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Cryptococcus neoformans survive and replicate in human microglia

S C Lee1, Y Kress, M L Zhao

  • 1Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, New York, USA.

Laboratory Investigation; a Journal of Technical Methods and Pathology
|December 1, 1995
PubMed
Summary
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Cryptococcus neoformans (CN) survives and replicates within human microglia by escaping phagolysosomes. This intracellular growth occurs in spacious phagosomes, suggesting a novel mechanism for fungal pathogenesis in the central nervous system.

Area of Science:

  • Mycology
  • Immunology
  • Neuroscience

Background:

  • Cryptococcus neoformans (CN) is an opportunistic pathogen causing fatal meningoencephalitis in immunocompromised individuals.
  • Microglia and macrophages are key central nervous system (CNS) cells infected by CN.
  • The cellular-level interaction between CN and CNS phagocytes remains poorly understood.

Purpose of the Study:

  • To investigate the fate of CN within human microglia at the cellular level.
  • To elucidate the mechanisms of CN survival and replication inside microglial cells.

Main Methods:

  • Human fetal microglial cultures were used to study Ab-opsonized CN.
  • Phase-contrast microscopy, transmission electron microscopy (TEM), and immunocytochemistry were employed.
  • Intracellular localization and capsular antigen of CN were analyzed.

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Main Results:

  • Microglia initially internalized CN in phagolysosomes, but CN escaped and resumed extracellular growth.
  • Intracellular CN were found in spacious phagosomes (SP) and close-fitting phagosomes (CP).
  • SP facilitated CN survival and replication, evidenced by multiple budding yeast cells and increased CN numbers over time. Modification of capsular polysaccharide was observed within SP.

Conclusions:

  • CN survives and replicates within spacious phagosomes in human microglia.
  • Alterations in CN capsular polysaccharide within SP may contribute to aberrant microglial-CN interactions.
  • This study reveals a novel mechanism for CN pathogenesis within the CNS.