Enhancement of Candida albicans Virulence After Exposition to Cigarette Mainstream Smoke

Abstract

The habit of cigarette smoking is associated with higher oral candidal carriage and possible predisposition to oral candidosis. The effects of exposure to smoke on the virulence properties of oral yeasts remain obscure. Hence, we showed in vitro the effect of cigarette smoke condensate (CSC) on ten clinical isolates of Candida albicans obtained from nonsmoking volunteers, as well the type-strain CBS562. CSC was generated by complete burn of five commercial cigarettes in an in-house smoking machine and used to prepare the culture broth in which the strains were grown. In 24-h intervals (T(24), T(48), and T(72)), the cells were harvested, washed, subcultured, and the resultant growth were evaluated for possible variations for secreted aspartyl protease, phospholipase, chondroitinase, and hemolysins, adhesion to acrylic and cell surface hydrophobicity (CSH). The results indicated a temporal increase in the secretion rates of enzymes, particularly when yeast cells were exposed to CSC for 48-72 h (P < 0.05). Similarly, adhesion to acrylic and CSH increased with exposure period (P < 0.05). Based on foregoing, we concluded that CSC may promote significant enhance in the secretion of candidal histolytic enzymes and adherence to denture surfaces, thereby promoting oral yeast carriage and possible infection.

Effect of tobacco tar on Staphylococcus aureus and Candida albicans biofilm formation

“…This is due to the growth inhibitory effect of the tobacco tar, while at low concentrations (sub MIC), the amount of adhered bacteria and fungi increased (Tables 4 and 5). The effect of cigarette smoke promoting cell adhesion in a dose dependent manner was previously reported by Baboni et al (2009). The adhesion can be promoted by CSC compounds at certain concentration, but inhibited when these compounds are high explaining the decrease of C. albicans adhesion/biofilm formation at 40 and 50% of CSC.…”

Cigarette Smoke-ExposedCandida albicansIncreased Chitin Production and Modulated Human Fibroblast Cell Responses

“…Exposure to cigarette smoke has also been shown to induce the formation of biofilm by various oral/respiratory pathogens in vitro , including P. gingivalis , S. aureus , S. pneumoniae , Klebsiella pneumonia , and P. aeruginosa , as well as Streptococcus mutans [30–32]. Cigarette smoke was also reported to increase C. albicans adhesion and growth, as well as biofilm formation [33, 34]. These effects were supported by the overexpression of EAP1 , HWP1 , and Sap2 genes known to be active players in C. albicans virulence [34].…”

Rifampicin induced virulence determinants increase Candida albicans biofilm formation

“…It has to be taken into account that a recent report failed to correlate the hydrophobicity of 50 clinical C. albicans isolates with their adhesiveness to polystyrene 35 . Other reports however, have shown hydrophobicity not only to correlate with Candida adhesiveness but to be part of concerted pathogenicity factor expression 23,36 . Fibronectin binding was also strongly increased after rifampicin treatment, showing the induction of an additional trait contributing to increased adherence.…”

“…As coumarin and phenol also upregulated Hsp90 and CDR1, the authors of this study concluded that the response to estrogen might be rather unspecific 21,22 . Cigarette smoke induced the expression of histolytic enzymes and increased candidal adhesion in vitro 23 . Rifampicin, a common antibiotic, induces MDR-1 expression by Candida albicans that in turn can lead to modestly elevated minimal inhibitory concentrations (MIC) for fluconazole by some isolates 24,25 .…”