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  • 1
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    Intracellular parasitism by the human granulocytic ehrlichiosis bacterium through the P-selectin ligand, PSGL-1 (2000)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2000-06-02
    Description: Human granulocytic ehrlichiosis (HGE) is a febrile tick-borne illness caused by a recently discovered intracellular bacterium remarkable for its tropism for professionally phagocytic neutrophils. Monoclonal antibodies against the P-selectin binding domain of the leukocyte P-selectin glycoprotein ligand, PSGL-1, prevented HGE cell binding and infection, as did enzymatic digestion of PSGL-1. Furthermore, simultaneous neoexpression in nonsusceptible cells of complementary DNAs for both PSGL-1 and its modifying alpha-(1,3) fucosyltransferase, Fuc-TVII, allowed binding and infection by HGE. Thus, the HGE bacterium specifically bound to fucosylated leukocyte PSGL-1. Selectin mimicry is likely central to the organism's unique ability to target and infect neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Herron, M J -- Nelson, C M -- Larson, J -- Snapp, K R -- Kansas, G S -- Goodman, J L -- R01AI40952/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2000 Jun 2;288(5471):1653-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Infectious Diseases, Department of Medicine, University of Minnesota School of Medicine, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10834846" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; B-Lymphocytes/microbiology ; Cell Line ; Ehrlichia/metabolism/*pathogenicity ; Fluorescent Antibody Technique, Indirect ; Fucosyltransferases/genetics/metabolism ; Glycosylation ; Granulocytes/metabolism/*microbiology ; HL-60 Cells ; Humans ; Ligands ; Membrane Glycoproteins/genetics/immunology/*metabolism ; Metalloendopeptidases/metabolism ; Molecular Mimicry ; Neutrophils/metabolism/*microbiology ; Oligosaccharides/genetics/immunology/metabolism ; P-Selectin/metabolism ; Transfection
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Venous levels of shear support neutrophil-platelet adhesion and neutrophil aggregation in blood via P-selectin and beta2-integrin (1998)
    In:  Other Sources
    Details
    Publication Date: 2019-07-13
    Description: BACKGROUND: After activation, platelets adhere to neutrophils via P-selectin and beta2-integrin. The molecular mechanisms and adhesion events in whole blood exposed to venous levels of hydrodynamic shear in the absence of exogenous activation remain unknown. METHODS AND RESULTS: Whole blood was sheared at approximately 100 s(-1). The kinetics of neutrophil-platelet adhesion and neutrophil aggregation were measured in real time by flow cytometry. P-selectin was upregulated to the platelet surface in response to shear and was the primary factor mediating neutrophil-platelet adhesion. The extent of neutrophil aggregation increased linearly with platelet adhesion to neutrophils. Blocking either P-selectin, its glycoprotein ligand PSGL-1, or both simultaneously by preincubation with a monoclonal antibody resulted in equivalent inhibition of neutrophil-platelet adhesion (approximately 30%) and neutrophil aggregation (approximately 70%). The residual amount of neutrophil adhesion was blocked with anti-CD11b/CD18. Treatment of blood with prostacyclin analogue ZK36374, which raises cAMP levels in platelets, blocked P-selectin upregulation and neutrophil aggregation to baseline. Complete abrogation of platelet-neutrophil adhesion required both ZK36374 and anti-CD18. Electron microscopic observations of fixed blood specimens revealed that platelets augmented neutrophil aggregation both by forming bridges between neutrophils and through contact-mediated activation. CONCLUSIONS: The results are consistent with a model in which venous levels of shear support platelet adherence to neutrophils via P-selectin binding PSGL-1. This interaction alone is sufficient to mediate neutrophil aggregation. Abrogation of platelet adhesion and aggregation requires blocking Mac-1 in addition to PSGL-1 or P-selectin. The described mechanisms are likely of key importance in the pathogenesis and progression of thrombotic disorders that are exacerbated by leukocyte-platelet aggregation.
    Keywords: Life Sciences (General)
    Type: Circulation (ISSN 0009-7322); 98; 9; 873-82
    Format: text
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