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Peter Hoglund - One of the best experts on this subject based on the ideXlab platform.

  • Adding to the complexity of fetal and neonatal alloimmune thrombocytopenia: Reduced fibrinogen binding in the presence of anti-HPA-1a antibody and hypo-responsive neonatal Platelets
    Thrombosis Research, 2018
    Co-Authors: Erle Refsum, Anna Wikman, S. Meinke, G. Gryfelt, Peter Hoglund
    Abstract:

    Background In fetal and neonatal alloimmune thrombocytopenia (FNAIT), maternal alloantibodies directed against paternally-derived Platelet antigens are transported across the placenta to the fetus, where they may cause thrombocytopenia. The most serious complication of FNAIT is an intracranial hemorrhage (ICH), which may cause death or life-long disability of the child. Apart from alloantibody-mediated Platelet destruction, the clinical outcome in FNAIT may be affected by properties of neonatal Platelets and possible functional effects on Platelets caused by maternal alloantibodies. Methods and results The function of umbilical cord blood Platelets was compared with adult Platelets in two assays, impedance aggregometry (Multiplate) and rotational thromboelastometry (Rotem). Both revealed a decreased in vitro neonatal Platelet function compared to adult Platelets. Consistent with this finding, activation using TRAP revealed less pronounced changes in the expression of CD62P, PAC-1, CD41 and CD42a in umbilical cord blood Platelets compared to adult Platelets. Furthermore, a monoclonal anti-HPA-1a antibody, derived from an immunized mother of two children with FNAIT, blocked fibrinogen binding to resting and activated umbilical cord blood and adult HPA-1aa and HPA-1ab Platelets, interfered with Platelet activation by TRAP, and impaired the function of umbilical cord blood HPA-1aa Platelets in rotational thromboelastometry. Discussion and conclusions Reduced fibrinogen binding in the presence of anti-HPA-1a antibodies may disturb the neonatal hemostatic balance, characterized by poorly responsive Platelets. This effect may operate in parallel to Platelet destruction and contribute to the clinical outcome in FNAIT.

Robert W. Alexander - One of the best experts on this subject based on the ideXlab platform.

  • Fat transfer with Platelet-rich plasma for breast augmentation
    Breast Augmentation: Principles and Practice, 2009
    Co-Authors: Robert W. Alexander
    Abstract:

    Tissue augmentation with autologous elements is considered the\nideal choice for transplantation and volume augmentation\nsurgery. It is well recognized that the ideal graft tissue\nshould offer the standard features of being readily available,\nhave low antigenicity, minimal donor site morbidity, predictable\nand reproducible retention, and avoid disease transmission.\nGradual standardization of consistent harvesting, manipulations,\nand transfer protocols is improving the ability to accurately\npredict volume enhancements and appreciate the long-term\nsurvival of the grafted tissues. Platelets actively extrude\nmultiple growth factors very important to early wound healing\nprocesses. In response to Platelet-to-Platelet or\nPlatelet-to-connective tissue contact, the Platelet cell\nmembrane is ``activated'' to release these products from the\nalpha granules via active extrusion. When these extruded growth\nfactors are released, histones and carbohydrate chains are added\nto receptor sites, thereby creating their unique chemistries and\nmake the ``active'' growth factors. Autologous fat grafting\noffers a viable and safe alternative means of breast\naugmentation in select patients. Platelet rich plasma enhances\nthe fat transfer to the breast.

Kristina L Modjeski - One of the best experts on this subject based on the ideXlab platform.

  • emerging roles for Platelets as immune and inflammatory cells
    Blood, 2014
    Co-Authors: Craig N Morrell, Angela A Aggrey, Lesley M Chapman, Kristina L Modjeski
    Abstract:

    Despite their small size and anucleate status, Platelets have diverse roles in vascular biology. Not only are Platelets the cellular mediator of thrombosis, but Platelets are also immune cells that initiate and accelerate many vascular inflammatory conditions. Platelets are linked to the pathogenesis of inflammatory diseases such as atherosclerosis, malaria infection, transplant rejection, and rheumatoid arthritis. In some contexts, Platelet immune functions are protective, whereas in others Platelets contribute to adverse inflammatory outcomes. In this review, we will discuss Platelet and Platelet-derived mediator interactions with the innate and acquired arms of the immune system and Platelet-vessel wall interactions that drive inflammatory disease. There have been many recent publications indicating both important protective and adverse roles for Platelets in infectious disease. Because of this new accumulating data, and the fact that infectious disease continues to be a leading cause of death globally, we will also focus on new and emerging concepts related to Platelet immune and inflammatory functions in the context of infectious disease.

