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Related Concept Videos

Fungal Phylum Microsporidia01:28

Fungal Phylum Microsporidia

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Microsporidia are a group of obligate intracellular fungi that were initially classified as protists but were later reclassified based on phylogenetic, molecular, and structural evidence linking them to the Chytridiomycota. These unicellular, non-motile organisms are highly specialized parasites that infect a wide range of animal hosts, including humans. They have evolved extensive genomic and metabolic reductions, making them highly dependent on their hosts for survival.Morphology and Genomic...
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Related Experiment Video

Updated: Jan 9, 2026

Macrophage Cholesterol Depletion and Its Effect on the Phagocytosis of Cryptococcus neoformans
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Cryptococcus exploits delayed microglial activation, and microglial osteopontin/Spp1 impairs peripheral host control.

Estefany Y Reyes1, Jae Yong2, Devon T DiPalma1

  • 1Department of Integrative Immunobiology, Duke University School of Medicine, Durham, NC 27705, USA.

Cell Host & Microbe
|December 2, 2025
PubMed
Summary

Cryptococcus causes deadly meningoencephalitis (CM). Host brain immune responses are surprisingly slow, allowing the fungus to establish infection before microglia fully activate.

Keywords:
Candida albicansCryptococcusIFN-γOPN/Spp1Th1 cellscryptococcal meningoencephalitisdisease-associated microgliafungal infectionmicroglianeuroimmunology

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Area of Science:

  • Neuroscience
  • Immunology
  • Mycology

Background:

  • Cryptococcus is a WHO critical-priority pathogen causing meningoencephalitis (CM).
  • CM is a leading cause of death in HIV/AIDS patients.
  • Host brain immune responses during CM are poorly understood.

Purpose of the Study:

  • To investigate host brain immune cell responses to Cryptococcus during CM.
  • To understand the kinetics of microglial activation and leukocyte recruitment in the brain.

Main Methods:

  • A mouse model of systemic Cryptococcus infection was used.
  • The timing of fungal brain infiltration, microglial activation, and leukocyte recruitment was analyzed.
  • The role of T-helper 1 (Th1) cell-derived interferon-gamma (IFN-γ) and microglia-derived osteopontin (OPN) was examined.

Main Results:

  • Cryptococcus infiltrates the brain rapidly (within 1 day).
  • Microglial activation and leukocyte recruitment are significantly delayed (14 days), unlike in Candida albicans infections.
  • Microglial activation depends on Th1 cell-derived IFN-γ, indicating adaptive immunity precedes innate responses.
  • Microglia-derived osteopontin exacerbates CM by increasing fungal loads.

Conclusions:

  • Host cellular response in the brain during Cryptococcus meningoencephalitis is uniquely slow.
  • This delay provides the fungus an extended window to establish infection.
  • Understanding this slow response is crucial for developing effective therapies against CM.