scholarly journals Candida albicans: The Ability to Invade Epithelial Cells and Survive under Oxidative Stress Is Unlinked to Hyphal Length

2017 ◽  
Vol 8 ◽  
Author(s):  
Paloma K. Maza ◽  
Alexis Bonfim-Melo ◽  
Ana C. B. Padovan ◽  
Renato A. Mortara ◽  
Cristina M. Orikaza ◽  
...  
2021 ◽  
Vol 9 (11) ◽  
pp. 2348
Author(s):  
Neftaha Tazi ◽  
Xavier Pigeon ◽  
Jérôme Mulamba Mbuyi-Boisvert ◽  
Simon Giret ◽  
François Béland ◽  
...  

The most common use of cannabis is smoking. The oral ecosystem, among other constituents, can be deregulated by the presence of cannabis smoke in the oral cavity. We evaluated the effect of cannabis smoke condensate (CSC) on the behavior of Candida albicans, a common yeast found in the oral cavity. The yeast was first cultured with different concentrations of CSC, and its growth was evaluated. The transition from the blastospore to the hyphal form and the hyphae size were assessed after 3 and 6 h, along with biofilm formation after 72 h of contact with CSC. The response of C. albicans to oxidative (H2O2) stress was also examined. Our results show that CSC contained high amounts of THC (about 1055 ppm), CBN (63 ppm), and CBG (about 47 ppm). The presence of various concentrations of CSC in the culture medium increased C. albicans growth. CSC also contributed to increases in both the hyphal length and biofilm mass. Following oxidative stress (H2O2 at either 100 or 500 μM), CSC prevented the damaging effect of H2O2 on both C. albicans shape and growth. These findings support clinical observations demonstrating that cannabis may promote C. albicans growth and oral candidiasis.


Author(s):  
Humidah Alanazi ◽  
Abdelhabib Semlali ◽  
Witold Chmielewski ◽  
Mahmoud Rouabhia

Electronic cigarette (e-cigarette) vapor comes in contact with the different constituents of the oral cavity, including such microorganisms as Candida albicans. We examined the impact of e-cigarettes on C. albicans growth and expression of different virulent genes, such as secreted aspartic proteases (SAPs), and the effect of e-cigarette vapor-exposed C. albicans on gingival epithelial cell morphology, growth, and lactate dehydrogenase (LDH) activity. An increase in C. albicans growth was observed with nicotine-rich e-cigarettes compared with non-exposed cultures. Following exposure to e-cigarette vapor, C. albicans produced high levels of chitin. E-cigarettes also increased C. albicans hyphal length and the expression of SAP2, SAP3, and SAP9 genes. When in contact with gingival epithelial cells, e-cigarette-exposed C. albicans adhered better to epithelial cells than the control. Indirect contact between e-cigarette-exposed C. albicans and gingival epithelial cells led to epithelial cell differentiation, reduced cell growth, and increased LDH activity. Overall, results indicate that e-cigarettes may interact with C. albicans to promote their pathogenesis, which may increase the risk of oral candidiasis in e-cigarette users.


2015 ◽  
Vol 83 (7) ◽  
pp. 2614-2626 ◽  
Author(s):  
Rohitashw Kumar ◽  
Darpan Saraswat ◽  
Swetha Tati ◽  
Mira Edgerton

Candida albicans, a commensal fungus of the oral microbiome, causes oral candidiasis in humans with localized or systemic immune deficiencies. Secreted aspartic proteinases (Saps) are a family of 10 related proteases and are virulence factors due to their proteolytic activity, as well as their roles in adherence and colonization of host tissues. We found that mice infected sublingually withC. albicanscells overexpressing Sap6 (SAP6OE and a Δsap8strain) had thicker fungal plaques and more severe oral infection, while infection with the Δsap6strain was attenuated. These hypervirulent strains had highly aggregative colony structurein vitroand higher secreted proteinase activity; however, the levels of proteinase activity ofC. albicansSaps did not uniformly match their abilities to damage cultured oral epithelial cells (SCC-15 cells). Hyphal induction in cells overexpressing Sap6 (SAP6OE and Δsap8cells) resulted in formation of large cell-cell aggregates. These aggregates could be produced in germinated wild-type cells by addition of native or heat-inactivated Sap6. Sap6 bound only to germinated cells and increasedC. albicansadhesion to oral epithelial cells. The adhesion properties of Sap6 were lost upon deletion of its integrin-binding motif (RGD) and could be inhibited by addition of RGD peptide or anti-integrin antibodies. Thus, Sap6 (but not Sap5) has an alternative novel function in cell-cell aggregation, independent of its proteinase activity, to promote infection and virulence in oral candidiasis.


2021 ◽  
Vol 7 (7) ◽  
pp. 540
Author(s):  
Ágnes Jakab ◽  
Tamás Emri ◽  
Kinga Csillag ◽  
Anita Szabó ◽  
Fruzsina Nagy ◽  
...  

The glucocorticoid betamethasone (BM) has potent anti-inflammatory and immunosuppressive effects; however, it increases the susceptibility of patients to superficial Candida infections. Previously we found that this disadvantageous side effect can be counteracted by menadione sodium bisulfite (MSB) induced oxidative stress treatment. The fungus specific protein phosphatase Z1 (CaPpz1) has a pivotal role in oxidative stress response of Candida albicans and was proposed as a potential antifungal drug target. The aim of this study was to investigate the combined effects of CaPPZ1 gene deletion and MSB treatment in BM pre-treated C. albicans cultures. We found that the combined treatment increased redox imbalance, enhanced the specific activities of antioxidant enzymes, and reduced the growth in cappz1 mutant (KO) strain. RNASeq data demonstrated that the presence of BM markedly elevated the number of differentially expressed genes in the MSB treated KO cultures. Accumulation of reactive oxygen species, increased iron content and fatty acid oxidation, as well as the inhibiting ergosterol biosynthesis and RNA metabolic processes explain, at least in part, the fungistatic effect caused by the combined stress exposure. We suggest that the synergism between MSB treatment and CaPpz1 inhibition could be considered in developing of a novel combinatorial antifungal strategy accompanying steroid therapy.


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