Pneumococcus-induced serotonin release from human platelets. Identification of the participating plasma/serum factor as immunoglobulin.

Zimmerman, Theodore S.; Spiegelberg, Hans L.

doi:10.1172/jci108161

Cited by 41 publications

(19 citation statements)

References 21 publications

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“…In vitro platelet serotonin release has been demonstrated when platelets were incubated with endotoxin [15] and pneumococci. [16] Also, activated complement [17] and thrombin [18] can cause platelet release reaction.…”

Section: Discussionmentioning

confidence: 99%

Platelet Parameters in Children with Upper Urinary Tract Infection: Is There a Specific Response?

et al. 2008

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Although complete blood count is routinely ordered in most upper urinary tract infections (UTI), and information regarding the patient's platelet indices is made available without added cost, the relationship between platelet count and mean platelet volume (MPV) and specific platelet responses to different infectious agents has not been extensively characterized in UTI. The objectives of this study were to examine platelet counts and platelet indices in children with culture-proven upper UTI to determine if there are organism-specific platelet responses. A retrospective analysis of data from all pediatric urine samples processed at Fatih University Medical School microbiology laboratory was undertaken for a period of two years (January 1, 2005, to December 31, 2006. Of the 200 patients with positive urine cultures, 146 (73%) were infected with gram-negative bacteria and 54 (27%) grew gram-positive bacteria. The platelet count during the episode of upper UTI and the incidence of thrombocytosis was significantly higher with the gram-positive infections than with the gram-negative infections or controls (p < 0.05). A statistically significant higher MPV was detected in the subjects with upper UTI (p < 0.05). Also, our data showed a statistically significant increase in MPV with gram-positive infections compared with the other groups (p < 0.05). In conclusion, based on the importance of the hemostatic component in the pathophysiology of infections, our findings of platelet count and MPV and predictivity of the type of the organism would suggest the usefulness of the routine measurements in children with upper UTI.

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Section: Discussionmentioning

confidence: 99%

Platelet Parameters in Children with Upper Urinary Tract Infection: Is There a Specific Response?

et al. 2008

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“…In such a situation, platelets and infectious agents become colocalized on a surface even without interacting directly with one another. Regardless of how the initial arrest takes place, adherent platelets are activated through an interaction of their IgG receptor, Fc␥RIIA, with specific antibodies bound to the microorganisms, 34 thus initiating the recruitment of additional platelets into a developing thrombus. This latter stage of the process involves the same pathways of platelet aggregation that have been identified previously for physiologic substrates of hemostasis, because platelet-platelet cohesion in bacteriainduced thrombi requires the distinct adhesive properties of fibrinogen, VWF, and their respective membrane receptors depending on flow conditions.…”

Section: Discussionmentioning

confidence: 99%

Induction of platelet thrombi by bacteria and antibodies

Sjöbring

Ringdahl

Ruggeri

2002

Blood

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We have characterized 2 distinct mechanisms through which infectious agents may promote platelet adhesion and thrombus formation in flowing blood, thus contributing to the progression of disease. In one case, the process initiates when the integrin ␣ IIb ␤ 3 mediates platelet arrest onto immobilized bacterial constituents that have bound plasma fibrinogen. If blood contains antibodies against the bacteria, immunoglobulin (Ig) G may cluster on the same surface and activate adherent platelets through the Fc␥RIIA receptor, leading to thrombus growth. As an alternative, bacteria that cannot bind fibrinogen may attach to substrates, such as immobilized plasma proteins or components of the extracellular matrix, which also support platelet adhesion. As a result of this colocalization, IgG bound to bacteria can activate neighboring platelets and induce thrombus growth regard- IntroductionPlatelet adhesion and aggregation at sites of tissue trauma involve interactions of membrane receptors with constituents of extracellular matrices, such as collagen, and circulating macromolecules, such as von Willebrand factor (VWF) and fibrinogen, 1 which contribute to arrest bleeding during hemostasis. Bacteria, too, can induce platelet aggregation [2][3][4] or uncontrolled clotting with disseminated intravascular coagulation (DIC), 5,6 which may become disease mechanisms when the causative agent intermittently invades the bloodstream. For example, coagulation and hemostasis are activated in some localized infections, such as necrotizing fasciitis, resulting in extensive thrombosis of arterioles and veins in and around lesions. 7,8 Moreover, experimental and clinical observations have demonstrated that platelets play a key pathogenetic role when certain microorganisms establish infection in the bloodstream, as in the case of bacterial endocarditis. 4,9 In particular, platelet aggregates may allow bacteria to settle and remain at the site of infection withstanding the shear forces of flowing arterial blood. In experimental models of this disease, early vegetations grow by accretion of layers of fibrin and platelets with bacterial colonies sandwiched between them. 10 Similar mechanisms may facilitate the establishment of bacteria on artificial devices, such as arterial grafts. 11 The number of strains that can settle in the arterial circulation is limited, but an array of different species can cause septic venous thrombosis, 12,13 a condition in which platelet activation may be involved.In these studies, we have used 2 invasive species, Streptococcus pyogenes (also designated group A streptococcus) and Staphylococcus aureus, as models to examine the mechanisms involved in bacteria-induced thrombus formation under conditions mimicking the macromolecular, cellular, and hemodynamic complexity of blood circulating in different vessels. Only bacteria capable of binding a platelet-reactive factor from blood, such as fibrinogen, could initiate adhesion on a surface not intrinsically conducive to platelet deposition. This step, however, was n...

