Smoking-aggravated oral candidiasis: Nrf2 pathway dampens NLRP3 inflammasome

被引:6
作者
Osman, Marwan [1 ,2 ]
Papon, Nicolas [3 ]
机构
[1] Lebanese Univ, Doctoral Sch Sci & Technol, Fac Publ Hlth, Lab Microbiol Sante & Environm LMSE, Tripoli, Lebanon
[2] Cornell Univ, Dept Populat Med & Diagnost Sci, Coll Vet Med, Ithaca, NY USA
[3] Univ Angers, Univ Brest, GEIHP, SFR ICAT, F-49000 Angers, France
关键词
Candida albicans; immunity; NLRP3; inflammasome; Nrf2; oxidative stress; smoking; IMMUNITY;
D O I
10.1111/jcmm.16901
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
While cigarette smoke compounds are known to have immunosuppressive effects on the oral mucosa, the relationship between in vivo immune dysfunction caused by smoking and the development of oral Candida infections remains largely unexplored. In a recent issue of The Journal of Cellular and Molecular Medicine, Ye and colleagues provide evidence that smoking increases oral mucosa susceptibility to Candida albicans infection via the activation of the Nrf2 pathway, which in turn negatively regulates the NLRP3 inflammasome. This opens new perspective in considering Nrf2 as a relevant target for smoking-induced C. albicans-related oral diseases.
引用
收藏
页码:9473 / 9475
页数:3
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