文献类型：期刊文献

英文题名：Candida albicans promotes tooth decay by inducing oral microbial dysbiosis

作者：Du, Qian[1,2];Ren, Biao[1];He, Jinzhi[1,2];Peng, Xian[1];Guo, Qiang[1];Zheng, Liwei[1,3];Li, Jiyao[1,2];Dai, Huanqin[4];Chen, Vivian[1];Zhang, Lixin[5,6];Zhou, Xuedong[1,2];Xu, Xin[1,2]

机构：[1]Sichuan Univ, West China Hosp Stomatol, Natl Clin Res Ctr Oral Dis, State Key Lab Oral Dis, Chengdu 610041, Peoples R China;[2]Sichuan Univ, West China Hosp Stomatol, Dept Cariol & Endodont, Chengdu 610041, Peoples R China;[3]Sichuan Univ, West China Hosp Stomatol, Dept Pediat Dent, Chengdu 610041, Peoples R China;[4]Chinese Acad Sci, Inst Microbiol, State Key Lab Mycol, Beijing 100101, Peoples R China;[5]Chinese Acad Sci, Inst Microbiol, Key Lab Pathogen Microbiol & Immunol, Beijing 100101, Peoples R China;[6]East China Univ Sci & Technol, State Key Lab Bioreactor Engn, Shanghai 200237, Peoples R China

年份：2021

卷号：15

期号：3

起止页码：894

外文期刊名：ISME JOURNAL

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000585771000003)】；

基金：We greatly thank Professors Williama A. Fonzi, Dominique Sanglard, Aaron P. Mitchell, David Kadosh, Joachim F. Ernst, Gerald R. Fink, Haoping Liu and Lo Hsiu-Jung for kindly providing fungal strains. Vivian Chen is a recipient of a 2017-2018 Fulbright Research grant to China. This work was supported by the National Natural Science Foundation of China (81771099 to XX, 81870754 to XZ, 81600858 to BR, 31720103901 to Lixin Zhang), the "111" Project of China (B18022 to Lixin Zhang), a research grant from the Department of Science & Technology Sichuan Province (2018SZ0121 to XX), and the Fundamental Research Funds for the Central Universities (22221818014S to Lixin Zhang).

语种：英文

摘要：Candida albicans has been detected in root carious lesions. The current study aimed to explore the action of this fungal species on the microbial ecology and the pathogenesis of root caries. Here, by analyzing C. albicans in supragingival dental plaque collected from root carious lesions and sound root surfaces of root-caries subjects as well as caries-free individuals, we observed significantly increased colonization of C. albicans in root carious lesions. Further in vitro and animal studies showed that C. albicans colonization increased the cariogenicity of oral biofilm by altering its microbial ecology, leading to a polymicrobial biofilm with enhanced acidogenicity, and consequently exacerbated tooth demineralization and carious lesion severity. More importantly, we demonstrated that the cariogenicity-promoting activity of C. albicans was dependent on PHR2. Deletion of PHR2 restored microbial equilibrium and led to a less cariogenic biofilm as demonstrated by in vitro artificial caries model or in vivo root-caries rat model. Our data indicate the critical role of C. albicans infection in the occurrence of root caries. PHR2 is the major factor that determines the ecological impact and caries-promoting activity of C. albicans in a mixed microbial consortium.