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Updated: Feb 8, 2026

Macrophage Cholesterol Depletion and Its Effect on the Phagocytosis of Cryptococcus neoformans
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Macrophage Cholesterol Depletion and Its Effect on the Phagocytosis of Cryptococcus neoformans

Published on: December 19, 2014

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Microglia sense fungal infections through capsular components from capillary-bound Cryptococcus neoformans via

Chenxu Feng1, Ge Wang1,2, Yixuan Wang1

  • 1Sheng Yushou Center of Cell Biology and Immunology, School of Life Sciences and Biotechnology, Shanghai Jiao Tong University, Shanghai, China.

Plos Biology
|February 6, 2026
PubMed

Insights

Brain-resident microglia detect fungal pathogens like Cryptococcus neoformans indirectly through released capsule components. This detection mechanism, involving endothelial cells and nucleotide signaling, offers new avenues for antifungal therapies targeting microglia.

Area of Science:

  • Neuroimmunology
  • Infectious Diseases
  • Cell Biology

Background:

  • Macrophages are crucial for host defense against pathogens.
  • The mechanism by which brain-resident macrophages (microglia) detect pathogens without direct contact is not fully understood.
  • Cryptococcus neoformans is an encapsulated fungal pathogen that can infect the brain.

Purpose of the Study:

  • To investigate how microglia detect Cryptococcus neoformans in the brain parenchyma.
  • To elucidate the role of fungal capsule components in microglia activation.
  • To explore potential therapeutic strategies targeting microglia for fungal brain infections.

Main Methods:

  • In situ imaging of a mouse model infected with Cryptococcus neoformans.
  • Analysis of microglia response to encapsulated vs. nonencapsulated fungi.
  • Investigation of the role of fungal capsule components, specifically glucuronoxylomannan (GXM).
  • Assessment of endothelial cell activation and nucleotide signaling pathways.

Main Results:

  • Microglia detect capillary-residing Cryptococcus neoformans before it crosses the blood-brain barrier.
  • Microglial response is triggered by released capsule components (e.g., GXM), not the intact capsule.
  • Microglia enwrap fungi in leaky capillaries, leading to uptake but not clearance, promoting fungal growth.
  • Glucuronoxylomannan (GXM) activates endothelial cells, leading to nucleotide release that signals microglia via P2Y12 receptors.

Conclusions:

  • Microglia possess a non-contact surveillance mechanism for detecting fungal pathogens in the brain.
  • Released fungal capsule components, particularly GXM, are key triggers for this microglial response.
  • The interaction promotes fungal uptake but hinders clearance, highlighting a complex host-pathogen dynamic.
  • Understanding this pathway opens new possibilities for microglia-directed antifungal therapies.

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