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Induction of Petite Colonies in Candida glabrate via Rose Bengal-Mediated Photodynamic Therapy

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Epithelial GM-CSF induction by Candida glabrata.

L Li¹, A Dongari-Bagtzoglou

¹Division of Periodontology, School of Dental Medicine, University of Connecticut, 263 Farmington Ave., Farmington, CT 06030-1710, USA.

Journal of Dental Research

|September 8, 2009

Summary

Candida glabrata triggers granulocyte monocyte colony-stimulating factor (GM-CSF) via NF-kappaB activation in oral cells. This interaction is adhesion-dependent and involves CDw17, independent of beta-glucans.

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Area of Science:

Immunology
Microbiology
Oral Biology

Background:

Candida glabrata is a fungal pathogen that interacts with oral epithelial cells.
Granulocyte-monocyte colony-stimulating factor (GM-CSF) is a key cytokine induced during this interaction.
The precise mechanisms regulating GM-CSF induction by C. glabrata remain largely unknown.

Purpose of the Study:

To investigate the molecular mechanisms underlying C. glabrata-induced GM-CSF synthesis in oral epithelial cells.
To test the hypothesis that viable C. glabrata triggers GM-CSF via NF-kappaB activation.
To identify specific cellular receptors and pathways involved in this immune response.

Main Methods:

Co-culture of oral epithelial cells with viable C. glabrata.
Assessment of GM-CSF synthesis and NF-kappaB activation.
Use of NF-kappaB inhibitors, anti-TLR4 antibodies, and anti-CDw17 antibodies.
Investigation of the role of fungal viability, adhesion, and endocytosis.
Evaluation of beta-glucan stimulation.

Main Results:

C. glabrata-induced GM-CSF synthesis was dependent on fungal adhesion and viability, and enhanced by endocytosis.
NF-kappaB activation was observed during C. glabrata interaction, and its inhibition partially reduced GM-CSF synthesis.
Blocking Toll-like receptor 4 (TLR4) did not affect GM-CSF production.
An anti-CDw17 antibody significantly inhibited both NF-kappaB activation and GM-CSF synthesis.
Beta-glucans did not stimulate GM-CSF production, suggesting a beta-glucan-independent pathway.

Conclusions:

The interaction of C. glabrata with oral epithelial cells induces GM-CSF production through a pathway involving CDw17 and NF-kappaB.
This pathway appears to be independent of beta-glucans and TLR4.
The findings elucidate a novel mechanism of innate immune activation in the oral cavity during fungal infection.