Differences in interleukin-1β release-inducing activity of Candida albicans toward dendritic cells and macrophages

Akira Hasebe1, Ayumi Saeki1, Yasuhiro Yoshida2

  • 1Departments of Oral Molecular Microbiology, Faculty of Dental Medicine and Graduate School of Dental Medicine, Hokkaido University, Kita 13, Nishi 7, Kita-ku, Sapporo 060-8586, Japan.

Insights

Candida albicans induces the proinflammatory cytokine IL-1β differently in dendritic cells and macrophages. Macrophages require direct contact and hyphal formation, unlike dendritic cells, for IL-1β release.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Interleukin-1 beta (IL-1β) is a critical proinflammatory cytokine in host defense against fungal infections like candidiasis.
  • Understanding how immune cells respond to Candida albicans is vital for developing effective antifungal strategies.

Purpose of the Study:

  • To investigate the distinct mechanisms by which Candida albicans triggers IL-1β release from dendritic cells and macrophages.
  • To identify key differences in cellular interactions and fungal morphology requirements for IL-1β induction.

Main Methods:

  • Utilized two Candida albicans strains: a uridine-auxotrophic strain (CAI4) and a naturally hyphae-forming strain (pACT1-GFP).
  • Stimulated LPS-primed murine macrophage and dendritic cell lines with the C. albicans strains.
  • Assessed IL-1β release, extracellular ATP levels, and the requirement for direct cell contact and fungal morphological changes.

Main Results:

  • Both C. albicans strains induced IL-1β release from dendritic cells.
  • Macrophages showed significant IL-1β release only with the hyphae-forming strain (pACT1-GFP), with minimal release from the CAI4 strain.
  • Macrophage IL-1β induction required direct contact and morphological transition of C. albicans to hyphae, while dendritic cells did not have this requirement.
  • Dead C. albicans induced IL-1β in dendritic cells but not macrophages.

Conclusions:

  • Candida albicans employs divergent mechanisms to induce IL-1β release in dendritic cells versus macrophages.
  • Differences in extracellular ATP release and fungal morphology significantly influence the immune response in these distinct cell types.
Abstract

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