Transcriptome profiling of endothelial cells during infections with high and low densities of C. albicans cells

Crystale S Y Lim1, Rozita Rosli, Heng-Fong Seow

  • 1Dept. of Biomedical Sciences, Faculty of Medicine & Health Sciences, Universiti Putra Malaysia, Serdang, Selangor, Malaysia.

Insights

High-density Candida albicans yeast infections trigger a strong host response, inducing apoptosis and cell death. These findings challenge the notion that yeast-form C. albicans is avirulent, suggesting a role in pathogenesis.

Area of Science:

  • Mycology
  • Infectious Diseases
  • Cell Biology

Background:

  • Systemic Candida albicans infections are increasing, yet its pathogenesis remains unclear.
  • Previous studies suggested yeast-form Candida albicans is avirulent, lacking host gene response.
  • This study investigates the pathogenic potential of yeast-form Candida albicans at high densities.

Purpose of the Study:

  • To determine the host response to different densities of Candida albicans infection.
  • To investigate the role of yeast-form Candida albicans in pathogenesis.
  • To analyze the transcriptional changes in human umbilical vein endothelial cells (HUVEC) during infection.

Main Methods:

  • Infection of HUVEC with high and low densities of Candida albicans.
  • Transcriptional profiling of HUVEC to analyze gene expression changes.
  • Assessment of HUVEC viability after exposure to conditioned media from infections.

Main Results:

  • High-density Candida albicans infections induced a stronger and broader transcriptional response in HUVEC compared to low-density infections.
  • Many differentially expressed genes were associated with apoptosis and cell death pathways.
  • Conditioned media from high-density infections reduced HUVEC viability, indicating cytotoxic molecule release.

Conclusions:

  • High-density yeast-form Candida albicans infections are not avirulent and can induce significant host cell responses.
  • Candida albicans may contribute to pathogenesis through mechanisms involving yeast-form proliferation and secreted factors.
  • Further research is needed to elucidate the specific molecules and pathways involved in yeast-form-mediated pathogenesis.

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