Open AccessSmoking increases oral mucosa susceptibility to Candida albicans infection via the Nrf2 pathway: In vitro and animal studies
Author(s) -
Ye Pei,
Chen Wei,
Huang Fan,
Liu Qin,
Zhu YaNan,
Wang Xiang,
Han XiaoDong,
Wang WenMei
Publication year - 2021
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.16724
Subject(s) - candida albicans , oral mucosa , corpus albicans , pathogenesis , immunology , in vitro , medicine , oxidative stress , biology , microbiology and biotechnology , pathology , biochemistry
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 .