Oxidative stress response and virulence factors in Candida glabrata clinical isolates
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Biofilms growth & development MeSH
- Candida glabrata drug effects isolation & purification pathogenicity physiology MeSH
- Diamide toxicity MeSH
- Virulence Factors metabolism MeSH
- Phospholipases metabolism MeSH
- Stress, Physiological * MeSH
- Hydrophobic and Hydrophilic Interactions MeSH
- Candidiasis microbiology MeSH
- Humans MeSH
- Hospitals, Teaching MeSH
- Oxidative Stress * MeSH
- Oxidants toxicity MeSH
- Hydrogen Peroxide toxicity MeSH
- Peptide Hydrolases metabolism MeSH
- Reactive Oxygen Species metabolism MeSH
- Triazines toxicity MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Geographicals
- Slovakia MeSH
- Names of Substances
- 7-chlorotetrazolo(5,1-c)benzo(1,2,4)triazine MeSH Browser
- Diamide MeSH
- Virulence Factors MeSH
- Phospholipases MeSH
- Oxidants MeSH
- Hydrogen Peroxide MeSH
- Peptide Hydrolases MeSH
- Reactive Oxygen Species MeSH
- Triazines MeSH
We determined the susceptibility to oxidative stress and assessed the four virulence factors of the 38 Candida glabrata clinical isolates originating from two teaching hospitals in Slovakia. All the isolates were susceptible to hydrogen peroxide, diamide, and 7-chlorotetrazolo[5,1-c]benzo[1,2,4]triazine (CTBT) inducing an increased formation of reactive oxygen species in fungal cells. The mean relative cell surface hydrophobicity (CSH) of isolates was 21.9, ranging from 1.92 to 56.96. All isolates showed biofilm formation. A high biofilm formation was observed among 60.5% of isolates. Positive correlations were observed between biofilm formation and moderate values of CSHs. The 76.3% and 84.2% of isolates displayed varying degrees of proteinase and phospholipase activity, respectively. These results demonstrate a differential distribution of factors contributing to virulence of C. glabrata clinical isolates and point to their significance in pathogenesis that would be targeted by novel antifungals.
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Antimicrob Agents Chemother. 1999 Nov;43(11):2753-65 PubMed
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Jpn J Infect Dis. 2007 Sep;60(5):280-3 PubMed
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PLoS Pathog. 2009 Jan;5(1):e1000268 PubMed
Infect Immun. 1985 Oct;50(1):97-101 PubMed
APMIS. 2002 Sep;110(9):601-10 PubMed
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