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Updated: Aug 9, 2026
Studying Interactions of Staphylococcus aureus with Neutrophils by Flow Cytometry and Time Lapse Microscopy
Published on: July 17, 2013
Interaction between human polymorphonuclear leucocytes and Staphylococcus aureus in the presence and absence of
Abstract:
Phagocytosis of Staphylococcus aureus by human polymorphonuclear leucocytes (PMN) in the presence and absence of opsonins was studied with an assay which allows interaction between PMN and bacteria on a surface. The kinetics of uptake, the activity of the metabolic burst, and the degranulation during phagocytosis of opsonized and unopsonized bacteria were compared. Uptake of unopsonized S. aureus proceeded at a slower rate, but unopsonized staphylococci induced metabolic activity and degranulation in the PMN to the same extent as opsonized bacteria. Treatment of PMN with a metabolic inhibitor (2-deoxy-D-glucose) or with an inhibitor of microfilament function (cytochalasin B) totally inhibited the capacity of PMN to ingest unopsonized S. aureus, whereas uptake of opsonized bacteria was much less affected. Treatment of the PMN with pronase prevented uptake of unopsonized bacteria, but had no effect on the uptake of opsonized bacteria. Uptake was not inhibited by mannose. Recognition of S. aureus by the PMN was not dependent on the presence of the cell wall components protein A or teichoic acid. The presence of a capsule inhibited uptake.
Insights
Human immune cells called polymorphonuclear leucocytes (PMN) can engulf Staphylococcus aureus. Opsonins enhance bacterial uptake, but PMN activation during phagocytosis occurs regardless of opsonins.
Area of Science:
- Immunology
- Microbiology
Background:
- Phagocytosis is a key immune mechanism for clearing bacterial infections.
- Staphylococcus aureus is a common pathogen, and its interaction with human immune cells is crucial for understanding infection dynamics.
Purpose of the Study:
- To investigate the mechanisms of Staphylococcus aureus phagocytosis by human polymorphonuclear leucocytes (PMN).
- To compare the uptake kinetics, metabolic activity, and degranulation of PMN when interacting with opsonized versus unopsonized S. aureus.
Main Methods:
- Utilized a surface-based assay for PMN-bacteria interaction.
- Compared phagocytosis of opsonized and unopsonized S. aureus.
- Assessed metabolic burst activity and degranulation.
- Employed metabolic inhibitors (2-deoxy-D-glucose) and microfilament inhibitors (cytochalasin B).
- Investigated the role of pronase, mannose, protein A, teichoic acid, and bacterial capsule.
Main Results:
- Uptake of unopsonized S. aureus was slower but induced similar PMN metabolic activity and degranulation as opsonized bacteria.
- Metabolic and microfilament inhibitors significantly impaired uptake of unopsonized bacteria, with less effect on opsonized bacteria.
- Pronase treatment blocked unopsonized bacterial uptake but not opsonized.
- Mannose did not inhibit uptake.
- Recognition was independent of protein A and teichoic acid; capsule presence inhibited uptake.
Conclusions:
- PMN phagocytosis of S. aureus involves complex interactions influenced by opsonins.
- While opsonins facilitate uptake rate, the induction of PMN activation (metabolic burst, degranulation) is not solely dependent on them.
- Specific bacterial surface components and host cell mechanisms play critical roles in S. aureus recognition and engulfment by PMN.
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