrombin concentration and paralleled the extent of serotonin and beta-thromboglobulin secretion. The degranulated platelets maintained their integrity, and many of their functional properties. Mixtures of degranulated platelets and normal platelets could be resolved by Stractan gradient centrifugation and the number of degranulated platelets quantitated. Using this method, increased levels of less dense platelets were shown to occur after cardiopulmonary bypass. Assay of changes in platelet density by Stractan gradient centrifugation is a useful method for detection of activated platelets in vitro and in vivo.

Cyclosporin A: antiparasite drug, modulator of the host-parasite relationship and immunosuppressant

Parasitology ◽  
1992 ◽  
Vol 105 (S1) ◽  
pp. S25-S40 ◽  
Author(s):  
L. H. Chappell ◽  
J. M. Wastling
Keyword(s):  
Cyclosporin A ◽  
Drug Administration ◽  
Gastrointestinal Nematodes ◽  
Laboratory Animals ◽  
Parasitic Infections ◽  
Filarial Nematodes ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Host Parasite

SUMMARYCyclosporin A (CsA), a cyclic undecapeptide with powerful properties of immunosuppression, acts on parasitic infections in laboratory animals in various ways. The outcome of drug administrationin vivovaries with timing of treatment relative to infection, route of administration, dose and number of treatments applied. CsA is clearly antiparasitic against malaria, schistosomes, adult tapeworms, metacestodes and filarial nematodes. By contrast, it acts as an immunomodulator against trypanosomes andGiardia, by exacerbating infection; in the case ofLeishmaniaspp. the drug acts variously. In some other infections CsA acts both as an antiparasite drug and as an immunosuppressant (Toxoplasma, avian coccidiosis and gastrointestinal nematodes).

Interactions between mosses (Bryophyta) and fungi

2006 ◽  
Vol 84 (10) ◽  
pp. 1509-1519 ◽  
Author(s):  
Marie L. Davey ◽  
Randolph S. Currah
Keyword(s):  
Host Cell ◽  
Mycorrhizal Fungi ◽  
Host Responses ◽  
Fungal Propagules ◽  
Parasite Relationship ◽  
Cellular Specificity ◽  
Host Parasite ◽  
Highly Evolved

A taxonomically diverse suite of fungi interacts with bryophytes as pathogens, parasites, saprobes, and commensals. Necrotrophic pathogens such as Tephrocybe palustris (Peck) Donk and Nectria mnii Döbbeler form patches of moribund gametophytes in otherwise healthy mats of mosses. These pathogens exhibit different methods of host cell disruption; N. mnii appears to displace the host cell protoplast with intracellular hyphae, while T. palustris causes host protoplast degeneration. Host responses to infection by bryopathogens are also variable. Host–pathogen relationships can be highly evolved, as in Bryophytomyces sphagni (Navashin) Cif., in which fungal propagules replace the bryophyte spores, and exploit the explosive dispersal mechanisms of the Sphagnum host. Bryophilous parasites tend to exhibit high tissue or cellular specificity with varying host specificity. For example, Octospora similis (Kirchstein) Benkert infects the rhizoids of species of Bryum, and Discinella schimperi (Navashin) Redhead specifically colonizes the mucilage producing cells of stems of Sphagnum squarrosum Crome. Eocronartium muscicola (Pers.) Fitzp. demonstrates a highly evolved host–parasite relationship in which the basidiocarp displaces the sporophyte and is fed directly by the gametophyte through specialized transfer tissues. Fungi such as Oidiodendron maius Barron are capable of decomposing moss cell walls that are generally resistant to decomposition because of their polyphenolic component. Mycorrhizal fungi, including Glomus, Suillus, and Endogone, have not been observed to form functional, nutrient-exchanging mycorrhizal interfaces with bryophytes, rather, they function as saprobes on moribund and senescent gametophytes. Finally, endophytic fungi may provide bryophyte hosts with greater tolerance to extreme pH or promote vegetative growth. In vivo observation of bryophyte–fungus interactions has provided insight into the types of interactions that occur; however to further understand the physiology, anatomy, and etiology of these interactions, it is necessary to culture bryophilous fungi in vitro and create artificial axenic systems for study.

