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• W1969458724 abstract "The main cytokine induced by the interaction of oral epithelial cells with C. glabrata is granulocyte monocyte colony-stimulating factor (GM-CSF); however, the mechanisms regulating this response are unknown. Based on previously published information on the interactions of C. albicans with oral epithelial cells, we hypothesized that interaction with viable C. glabrata triggers GM-CSF synthesis via NF-kappaB activation. We found that C. glabrata-induced GM-CSF synthesis was adhesion-dependent, enhanced by endocytosis, and required fungal viability. NF-kappaB activation was noted during interaction of epithelial cells with C. glabrata, and pre-treatment with an NF-kappaB inhibitor partly inhibited GM-CSF synthesis. Blocking TLR4 with anti-TLR4 antibody did not inhibit GM-CSF production. In contrast, an anti-CDw17 antibody triggered significant inhibition of NF-kappaB activation and GM-CSF synthesis. beta-glucans did not stimulate GM-CSF synthesis, suggesting that the CDw17/NF-kappaB/GM-CSF pathway may be beta-glucan-independent. This study provides new insights into the mechanism of GM-CSF induction by C. glabrata." @default.
• W1969458724 created "2016-06-24" @default.
• W1969458724 creator A5017105081 @default.
• W1969458724 creator A5091563483 @default.
• W1969458724 date "2009-08-01" @default.
• W1969458724 modified "2023-10-12" @default.
• W1969458724 title "Epithelial GM-CSF Induction by <i>Candida glabrata</i>" @default.
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• W1969458724 doi "https://doi.org/10.1177/0022034509341266" @default.
• W1969458724 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2836204" @default.
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