Comment on "Sterilizing immunity in the lung relies on targeting fungal apoptosis-like programmed cell death"

Abdel Aouacheria1, Kyle W Cunningham2, J Marie Hardwick3

  • 1ISEM, Institut des Sciences de l'Evolution de Montpellier, Université de Montpellier, CNRS, EPHE, IRD, Montpellier, France.

Science (New York, N.Y.)
|June 23, 2018
PubMed

Insights

The fungus Aspergillus fumigatus may not undergo programmed cell death triggered by human neutrophils. Current evidence is insufficient to confirm protease signaling or a fungal caspase inhibitor

Area of Science:

  • Mycology
  • Immunology
  • Cell Biology

Background:

  • Aspergillus fumigatus is a common fungus that causes aspergillosis in humans.
  • Lung neutrophils are known to trigger cell death in fungal pathogens.
  • Previous studies suggested caspase-dependent apoptosis-like cell death in A. fumigatus.

Purpose of the Study:

  • To investigate the mechanism of cell death in Aspergillus fumigatus upon interaction with lung neutrophils.
  • To determine if fungal cell death is mediated by a protease signaling cascade.
  • To assess the role of a fungal caspase inhibitor homologous to human survivin.

Main Methods:

  • The study by Shlezinger et al. utilized specific technologies to observe fungal cell death.
  • Analysis focused on caspase-dependent pathways and protease signaling.
  • Investigated the effect of a fungal caspase inhibitor.

Main Results:

  • The study reports that Aspergillus fumigatus undergoes caspase-dependent apoptosis-like cell death.
  • This cell death is triggered by lung neutrophils.
  • However, the evidence for a protease signaling cascade thwarted by a fungal caspase inhibitor was found to be unreliable.

Conclusions:

  • The findings question the previously reported mechanism of fungal cell death in aspergillosis.
  • Further research is needed to confirm the role of protease signaling and fungal caspase inhibitors in A. fumigatus pathogenesis.
  • Reliable technologies are crucial for accurate investigation of fungal-host interactions.

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