Glycosaminoglycan profile in macrophages exposed to Candida albicans and interleukins

M Bodo1, E Blasi, E Becchetti

  • 1Dipartimento di Morfologia ed Embriologia, Università di Ferrara, Italy. pzf@ifeuniv.unife.it

Insights

Macrophages interacting with Candida albicans alter glycosaminoglycan (GAG) profiles, particularly in ANA-1 cells, impacting their function. These changes, influenced by interleukins, suggest a role in macrophage heterogeneity.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Glycosaminoglycans (GAGs) are key extracellular matrix components influencing macrophage phagocytosis.
  • Macrophage phenotype and function are critical in host defense against pathogens like Candida albicans.

Purpose of the Study:

  • To investigate how Candida albicans (iCa) interaction affects glycosaminoglycan (GAG) profiles in ANA-1 and BV-2 macrophage cell lines.
  • To determine the modulatory effects of interleukin-1alpha (IL-1α) and interleukin-6 (IL-6) on GAG expression during iCa exposure.

Main Methods:

  • Analysis of GAG profiles in ANA-1 and BV-2 macrophage cell lines.
  • Treatment with Candida albicans (iCa), IL-1α, and IL-6, followed by GAG quantification and characterization.
  • Comparison of GAG changes between cell lines and treatment groups.

Main Results:

  • ANA-1 cells showed reduced total GAG accumulation upon iCa treatment, with IL-1α altering specific GAG chain percentages (decreased heparan sulfate/chondroitin sulfate, increased hyaluronic acid).
  • IL-6 treatment decreased the hyaluronic acid/sulfated GAG ratio in ANA-1 cells, with or without iCa.
  • BV-2 cells exhibited a distinct GAG pattern, with less modulation by iCa and ILs compared to ANA-1 cells.

Conclusions:

  • Macrophage-pathogen interactions and cytokine signaling significantly alter GAG expression profiles.
  • Differential GAG modulation in ANA-1 versus BV-2 cells highlights cell-type-specific responses.
  • Changes in individual GAG classes may underlie the observed functional heterogeneity in macrophages.