Epithelial GM-CSF Induction by Candida glabrata

Li, L.; Dongari-Bagtzoglou, A.

doi:10.1177/0022034509341266

Cited by 39Antifungal resistance and susceptibilityOral microbiology and periodontitis researchImmune Response and Inflammation

Epithelial GM-CSF Induction by Candida glabrata

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Li, L., Dongari-Bagtzoglou, A.·2009·Journal of Dental Research

DOI 10.1177/0022034509341266PMC PMC2836204

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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.

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GM-CSF production in oral epithelial cells is dependent upon the lactosylceramide receptor CDw17-mediated activation of NF-kB.
“This GM-CSF production in oral epithelial cells was later shown to be dependent upon the lactosylceramide receptor CDw17-mediated activation of NF (nuclear factor)-kB [134].”
From Candida glabrata: A Lot More Than Meets the Eye (2019) · cites this paper as [134]

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Authors: Li, L., & Dongari-Bagtzoglou, A.
Affiliations: University of Connecticut (US)
Division of Periodontology, School of Dental Medicine, University of Connecticut, 263 Farmington Ave., Farmington, CT 06030-1710, USA
Venue: Journal of Dental Research
Publisher: SAGE Publications
Published: 2009-08
Volume: 88
Issue: 8
Pages: 746-751
ISSN: 0022-0345 (ISSN-L)
1544-0591
DOI: 10.1177/0022034509341266
PMC: PMC2836204
OpenAlex: W1969458724
Cited by: 39
References: 31
Citations by year: 2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 2 · 2020: 3 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 4 · 2012: 2
FWCI: 3.22
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Dental Research (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute of Dental and Craniofacial Research (R01 DE 13986, R01DE013986)
Topics: Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords: Candida glabrata, GM-CSF, oral epithelial cells, NF-κB activation, fungal viability, endocytosis, TLR4, fungal-host interactions, oral candidiasis
MeSH terms: Antibodies, Cell Line, Endocytosis, Epithelial Cells, Glucans, Humans, Lactosylceramides, Mouth Mucosa, Polysaccharides, Polysaccharides, Bacterial, Zymosan, Cytochalasin D, Antigens, CD, Granulocyte-Macrophage Colony-Stimulating Factor, NF-kappa B, Nucleic Acid Synthesis Inhibitors, Candida glabrata, Cell Line, Tumor, beta-Glucans, Toll-Like Receptor 4

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Epithelial GM-CSF Induction by Candida glabrata

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