The Role of Ca2+I in Procoagulant Surface Expression and Apoptosis in Human Platelets.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3569-3569
Author(s):  
Adam M. Gwozdz ◽  
Hong Wang ◽  
K.W. Annie Bang ◽  
Marian A. Packham ◽  
John Freedman ◽  
...  
Keyword(s):  
In Vitro Study ◽  
Fold Increase ◽  
Surface Expression ◽  
Human Platelets ◽  
Apoptotic Pathway ◽  
Outer Leaflet ◽  
Activated Platelets

Abstract Asymmetry of phospholipids across the plasma membrane bilayer is a feature of all eukaryotic cells. When platelets are stimulated with certain agonsists, phospholipids are randomized by the action of a Ca2+-dependent scramblase enzyme, resulting in exposure of the anionic aminophospholipid phosphatidylserine (PS) on the outer leaflet that provides a procoagulant surface, catalyzing thrombin formation. We have previously demonstrated that the procoagulant surface of activated platelets persists in vitro for at least 4 hrs (Blood100:63b, 2002). Such persistence may propagate thrombosis in vivo when activated procoagulant platelets re-enter the circulation after fibrinolysis. There is currently little information concerning the mechanisms by which the procoagulant surface persists on activated platelets. In this in vitro study, the Ca2+-chelator BAPTA (0.1 μmol/109 platelets) was used to investigate the role of intracellular Ca2+ (Ca2+i) in procoagulant surface expression and persistence; PS expression was determined flow cytometrically by the binding of annexin A5-FITC. Unexpectedly, chelation of Ca2+i resulted in a 2–2.5x-fold increase in PS expression on the surface of platelets 5 min after activation with thrombin or thrombin+collagen (T+C), and this persisted for up to 4 hrs (last time point tested). Since PS expression is a hallmark of apoptosis in nucleated cells, we also examined another platelet apoptosis marker, the collapse of the mitochondrial inner membrane potential (ΔΨm), by flow cytometry using the potential-sensitive dye TMRM; PS expression was measured concurrently. This allowed us to distinguish between activated platelets expressing PS with an intact ΔΨm and apoptotic platelets expressing PS with a dissipated ΔΨm. 70–85% of the thrombin- or T+C-activated platelets expressing PS had an intact ΔΨm, which persisted for up to 4 hrs after activation. Thus, PS expression can occur independently of ΔΨm loss. However, chelation of Ca2+i with BAPTA resulted in 60–70% of the thrombin- or T+C-activated platelets persistently expressing PS to also have a collapsed ΔΨm, indicating that apoptotic pathways similar to those found in nucleated cells may modulate PS expression in platelets and may depend on Ca2+i concentrations. Caspases and calpain are centrally involved in apoptotic signaling and execution in nucleated cells. Caspases-9 and -3 have been identified in human platelets and may be responsible for downstream activation of calpain. We examined the effects of Ca2+i chelation in thrombin- and T+C- activated platelets on the activation of procaspases and calpain by Western blotting. In keeping with our observations of increased PS expression with concurrent ΔΨm loss in activated platelets with Ca2+i chelation, we observed cleavage of both procaspase-9, procaspase-3 and calpain, which did not occur in activated platelets without Ca2+i chelation. Taken together, our results indicate that Ca2+i levels in activated platelets may serve as a decisional checkpoint for the apoptotic pathway in human platelets, where procaspase-9 and procaspase-3 along with downstream calpain may function in a Ca2+-sensitive manner to protect platelets against PS exposure and ΔΨm collapse.

scholarly journals The effect of thrombin on the density distribution of blood platelets: detection of activated platelets in the circulation

