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Updated: Jun 22, 2026
Live-cell Video Microscopy of Fungal Pathogen Phagocytosis
Published on: January 9, 2013
Escherichia coli and TNF-alpha modulate macrophage phagocytosis of Candida glabrata
Donavon J Hess1, Michelle J Henry-Stanley, Catherine M Bendel
1Department of Surgery, University of Minnesota, Minneapolis, Minnesota, USA.
Background:
The incidence of systemic nonalbicans Candida (especially C. glabrata) infections is increasing dramatically in intensive care units, but relatively little is known about the pathogenesis or host defenses associated with these life threatening infections.
Materials And Methods:
The course of systemic C. glabrata infection was assessed as the fungal burden in the kidneys and livers of mice sacrificed 1, 8, and 15 d after intravenous C. glabrata. Sixteen hours before each sacrifice, half of the mice were injected intraperitoneally with intact viable or nonviable E. coli cells, or with E. coli lipopolysaccharide (LPS), or with tumor necrosis factor (TNF)-alpha. To clarify the effect of LPS and TNF-alpha on phagocytosis, resident (unstimulated) mouse peritoneal macrophages were harvested, cultivated ex vivo, and some cultures were treated with LPS or TNF-alpha prior to 30 min incubation with C. glabrata.
Results:
Compared with mice injected with vehicle, each agent (intact E. coli cells or E. coli LPS or TNF-alpha) was consistently associated with decreased numbers of tissue C. glabrata, and some of these decreases were significant (P < 0.05). Compared with untreated macrophages, phagocytosis of C. glabrata was increased with LPS-treated macrophages (P < 0.01), and phagocytosis was also increased in the presence of TNF-alpha (P < 0.01).
Conclusion:
E. coli LPS and TNF-alpha may participate in host defense against C. glabrata by a mechanism involving increased macrophage phagocytosis, suggesting that stimulation of inflammatory cytokines may facilitate host clearance of C. glabrata.
Insights
Systemic Candida glabrata infections are rising in ICUs. Escherichia coli lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) boost macrophage phagocytosis, aiding host defense against C. glabrata.
Area of Science:
- Infectious Diseases
- Immunology
- Critical Care Medicine
Background:
- Systemic non-albicans Candida infections, particularly Candida glabrata, are increasing in intensive care units.
- Pathogenesis and host defenses for these severe infections remain poorly understood.
Purpose of the Study:
- To investigate the host response to systemic Candida glabrata infection.
- To evaluate the role of Escherichia coli components in modulating host defenses against C. glabrata.
Main Methods:
- Assessed fungal burden in mouse kidneys and livers following systemic C. glabrata infection.
- Administered E. coli cells, lipopolysaccharide (LPS), or tumor necrosis factor-alpha (TNF-alpha) to mice.
- Ex vivo analysis of macrophage phagocytosis of C. glabrata after LPS or TNF-alpha treatment.
Main Results:
- E. coli LPS and TNF-alpha significantly reduced fungal burden in infected mice.
- LPS and TNF-alpha treatments markedly increased the phagocytosis of C. glabrata by macrophages.
- These effects were observed in vivo and ex vivo.
Conclusions:
- E. coli LPS and TNF-alpha may enhance host defense against C. glabrata infections.
- Increased macrophage phagocytosis is a likely mechanism for this enhanced defense.
- Stimulating inflammatory cytokines could be a therapeutic strategy for C. glabrata infections.
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