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CD66b overexpression and homotypic aggregation of human peripheral blood neutrophils after activation by a gram-positive stimulus.

Abstract

Neutrophils represent the main component of innate immunity in the clearance of bacterial infections. To pass the tissue and to localize and reach the site of infection, the peripheral blood neutrophils have to pass through a complex receptor-mediated interaction with the endothelial layer. Under pathophysiological conditions, such as severe sepsis, this process is impaired and often characterized by neutrophil aggregation. In this study, we examined the impact of three different Staphylococcus aureus strains on the activation status of human peripheral blood neutrophils by coincubation of bacterial culture supernatant with whole blood. This complex interaction of a gram-positive stimulus with blood components leads to a special neutrophil activation phenotype, which is characterized by an overexpression of the cell-surface molecule CD66b. The process is accompanied by a strong increase of homotypic aggregates and seems to be initialized by a massive activation impulse caused by the interplay of plasma components. This maximum activation of neutrophils prior to the complex and highly regulated activation required for transmigration might play a key role in the neutrophil dysfunction in gram-positive sepsis.

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  • Publisher Full Text
  • Authors

    Schmidt T, Zündorf J, Grüger T, Brandenburg K, Reiners AL, Zinserling J, Schnitzler N

    Institution

    Federal Institute for Drugs and Medical Devices, L2-Biosafety Laboratory, Bonn, Germany.

    Source

    Journal of leukocyte biology 91:5 2012 May pg 791-802

    MeSH

    Adult
    Animals
    Antigens, CD
    Blotting, Western
    Cell Adhesion
    Cell Adhesion Molecules
    Cells, Cultured
    Enzyme-Linked Immunosorbent Assay
    Flow Cytometry
    GPI-Linked Proteins
    Humans
    Middle Aged
    Neutrophil Activation
    Neutrophils
    Staphylococcal Infections
    Staphylococcus aureus
    Swine
    Young Adult

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    22319104