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Fas-FasL interactions modulate host defense against systemic Candida albicans infection

M G Netea1, J W van Der Meer, J F Meis

  • 1Departments of Medicine, Catholic University Nijmegen, University Hospital, Nijmegen, The Netherlands.

The Journal of Infectious Diseases
|October 9, 1999
PubMed

Insights

Fas-FasL interactions are crucial for host defense against Candida albicans infection. Blocking these interactions in mice increased protective cytokines and reduced fungal infections.

Area of Science:

  • Immunology
  • Microbiology
  • Infectious Diseases

Background:

  • Fas-FasL costimulation influences proinflammatory cytokine production.
  • MRL/lpr mice, deficient in functional Fas, exhibit elevated cytokine levels.
  • Fas-FasL interactions' role in Candida albicans infection is not fully understood.

Purpose of the Study:

  • To investigate the role of Fas-FasL interactions in host defense against lethal Candida albicans infection.
  • To determine the impact of Fas deficiency on cytokine production and disease progression in candidiasis.

Main Methods:

  • Comparison of cytokine production by macrophages from MRL/lpr and MRL+/+ mice stimulated with C. albicans.
  • Assessment of mortality, fungal load, and hyphal formation in Fas-deficient and control mice with disseminated candidiasis.
  • Evaluation of neutrophil recruitment and phagocytic activity in response to C. albicans infection.

Main Results:

  • MRL/lpr macrophages produced significantly more tumor necrosis factor and interleukin-1 upon C. albicans stimulation.
  • Fas-deficient mice showed significantly lower mortality and fungal burden in disseminated candidiasis.
  • Increased neutrophil recruitment was observed in Fas-deficient mice, correlating with reduced fungal growth and hyphal invasion.

Conclusions:

  • Fas-FasL interactions are involved in host defense against Candida albicans.
  • Absence of Fas-FasL signaling enhances cytokine production, leading to protection against disseminated candidiasis.
  • Neutrophil recruitment is a key mechanism underlying the protective effects of Fas deficiency in C. albicans infection.

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