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Opsonization of Staphylococcus aureus protects endothelial cells from damage by phagocytosing polymorphonuclear
Abstract:
When phagocytosis of Staphylococcus aureus by human polymorphonuclear leukocytes (PMN) takes place on the surface of cultured human endothelial cells, the endothelial monolayers are damaged by lysosomal enzymes that are released by the PMN. Because PMN can phagocytose opsonized as well as unopsonized staphylococci on an endothelial surface, we studied the role of bacterial opsonization in the damage caused to the endothelium. Phagocytosis of unopsonized S. aureus was accompanied by greater damage (expressed as the percentage of the endothelial cells detached from the culture plates) of the monolayers than was phagocytosis of opsonized S. aureus: 52 +/- 10% and 24 +/- 7%, respectively, after 30 min of phagocytosis and 73 +/- 5% and 50 +/- 6%, respectively, after 60 min of phagocytosis. When correlated to the amount of phagocytosis, this difference was even greater (uptake was 35 +/- 4% for unopsonized S. aureus and 56 +/- 5% for opsonized S. aureus after 30 min and 42 +/- 3% and 60 +/- 5%, respectively, after 60 min). Total release of lysozyme and myeloperoxidase and generation of superoxide anion were the same during phagocytosis of opsonized or unopsonized staphylococci. Adherence of PMN to the endothelial cells was greater during phagocytosis of unopsonized S. aureus: 42 +/- 4% verus 27 +/- 3% during phagocytosis of opsonized staphylococci. Possibly, increased adherence of the PMN resulted in a locally higher concentration of enzymes which induced more damage. We conclude that opsonization of bacteria not only improves bacterial uptake, but also protects bystander cells from damage by the phagocytosing PMN.
Insights
Bacterial opsonization reduces damage to endothelial cells during Staphylococcus aureus phagocytosis by human polymorphonuclear leukocytes (PMN). Opsonization improves bacterial uptake and protects bystander cells from PMN-induced damage.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Human polymorphonuclear leukocytes (PMN) phagocytose Staphylococcus aureus on endothelial cells.
- PMN-released lysosomal enzymes can damage endothelial monolayers during phagocytosis.
- Bacterial opsonization influences phagocytosis and potential endothelial damage.
Purpose of the Study:
- To investigate the role of bacterial opsonization in endothelial cell damage caused by PMN phagocytosis of S. aureus.
- To compare the extent of endothelial damage when phagocytosing opsonized versus unopsonized S. aureus.
Main Methods:
- Cultured human endothelial cells were exposed to opsonized or unopsonized S. aureus.
- Phagocytosis by human PMN was allowed on the endothelial monolayers.
- Endothelial cell damage was quantified by measuring cell detachment.
- PMN adherence, bacterial uptake, lysozyme release, myeloperoxidase release, and superoxide anion generation were measured.
Main Results:
- Phagocytosis of unopsonized S. aureus caused significantly greater endothelial cell detachment (52-73%) compared to opsonized S. aureus (24-50%).
- Despite lower uptake of unopsonized bacteria, endothelial damage was higher, suggesting opsonization protects bystander cells.
- PMN adherence to endothelial cells was greater during phagocytosis of unopsonized S. aureus.
- Enzyme release and superoxide generation were similar for both opsonized and unopsonized bacteria.
Conclusions:
- Bacterial opsonization enhances bacterial uptake by PMN.
- Opsonization of S. aureus protects endothelial cells from damage induced by phagocytosing PMN.
- Increased PMN adherence to endothelial cells during unopsonized bacterial phagocytosis may contribute to greater endothelial damage.