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Ingestion of yeast forms of Sporothrix schenckii by mouse peritoneal macrophages

Infection and Immunity
|February 1, 1983
PubMed

Insights

Phagocytosis of Sporothrix schenckii yeasts by macrophages is enhanced by concanavalin A (ConA) and inhibited by specific sugars. Neuraminidase treatment boosts yeast ingestion, suggesting macrophage receptors bind S. schenckii surface components.

Area of Science:

  • Immunology
  • Mycology
  • Cell Biology

Background:

  • Sporothrix schenckii is a fungus causing sporotrichosis.
  • Macrophage phagocytosis is crucial for controlling fungal infections.
  • Understanding fungal-macrophage interactions is key to developing treatments.

Purpose of the Study:

  • To investigate the phagocytosis of Sporothrix schenckii yeast forms by mouse peritoneal macrophages.
  • To determine the role of yeast surface components and macrophage receptors in phagocytosis.
  • To explore the effects of lectins and specific sugars on fungal uptake.

Main Methods:

  • Incubation of thioglycolate-elicited mouse peritoneal macrophages with S. schenckii yeast forms.
  • Use of concanavalin A (ConA) for opsonization and assessment of phagocytic indexes.
  • Treatment of yeast cells with neuraminidase and evaluation of phagocytosis.
  • Inhibition studies using various monosaccharides, derivatives, and purified polysaccharides.
  • Control experiments with latex particles and sheep erythrocytes.

Main Results:

  • Concanavalin A (ConA) opsonization significantly increased yeast phagocytosis, dependent on ConA concentration and yeast surface receptors.
  • Neuraminidase treatment of S. schenckii enhanced the ingestion of unopsonized yeasts by 7.7-fold.
  • Specific monosaccharides (mannose, rhamnose, galactose, glucosamine, N-acetylglucosamine, N-acetylneuraminic acid) partially inhibited phagocytosis.
  • Purified rhamnomannan and galactomannan inhibited phagocytosis, while certain peptidopolysaccharides showed toxicity or no effect.
  • Macrophage pretreatment with inhibitory sugars did not affect phagocytosis of non-fungal particles.

Conclusions:

  • Macrophage phagocytosis of S. schenckii is mediated by specific interactions with yeast surface carbohydrates.
  • Lectins like ConA can enhance fungal uptake by binding to yeast surface receptors.
  • Specific sugars and their derivatives act as inhibitors, suggesting the presence of corresponding receptors on macrophages.
  • These findings indicate the existence of specific receptors on peritoneal macrophages that recognize and bind S. schenckii cell surface components, influencing phagocytosis.

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