Smoking increases oral mucosa susceptibility to Candida albicans infection via the Nrf2 pathway: In vitro and animal studies. Issue 16 (21st June 2021)

• Record Type: Journal Article
• Authors: Ye, Pei; Chen, Wei; Huang, Fan; Liu, Qin; Zhu, Ya‐Nan; Wang, Xiang; Han, Xiao‐Dong; Wang, Wen‐Mei
• Is Part Of: Journal of cellular and molecular medicine. Volume 25:Issue 16(2021)
• Page Start: 7948
• Page End: 7960
• Publication Date: 2021-06-21
• Subjects: Candida albicans -- NLRP3 inflammasome -- Nrf2 -- oral immunity -- oxidative stress -- smoking; Cytology; Medicine; Molecular Biology; Cytologie -- Périodiques; Médecine -- Périodiques; Biologie moléculaire -- Périodiques; Cytology -- Periodicals; Medicine -- Periodicals; Molecular biology -- Periodicals; 611.01805
• DOI: 10.1111/jcmm.16724
• Languages: English
• ISSNs: 1582-1838

Abstract

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 .