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Background  Smokers are more prone to oral infections than are non-smokers. Cigarette smoke reaches the host cells but also microorganisms present in the oral cavity. The contact between cigarette smoke and oral bacteria promotes such oral diseases as periodontitis. Cigarette smoke can also modulate  C. albicans  activities that promote oral candidiasis. The goal of this study was to investigate the effect of cigarette smoke condensate on  C. albicans  adhesion, growth, and biofilm formation as well as the activation of  EAP1 ,  HWP1  and secreted aspartic protease 2.    Results  Cigarette smoke condensate (CSC) increased  C. albicans  adhesion and growth, as well as biofilm formation. These features may be supported by the activation of certain important genes. Using quantitative RT-PCR, we demonstrated that CSC-exposed  C. albicans  expressed high levels of  EAP1 ,  HWP1  and  SAP2  mRNA and that this gene expression increased with increasing concentrations of CSC.    Conclusion  CSC induction of  C. albicans  adhesion, growth, and biofilm formation may explain the increased persistence of this pathogen in smokers. These findings may also be relevant to other biofilm-induced oral diseases.

Cigarette smoke condensate increases C. albicans adhesion, growth, biofilm formation, and EAP1, HWP1 and SAP2 gene expression