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Fungal surfaces: effects of interactions with phagocytic cells
1Evans Memorial Department of Clinical Research, University Hospital, Boston, Massachusetts 02118.
Abstract:
Fungal surfaces undergo profound changes during morphogenesis that modify host responses. For example, inhaled spores or conidia of Rhizopus or Aspergillus lose their surface hydrophobic outer layers, initially swell, and then germinate to form mycelia that may invade tissues. These various fungal forms not only elicit differing response from host phagocytic cells but also differ in their susceptibilities to cellular microbicidal mechanisms. In addition, studies comparing neutrophil activation responses to opsonized and unopsonized Candida hyphae indicate that the presence or absence of antibody or complement on fungal surfaces determines distinct patterns of the early responses of neutrophils to stimulation, such as membrane depolarization, cytosolic increase in calcium, and phosphoinositide turnover. These initial events in the neutrophil activation sequence are followed by release of both fungicidal granule constituents and oxidants from the respiratory burst. The quantity and specificity of delivery of these toxic neutrophil products ultimately determine the relative efficiency of fungicidal activity versus inflammatory cytotoxicity to host cells.
Insights
Fungal surface changes during morphogenesis alter host immune cell responses. Opsonization of fungi significantly impacts neutrophil activation, influencing the effectiveness of fungal clearance and host tissue damage.
Area of Science:
- Mycology
- Immunology
- Cell Biology
Background:
- Fungal morphogenesis involves significant surface alterations.
- These changes influence host immune cell interactions and susceptibility to microbicidal mechanisms.
- Different fungal forms elicit varied responses from phagocytic cells.
Purpose of the Study:
- To investigate how fungal surface changes during morphogenesis affect host responses.
- To compare neutrophil activation to opsonized versus unopsonized fungal forms.
- To understand the role of opsonization in determining the efficacy of host defense.
Main Methods:
- Comparative analysis of host immune cell responses to different fungal morphotypes.
- Assessment of neutrophil activation markers (e.g., membrane depolarization, calcium influx) upon exposure to opsonized and unopsonized fungi.
- Evaluation of fungal susceptibility to cellular microbicidal mechanisms.
Main Results:
- Fungal surface hydrophobicity changes during morphogenesis (e.g., spore to mycelia).
- Opsonization (antibody or complement) on fungal surfaces dictates distinct neutrophil activation patterns.
- Neutrophil responses include membrane depolarization, calcium flux, and phosphoinositide turnover.
Conclusions:
- Fungal morphogenesis dynamically alters surface properties, impacting host immune recognition.
- Opsonization status is critical in modulating early neutrophil activation events.
- The efficiency of fungal killing versus host cell damage by neutrophils depends on the targeted delivery of microbicidal products.