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

BMC Microbiology

Mahmoud Rouabhia¹  Witold Chmielewski¹  Humidah Alanazi¹  Kerstin Killer¹  Abdelhabib Semlali² 

[1] Groupe de Recherche en Écologie Buccale, Faculté de Médecine Dentaire, Université Laval, 2420 rue de la Terrasse, Québec G1V 0A6, Canada;Genome Research Chair, Department of Biochemistry, College of Science King Saud University, Riyadh, Kingdom of Saudi Arabia

关键词: Sap2;    HWP-1;    EAP-1;    Genes;    Biofilm;    Growth;    Adhesion;    C albicans;    Tobacco;    Cigarette smoke;   

Others  :  1141735
DOI  :  10.1186/1471-2180-14-61

 received in 2013-12-03, accepted in 2014-03-07,  发布年份 2014

【 摘 要 】

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.

【 授权许可】

   
2014 Semlali et al.; licensee BioMed Central Ltd.

【 图 表 】

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