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The zinc-reversible antimicrobial activity of neutrophil lysates and abscess fluid supernatants
P G Sohnle1, C Collins-Lech, J H Wiessner
1Department of Medicine, Medical College of Wisconsin, Milwaukee.
Abstract:
There is some evidence to suggest that microbial growth inhibition may occur in chronic abscesses. A substance perhaps responsible for this phenomenon is calprotectin, a neutrophil cytoplasmic protein that inhibits microbial growth and that belongs to a class of proteins often having specific binding sites for zinc. In the present study, the suppressive effects of either human or mouse neutrophil lysates on Candida albicans growth were found to be completely reversed by micromolar quantities of zinc but not by iron or other trace elements. Similarly, supernatants of exudates from experimental abscesses in mice or from clinical specimens of abscesses in humans markedly inhibited the proliferation of C. albicans, and this effect was also completely reversed by zinc. A protein complex characteristic of calprotectin was identified in the abscess fluids. Preparations of the neutrophil growth-inhibiting protein, containing predominantly calprotectin, were shown to have zinc-binding activity by a dialysis technique. These findings suggest that the major mechanism of C. albicans growth inhibition by abscess fluids is through competition for zinc by a cytoplasmic protein apparently released from dying neutrophils.
Insights
Calprotectin, a neutrophil protein, inhibits Candida albicans growth in abscesses by binding zinc. This microbial growth inhibition is reversed by adding zinc, suggesting a key role for zinc competition.
Area of Science:
- Microbiology
- Immunology
- Biochemistry
Background:
- Chronic abscesses may exhibit microbial growth inhibition.
- Calprotectin, a neutrophil protein, is a potential mediator of this inhibition due to its zinc-binding properties.
Purpose of the Study:
- To investigate the mechanism of microbial growth inhibition in abscesses.
- To determine the role of calprotectin and zinc in inhibiting Candida albicans proliferation.
Main Methods:
- Assessing the effect of neutrophil lysates and abscess exudates on Candida albicans growth.
- Investigating the impact of zinc, iron, and other trace elements on microbial inhibition.
- Identifying calprotectin in abscess fluids using protein complex analysis.
- Measuring zinc-binding activity of purified neutrophil proteins via dialysis.
Main Results:
- Human and mouse neutrophil lysates inhibited Candida albicans growth, an effect reversed by zinc.
- Abscess exudates also inhibited C. albicans proliferation, with zinc reversal observed.
- Calprotectin-characteristic protein complexes were found in abscess fluids.
- Purified neutrophil proteins showed zinc-binding activity.
Conclusions:
- The primary mechanism for Candida albicans growth inhibition in abscesses involves zinc competition.
- Calprotectin released from dying neutrophils likely mediates this zinc sequestration, thereby inhibiting microbial growth.