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The effect of zinc on bacterial phagocytosis, killing and cytoprotection in human polymorphonuclear leucocytes
B Sunzel1, S Holm, C O Reuterving
1Department of Oral & Maxillofacial Surgery, University of Umeå, Sweden.
Abstract:
An in vitro study examining the effects of zinc treatment on human PMN cell phagocytosis and killing of Staphylococcus aureus and Staphylococcus epidermidis and the cytoprotection of zinc against staphylococcal toxins. Phagocytosis was studied by transmission electron microscopy using different microbiological techniques, one of which was designed to follow the kinetics of bacterial killing. No effect was found on phagocytosis and bacterial killing. The cytotoxic effects of a crude toxin and an alpha-toxin extracted from Staphylococcus aureus preparations were studied on human PMN cells using the standard 51Cr release assay. Both toxins induced a dose-dependent leakage of 51Cr, indicating cell membrane damage. These results were confirmed by electron microscopy during the phagocytosis of S. aureus, where severe PMN cellular degeneration was observed. The addition of zinc to PMN cells strongly inhibited the release of 51Cr. In conclusion, our results show that zinc in higher than physiological concentrations does not inhibit PMN cell functions such as phagocytosis and intracellular killing of S. aureus and S. epidermidis. The addition of zinc may be beneficial in certain clinical situations, such as wound healing, zinc deficiency and infections involving toxin-producing bacteria, e.g. S. aureus.
Insights
Zinc protects human immune cells from staphylococcal toxins without impairing phagocytosis or bacterial killing. This suggests zinc may benefit infections involving toxin-producing bacteria like Staphylococcus aureus.
Area of Science:
- Immunology
- Microbiology
- Toxicology
Background:
- Staphylococcus aureus and S. epidermidis are common human pathogens.
- Staphylococcal toxins can damage human immune cells, potentially hindering infection control.
- Zinc's role in modulating immune cell function against bacterial toxins requires further investigation.
Purpose of the Study:
- To investigate the effect of zinc on human polymorphonuclear leukocyte (PMN) cell functions.
- To assess zinc's cytoprotective capacity against staphylococcal toxins.
- To determine if zinc impacts PMN phagocytosis and killing of Staphylococcus species.
Main Methods:
- In vitro study using human PMN cells.
- Transmission electron microscopy to observe phagocytosis and bacterial killing kinetics.
- 51Cr release assay to measure cell membrane damage induced by staphylococcal toxins.
- Exposure of PMN cells to Staphylococcus aureus and Staphylococcus epidermidis.
Main Results:
- Zinc did not affect PMN phagocytosis or the killing of S. aureus and S. epidermidis.
- Staphylococcal toxins caused dose-dependent PMN cell membrane damage, confirmed by 51Cr release and electron microscopy.
- Zinc significantly inhibited toxin-induced 51Cr release, indicating cytoprotection.
Conclusions:
- Zinc, even at supra-physiological concentrations, does not impede PMN phagocytosis or intracellular killing of S. aureus and S. epidermidis.
- Zinc demonstrates a protective effect against staphylococcal toxin-induced cell damage.
- Zinc supplementation may be beneficial in clinical scenarios like wound healing, zinc deficiency, and infections caused by toxin-producing bacteria.