Research Article Cigarette Smoke-Exposed Candida albicans Increased Chitin Production and Modulated Human Fibroblast Cell Responses Humidah Alanazi, 1 Abdelhabib Semlali, 1,2 Laura Perraud, 1 Witold Chmielewski, 1 Andrew Zakrzewski, 1 and Mahmoud Rouabhia 1 1 Groupe de Recherche en ´ Ecologie Buccale, Facult´ e de M´ edecine Dentaire, Universit´ e Laval, 2420 rue de la Terrasse, Qu´ ebec, QC, Canada G1V 0A6 2 Genome Research Chair, Department of Biochemistry, College of Science, King Saud University, Riyadh 12371, Saudi Arabia Correspondence should be addressed to Mahmoud Rouabhia; mahmoud.rouabhia@fmd.ulaval.ca Received 24 July 2014; Revised 29 August 2014; Accepted 29 August 2014; Published 11 September 2014 Academic Editor: John B. Vincent Copyright © 2014 Humidah Alanazi et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Te predisposition of cigarette smokers for development of respiratory and oral bacterial infections is well documented. Cigarette smoke can also contribute to yeast infection. Te aim of this study was to investigate the efect of cigarette smoke condensate (CSC) on C. albicans transition, chitin content, and response to environmental stress and to examine the interaction between CSC- pretreated C. albicans and normal human gingival fbroblasts. Following exposure to CSC, C. albicans transition from blastospore to hyphal form increased. CSC-pretreated yeast cells became signifcantly ( < 0.01) sensitive to oxidation but signifcantly ( < 0.01) resistant to both osmotic and heat stress. CSC-pretreated C. albicans expressed high levels of chitin, with 2- to 8-fold recorded under hyphal conditions. CSC-pretreated C. albicans adhered better to the gingival fbroblasts, proliferated almost three times more and adapted into hyphae, while the gingival fbroblasts recorded a signifcantly ( < 0.01) slow growth rate but a signifcantly higher level of IL-1 when in contact with CSC-pretreated C. albicans. CSC was thus able to modulate both C. albicans transition through the cell wall chitin content and the interaction between C. albicans and normal human gingival fbroblasts. Tese fndings may be relevant to fungal infections in the oral cavity in smokers. 1. Introduction Mucosal candidiasis, especially the oropharyngeal type (OPC), is a common opportunistic infection in both immun- ocompromised and immunocompetent persons [1]. Te lead- ing cause of candidiasis is Candida albicans, a commensal dimorphic yeast that colonizes up to 60% of normally healthy individuals [2]. Symptomatic OPC appears under a num- ber of predisposing conditions [3, 4]. From these, tobacco smoking was considered predisposing to oral candidiasis [5]. Indeed, epidemiological studies in immunocompromised patients have identifed tobacco as a major risk factor for symptomatic infection [6, 7]. Furthermore, the rate of oral candidal carriage in tobacco smokers was reported to be higher in smokers than in nonsmokers [8, 9]. Tis may explain why 98% of Indian villager’s smokers sufer candidal leukoplakia that can be resolved afer cessation of tobacco [10, 11]. Te exact mechanism by which candidal carriage may be afected by tobacco is still to be discovered. Previous studies have demonstrated that smoking leads to innate immune reduction facilitating candida colonization and host infection [12]. Tis may suggest the use of tobacco compounds by C. albicans as nutritional factors, since aromatic hydrocarbons contained in cigarette smoke can be converted by Candida species to carcinogen end products [13]. It has also been reported that C. albicans can catalyze the formation of N-nitrosobenzylmethylamine supporting the high candidal leukoplakia level in smokers [14]. During the development of candidiasis, C. albicans adheres to and invades the tissue [15, 16]. Tis adhesion is promoted by yeast cell wall proteins [17]. Candida cell walls Hindawi Publishing Corporation BioMed Research International Volume 2014, Article ID 963156, 11 pages http://dx.doi.org/10.1155/2014/963156