PUBLICATION

Survival in macrophages induces enhanced virulence in Cryptococcus

Authors
Nielson, J.A., Jezewski, A.J., Wellington, M., Davis, J.M.
ID
ZDB-PUB-231211-6
Date
2023
Source
mSphere   9(1): e0050423 (Journal)
Registered Authors
Keywords
Cryptococcus, capsule, dissemination, macrophage, phagocytosis
MeSH Terms
  • Macrophages/microbiology
  • Cryptococcosis*/microbiology
  • Zebrafish/microbiology
  • Mannose
  • Animals
  • Mice
  • Humans
  • Cryptococcus neoformans*
  • Chitin/metabolism
  • Virulence
PubMed
38073033 Full text @ mSphere
Abstract
Cryptococcosis begins in the lungs and can ultimately travel through the bloodstream to cause devastating infection in the central nervous system. In the zebrafish model, small amounts of cryptococcus inoculated into the bloodstream are initially phagocytosed and become far more capable of dissemination after they exit macrophages. Similarly, survival in the mouse lung produces cryptococcal cell types with enhanced dissemination. In this study, we have evaluated how phagocytosis changes the properties of Cryptococcus during pathogenesis. Macrophage-experienced cells (MECs) become "licensed" for enhanced virulence. They out-disseminate culture-grown cells in the fish and out-compete non-MECs in the mouse lung. Analysis of their cell surface demonstrates that MECs have increased availability of cell wall components mannose and chitin substances involved in provoking phagocytosis. These findings suggest how Cryptococcus might tune its cell surface to induce but survive repeated phagocytosis during early pathogenesis in the lung.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping