Oral epithelium–<i>Candida glabrata</i> interactions <i>in vitro</i>

Li, L.; Dongari-Bagtzoglou, Anna

doi:10.1111/j.1399-302x.2007.00342.x

Cited by 26 publications

(25 citation statements)

References 38 publications

(67 reference statements)

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“…Previous dose response studies showed that a maximal GM-CSF response is detected after prolonged incubation at a 0.1:1 C. glabrata- to-epithelial-cell ratio (Li and Dongari-Bagtzoglou, 2007; Li et al ., 2007), and we obtained similar data with strain MRL2302 in this study (Fig. 1A).…”

Section: Resultsmentioning

confidence: 99%

“…We have shown that C. glabrata is a potent inducer of granulocyte monocyte colony-stimulating factor (GM-CSF) in human oral keratinocytes (Li and Dongari-Bagtzoglou, 2007; Li et al ., 2007), and that strains differ in eliciting GM-CSF responses, with certain oroesophageal candidiasis isolates possessing higher GM-CSF induction capacity than oral commensal isolates (Li and Dongari-Bagtzoglou, 2007). By enhancing the proliferation, activation, as well as fungicidal activity of immuno-effector cells such as neutrophils and monocytes, GM-CSF may play a major role in local control of Candida and the prevention of invasive infection, as suggested in clinical reports (Nicolatou-Galitis et al ., 2001).…”

Section: Introductionmentioning

confidence: 99%

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Epithelial GM-CSF Induction by Candida glabrata

Dongari-Bagtzoglou

2009

J Dent Res

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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-κB activation. We found that C. glabrata-induced GM-CSF synthesis was adhesion-dependent, enhanced by endocytosis, and required fungal viability. NF-κB activation was noted during interaction of epithelial cells with C. glabrata, and pre-treatment with an NF-κB 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-κB activation and GM-CSF synthesis. β-glucans did not stimulate GM-CSF synthesis, suggesting that the CDw17/NF-κB/GM-CSF pathway may be β-glucan-independent. This study provides new insights into the mechanism of GM-CSF induction by C. glabrata.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Epithelial GM-CSF Induction by Candida glabrata

Dongari-Bagtzoglou

2009

J Dent Res

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“…Most of the proteins found from C. glabrata are involved in transcriptional regulation. It has been suggested that C. glabrata and C. albicans have a “synergistic” relationship in the pathogenesis of oral infection 39 . It may be possible that proteins from C. glabrata have some mechanism of control over expression of inflammatory factors originating from C. albicans species.…”

Section: Discussionmentioning

confidence: 99%

Role of salivary and candidal proteins in denture stomatitis: an exploratory proteomic analysis

et al. 2014

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Denture stomatitis, inflammation and redness beneath a denture, affects nearly half of all denture wearers. Candida organism, the presence of a denture, saliva, and host immunity are the key etiological factors for the condition. The role of salivary proteins in denture stomatitis is not clear. In this study 30 edentulous subjects wearing a maxillary complete denture were recruited. Unstimulated whole saliva from each subject was collected and pooled into two groups (n=15 each); healthy and stomatitis (Newton classification II and III). Label-free multidimensional liquid chromatography/tandem mass spectrometry (2D-LC-MS/MS) proteomics on two mass spectrometry platforms were used to determine peptide mass differences between control and stomatitis groups. Cluster analysis and principal component analysis were used to determine differential expression among the groups. The two proteomic platforms identified 97 and 176 proteins (ANOVA; p<0.01) differentially expressed among the healthy, type 2 and 3 stomatitis groups. Three proteins including carbonic anhydrase 6, cystatin C, and cystatin SN were found to be the same as previous study. Salivary proteomic profiles of patients with denture stomatitis were found to be uniquely different from controls. Analysis of protein components suggests that certain salivary proteins may predispose some patients to denture stomatitis while others are believed to be involved in the reaction to fungal infection. Analysis of candidal proteins suggest that multiple species of candidal organisms play a role in denture stomatitis.

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“…In contrast, another group documented GM-CSF production by oral epithelial cells in response to C. glabrata rather than C. albicans . In the same study, oral epithelial cells were more resistant to killing by C. glabrata compared to C. albicans [117]. Clearly, much remains to be learned on the interaction between epithelial cells and NAC species.…”

Section: Cellular Immunity To Candida Species: the First Line Of Defensementioning

confidence: 99%

“…For example, C. albicans , C. tropicalis and C. krusei induced IL-1β production by BMDMs, whereas C. glabrata did not [148]. Similarly, C. albicans but not C. glabrata promoted epithelial cell production of IL-8 and IL-1α [117]. However, several studies suggest that C. glabrata may favor GM-CSF production, as this NAC species induced production of GM-CSF by both epithelial cells and BMDMs in vitro [101, 117].…”

Section: Antifungal Mechanisms: Soluble Factorsmentioning

confidence: 99%

Beyond Candida albicans: Mechanisms of immunity to non-albicans Candida species

Whibley

Gaffen

2015

Cytokine

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The fungal genus Candida encompasses numerous species that inhabit a variety of hosts, either as commensal microbes and/or pathogens. Candida species are a major cause of fungal infections, yet to date there are no vaccines against Candida or indeed any other fungal pathogen. Our knowledge of immunity to Candida mainly comes from studies on C. albicans, the most frequent species associated with disease. However, non-albicans Candida (NAC) species also cause disease and their prevalence is increasing. Although research into immunity to NAC species is still at an early stage, it is becoming apparent that immunity to C. albicans differs in important ways from non-albicans species, with important implications for treatment, therapy and predicted demographic susceptibility. This review will discuss the current understanding of immunity to NAC species in the context of immunity to C. albicans, and highlight as-yet unanswered questions.

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Oral epithelium–Candida glabrata interactions in vitro

Abstract: C. glabrata is less cytotoxic than C. albicans and induces different proinflammatory cytokine responses in oral epithelial cells.

Cited by 26 publications

References 38 publications

Epithelial GM-CSF Induction by Candida glabrata

Epithelial GM-CSF Induction by Candida glabrata

Role of salivary and candidal proteins in denture stomatitis: an exploratory proteomic analysis

Beyond Candida albicans: Mechanisms of immunity to non-albicans Candida species

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