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Smoking increases oral mucosa susceptibility to Candida albicans infection via the Nrf2 pathway: In vitro and animal studies |
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| Authors: | Pei Ye Wei Chen Fan Huang Qin Liu Ya-Nan Zhu Xiang Wang Xiao-Dong Han Wen-Mei Wang |
| Affiliation: | 1. Nanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing, China Contribution: Data curation (equal), Formal analysis (lead), Methodology (lead), Software (equal), Writing - original draft (lead), Writing - review & editing (lead);2. Nanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China Contribution: Data curation (equal), Investigation (equal), Methodology (equal), Software (equal);3. Nanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China Contribution: Investigation (equal);4. Nanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China Contribution: Funding acquisition (supporting), Investigation (equal);5. Nanjing Stomatological Hospital & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, China |
| Abstract: | Smoking and Candida albicans (C. albicans) infection are risk factors for many oral diseases. Several studies have reported a close relationship between smoking and the occurrence of C. albicans infection. However, the exact underlying mechanism of this relationship remains unclear. We established a rat infection model and a C. albicans-Leuk1 epithelial cell co-culture model with and without smoke exposure to investigate the mechanism by which smoking contributes to C. albicans infection. Oral mucosa samples from healthy individuals and patients with oral leucoplakia were also analysed according to their smoking status. Our results indicated that smoking induced oxidative stress and redox dysfunction in the oral mucosa. Smoking-induced Nrf2 negatively regulated the NLRP3 inflammasome, impaired the oral mucosal defence response and increased the oral mucosa susceptibility to C. albicans. The results suggest that the Nrf2 pathway could be involved in the pathogenesis of oral diseases by mediating an antioxidative response to cigarette smoke exposure and suppressing host immunity against C. albicans. |
| Keywords: | Candida albicans NLRP3 inflammasome Nrf2 oral immunity oxidative stress smoking |