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“…The existence of Fc'y receptors on human platelets has been supported by several lines of evidence, including Fc-dependent secretory and aggregation responses to IgG aggregates and IgGbearing immune complexes (1)(2)(3)(4)(5)(6), direct radioligand binding studies with IgG dimers and larger oligomers (7), and a report of a KBr-solubilized 255,000-mol-wt platelet membrane glycoprotein exhibiting reactivity with aggregated IgG (8).…”

Section: Introductionmentioning

confidence: 98%

“…The Sepharose pellets were suspended in 80 gl Laemmli's (16) sample buffer containing 2% SDS with or without 20 mM dithiothreitol (DTT) (Pierce Chemical Co.), in place of 2-mercaptoethanol, followed by mixing and boiling for 2 min. Addition of 5 Al I M iodoacetamide (Sigma Chemical Co.) was followed by microcentrifugation (Beckman Instruments Inc., Spinco Div., Palo Alto, CA) for 30 s. The supernatants were removed and applied to a 5-15% polyacrylamide gradient slab gel in 0.1% SDS. The gels were stained with Coomassie Blue, dried on filter paper, and then analyzed by autoradiography using XAR-2 film (Eastman Kodak Co., Rochester, NY).…”

Section: Introductionmentioning

confidence: 99%

Human platelet Fc receptor for immunoglobulin G. Identification as a 40,000-molecular-weight membrane protein shared by monocytes.

Rosenfeld¹,

Looney²,

Leddy³

et al. 1985

J. Clin. Invest.

224

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We have recently shown that human monocytes and U937 cells possess two molecular classes of Fcy receptor. One, a 72,000-mol-wt sialoglycoprotein, has high affinity for certain subclasses of human and murine monomeric IgG. The other is a 40,000-mol-wt protein (p40) with low affinity for monomeric IgG but with the capacity to bind IgG aggregates or IgG-coated particles.In the present study, a 40,000-mol-wt single chain protein, apparently identical to p40 from U937 cells, was isolated from surface-radioiodinated human platelets by affinity purification using a murine IgG2b monoclonal antibody to p40. This 40,000-mol-wt protein was not seen when control IgG2b or unrelated murine monoclonal antibodies were employed in place of antip40. The same 40,000-mol-wt protein was also recovered from an IgG-Sepharose affinity adsorbent, but not from ovalbuminor myoglobin-Sepharose. The 72,000-mol-wt Fcvy receptor of monocytes was not identified on platelets.Monoclonal anti-p4O and Fab fragments derived from this antibody blocked platelet aggregation by heat-aggregated human IgG, whereas a control murine IgG2b protein had little or no inhibitory effect at 500-1,000-fold higher concentrations. A murine IgG1 monoclonal antibody, reactive with an unrelated platelet-specific membrane antigen, did not inhibit platelet responses to aggregated IgG. Anti-p4O did not affect platelet aggregation by thrombin, collagen, or fibrinogen plus ADP. Although antip40 did not directly aggregate platelets in the concentrations employed, cross-linking with F(ab'`) goat anti-murine Ig induced apyrase-sensitive aggregation of anti-p40-treated platelets. This indicates that p40 possesses transmembrane linkage for platelet activation and secretion.These observations strongly suggest that this newly recognized 40,000-mol-wt platelet membrane protein serves as an Fcy receptor.

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Pneumococcus-induced serotonin release from human platelets. Identification of the participating plasma/serum factor as immunoglobulin.

Abstract: A B S T R A C T Pneumococcus-induced

Cited by 41 publications

References 21 publications

Platelet Parameters in Children with Upper Urinary Tract Infection: Is There a Specific Response?

Platelet Parameters in Children with Upper Urinary Tract Infection: Is There a Specific Response?

Induction of platelet thrombi by bacteria and antibodies

Human platelet Fc receptor for immunoglobulin G. Identification as a 40,000-molecular-weight membrane protein shared by monocytes.

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