Blood ◽  
1983 ◽  
Vol 62 (2) ◽  
pp. 433-438 ◽  
Author(s):  
B van Oost ◽  
IH van Hien-Hagg ◽  
AP Timmermans ◽  
JJ Sixma
Keyword(s):  
Cardiopulmonary Bypass ◽  
Density Distribution ◽  
Density Gradient Centrifugation ◽  
Blood Platelets ◽  
Gradient Centrifugation ◽  
Buoyant Density ◽  
Human Platelets ◽  
Activated Platelets

Abstract The buoyant density of human platelets is decreased after they have been aggregated and induced to secrete their granule content by thrombin. This change in density was detected by discontinuous density gradient centrifugation using arabinogalactan (Stractan) solutions. The density decrease was dependent on the thrombin concentration and paralleled the extent of serotonin and beta-thromboglobulin secretion. The degranulated platelets maintained their integrity, and many of their functional properties. Mixtures of degranulated platelets and normal platelets could be resolved by Stractan gradient centrifugation and the number of degranulated platelets quantitated. Using this method, increased levels of less dense platelets were shown to occur after cardiopulmonary bypass. Assay of changes in platelet density by Stractan gradient centrifugation is a useful method for detection of activated platelets in vitro and in vivo.

Host/parasite relationship in the in vitro infection of rat gliocytes by Neospora caninum: Evaluation of cell respiration

2007 ◽  
Vol 83 (1) ◽  
pp. 27-29 ◽  
Author(s):  
Alexandre M. Pinheiro ◽  
Cláudia Valle Santos ◽  
Maria de Fátima D. Costa ◽  
Luiz Erlon A. Rodrigues
Keyword(s):  
Neospora Caninum ◽  
Cell Respiration ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Host Parasite

A Comparison of the Effect of Decorsin and Two Disintegrins, Albolabrin and Eristostatin, on Platelet Function

1995 ◽  
Vol 74 (05) ◽  
pp. 1316-1322 ◽  
Author(s):  
Mary Ann McLane ◽  
Jagadeesh Gabbeta ◽  
A Koneti Rao ◽  
Lucia Beviglia ◽  
Robert A Lazarus ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Sequence Similarity ◽  
Platelet Aggregation Inhibitors ◽  
Antiplatelet Drug ◽  
Rgd Sequence ◽  
Fibrinogen Receptor ◽  
Activated Platelets

SummaryNaturally-occurring fibrinogen receptor antagonists and platelet aggregation inhibitors that are found in snake venom (disintegrins) and leeches share many common features, including an RGD sequence, high cysteine content, and low molecular weight. There are, however, significant selectivity and potency differences. We compared the effect of three proteins on platelet function: albolabrin, a 7.5 kDa disintegrin, eristostatin, a 5.4 kDa disintegrin in which part of the disintegrin domain is deleted, and decorsin, a 4.5 kDa non-disintegrin derived from the leech Macrobdella decora, which has very little sequence similarity with either disintegrin. Decorsin was about two times less potent than albolabrin and six times less potent than eristostatin in inhibiting ADP- induced human platelet aggregation. It had a different pattern of interaction with glycoprotein IIb/IIIa as compared to the two disintegrins. Decorsin bound with a low affinity to resting platelets (409 nM) and to ADP-activated platelets (270 nM), and with high affinity to thrombin- activated platelets (74 nM). At concentrations up to 685 nM, it did not cause expression of a ligand-induced binding site epitope on the (β3 subunit of the GPIIb/IIIa complex. It did not significantly inhibit isolated GPIIb/IIIa binding to immobilized von Willebrand Factor. At low doses (1.5-3.0 μg/mouse), decorsin protected mice against death from pulmonary thromboembolism, showing an effect similar to eristostatin. This suggested that decorsin is a much more potent inhibitor of platelet aggregation in vivo than in vitro, and it may have potential as an antiplatelet drug.

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