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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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 791-802MeSH
AdultAnimals
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 ArticleResearch Support, Non-U.S. Gov't
Language
eng
PubMed ID
22319104
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