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Interactions of Aspergillus fumigatus with endothelial cells: internalization, injury, and stimulation of tissue

Leila M Lopes Bezerra1, Scott G Filler

  • 1Department of Internal Medicine, Harbor-UCLA Research and Education Institute, 1124 W Carson St, Torrance, CA 90502, USA.

Blood
|November 25, 2003
PubMed

Insights

Investigating Aspergillus fumigatus interactions with endothelial cells reveals distinct mechanisms of injury. Hyphae, not conidia, promote thrombosis by increasing tissue factor activity, contributing to invasive aspergillosis pathogenesis.

Area of Science:

  • Mycology
  • Pathogenesis
  • Endothelial Cell Biology

Background:

  • Invasive aspergillosis presents a high mortality risk in hematologic malignancy patients.
  • The infection is marked by vascular invasion and thrombosis.
  • Understanding Aspergillus fumigatus interactions with endothelial cells is crucial for elucidating disease mechanisms.

Purpose of the Study:

  • To investigate the in vitro interactions between Aspergillus fumigatus conidia and hyphae with endothelial cells.
  • To determine the mechanisms by which these fungal forms induce endothelial cell injury and affect tissue factor activity.

Main Methods:

  • In vitro study using endothelial cells exposed to Aspergillus fumigatus conidia and hyphae.
  • Assessment of microfilament rearrangement, endocytosis, endothelial cell injury, and tissue factor activity.
  • Comparison of effects between live and killed fungal forms.

Main Results:

  • Both conidia and hyphae induced endothelial cell microfilament rearrangement and endocytosis; conidia were endocytosed more readily.
  • Endocytosed conidia and hyphae caused progressive endothelial cell injury, with live conidia causing more injury than live hyphae.
  • Hyphae, but not conidia, significantly increased endothelial cell tissue factor activity and antigen expression, regardless of viability.

Conclusions:

  • Aspergillus fumigatus conidia and hyphae interact differently with endothelial cells, leading to distinct pathogenic mechanisms.
  • Endothelial cell invasion and injury by hyphae, coupled with increased tissue factor activity, likely contribute to angioinvasion and thrombosis in invasive aspergillosis.

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