Jamey D Marth - One of the best experts on this subject based on the ideXlab platform.

  • dual actions of group b streptococcus capsular sialic acid provide resistance to Platelet mediated antimicrobial killing
    Proceedings of the National Academy of Sciences of the United States of America, 2019
    Co-Authors: Satoshi Uchiyama, Kyoko Fukahori, Nao Ando, Mengyou Wu, Flavio Schwarz, Shoib S Siddiqui, Ajit Varki, Jamey D Marth
    Abstract:

    Circulating Platelets have important functions in thrombosis and in modulating immune and inflammatory responses. However, the role of Platelets in innate immunity to bacterial infection is largely unexplored. While human Platelets rapidly kill Staphylococcus aureus, we found the neonatal pathogen group B Streptococcus (GBS) to be remarkably resistant to Platelet killing. GBS possesses a capsule polysaccharide (CPS) with terminal α2,3-linked sialic acid (Sia) residues that mimic a common epitope present on the human cell surface glycocalyx. A GBS mutant deficient in CPS Sia was more efficiently killed by human Platelets, thrombin-activated Platelet releasate, and synthetic Platelet-associated antimicrobial peptides. GBS Sia is known to bind inhibitory Sia-recognizing Ig superfamily lectins (Siglecs) to block neutrophil and macrophage activation. We show that human Platelets also express high levels of inhibitory Siglec-9 on their surface, and that GBS can engage this receptor in a Sia-dependent manner to suppress Platelet activation. In a mouse i.v. infection model, antibody-mediated Platelet depletion increased susceptibility to Platelet-sensitive S. aureus but did not alter susceptibility to Platelet-resistant GBS. Elimination of murine inhibitory Siglec-E partially reversed Platelet suppression in response to GBS infection. We conclude that GBS Sia has dual roles in counteracting Platelet antimicrobial immunity: conferring intrinsic resistance to Platelet-derived antimicrobial components and inhibiting Platelet activation through engagement of inhibitory Siglecs. We report a bacterial virulence factor for evasion of Platelet-mediated innate immunity.

Waander L. Van Heerde - One of the best experts on this subject based on the ideXlab platform.

  • Multicolor flow cytometry for evaluation of Platelet surface antigens and activation markers
    Thrombosis Research, 2012
    Co-Authors: Jeroen F. Van Velzen, Britta A P Laros-van Gorkom, Gheorghe A M Pop, Waander L. Van Heerde
    Abstract:

    Introduction: Flow cytometry allows the analysis of multiple antigens in a single tube at a single cell level. We present a rapid and sensitive two tube flow cytometric protocol for the detection of multiple Platelet antigens and activation markers gated on a pure Platelet population. Materials and methods: The presence of Platelet specific antigens was analyzed in citrated whole blood of normal Platelets and from patients diagnosed with Platelet abnormalities. Quiescent Platelets as well as stimulated Platelets were analyzed using a gating strategy based on ubiquitously expressed Platelet membrane markers. A ubiquitously expressed Platelet marker was combined with antibodies against the activated alpha2b-beta3 (PAC-1), Lysosomal Activated Membrane Protein (CD63) and P-selectin (CD62P). Results: We were able to detect the Platelet antigens CD36, CD41, CD42a, CD42b and CD61 in one single tube. Our approach allowed the single tube determination of PAC-1, CD63 and CD62P after activation of Platelets by thrombin, collagen, ADP and PAR-1, and determination of Platelet abnormalities. Conclusions: Our two tube multi-parameter screening protocol is suited for the analysis of Platelet antigens expressed on quiescent and activated Platelets and allows the detection of aberrancies as found in blood of patients with thrombocytopathy such as Glanzmann Thrombasthenia, storage pool disease with diminished granule content and patients treated with clopidogrel and acetylsalicylic acid. © 2012 Elsevier Ltd. All rights reserved.